Subjects -> MEDICAL SCIENCES (Total: 8186 journals)
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    - UROLOGY, NEPHROLOGY AND ANDROLOGY (151 journals)

HEMATOLOGY (160 journals)                     

Showing 1 - 153 of 153 Journals sorted alphabetically
Acta Angiologica     Open Access   (Followers: 3)
Acta Haematologica     Full-text available via subscription   (Followers: 18)
Acta Haematologica Polonica     Open Access  
Adipocyte     Open Access  
Advances in Hematology     Open Access   (Followers: 13)
Africa Sanguine     Full-text available via subscription  
American Journal of Hematology     Hybrid Journal   (Followers: 46)
Anemia     Open Access   (Followers: 6)
Annals of Hematology     Hybrid Journal   (Followers: 14)
Archives of Hematology Case Reports and Reviews     Open Access  
Arteriosclerosis, Thrombosis and Vascular Biology     Full-text available via subscription   (Followers: 25)
Artery Research     Hybrid Journal   (Followers: 4)
Artificial Cells, Nanomedicine and Biotechnology     Hybrid Journal   (Followers: 3)
ASAIO Journal     Hybrid Journal   (Followers: 2)
Best Practice & Research Clinical Haematology     Hybrid Journal   (Followers: 5)
Blood     Hybrid Journal   (Followers: 291)
Blood Advances     Open Access   (Followers: 9)
Blood and Lymphatic Cancer : Targets and Therapy     Open Access   (Followers: 7)
Blood Cancer Journal     Open Access   (Followers: 21)
Blood Cells, Molecules, and Diseases     Hybrid Journal   (Followers: 5)
Blood Coagulation & Fibrinolysis     Hybrid Journal   (Followers: 27)
Blood Pressure     Open Access   (Followers: 1)
Blood Pressure Monitoring     Hybrid Journal   (Followers: 2)
Blood Purification     Full-text available via subscription   (Followers: 5)
Blood Reviews     Hybrid Journal   (Followers: 20)
BMC Hematology     Open Access   (Followers: 6)
BMJ Open Diabetes Research & Care     Open Access   (Followers: 23)
Bone Marrow Transplantation     Hybrid Journal   (Followers: 15)
British Journal of Diabetes & Vascular Disease     Open Access   (Followers: 14)
British Journal of Haematology     Hybrid Journal   (Followers: 54)
British Journal of Primary Care Nursing - Cardiovascular Disease, Diabetes and Kidney Care     Full-text available via subscription   (Followers: 7)
Canadian Journal of Diabetes     Hybrid Journal   (Followers: 9)
Case Reports in Hematology     Open Access   (Followers: 10)
Clinical and Applied Thrombosis/Hemostasis     Open Access   (Followers: 28)
Clinical Diabetes     Full-text available via subscription   (Followers: 30)
Clinical Diabetes and Endocrinology     Open Access   (Followers: 14)
Clinical Lymphoma & Myeloma     Full-text available via subscription   (Followers: 2)
Clinical Lymphoma Myeloma and Leukemia     Hybrid Journal   (Followers: 6)
Conquest : The Official Journal of Diabetes Australia     Full-text available via subscription   (Followers: 1)
Current Angiogenesis     Hybrid Journal   (Followers: 1)
Current Diabetes Reports     Hybrid Journal   (Followers: 14)
Current Diabetes Reviews     Hybrid Journal   (Followers: 13)
Current Hematologic Malignancy Reports     Hybrid Journal   (Followers: 2)
Current Opinion in Hematology     Hybrid Journal   (Followers: 14)
Cytotherapy     Full-text available via subscription   (Followers: 1)
Der Diabetologe     Hybrid Journal  
Diabetes     Full-text available via subscription   (Followers: 257)
Diabetes aktuell     Hybrid Journal   (Followers: 2)
Diabetes and Vascular Disease Research     Hybrid Journal   (Followers: 8)
Diabetes Care     Full-text available via subscription   (Followers: 283)
Diabetes Case Reports     Open Access  
Diabetes Educator     Hybrid Journal   (Followers: 10)
Diabetes Management     Full-text available via subscription   (Followers: 7)
Diabetes Research and Clinical Practice     Hybrid Journal   (Followers: 18)
Diabetes Spectrum     Full-text available via subscription   (Followers: 14)
Diabetes Technology & Therapeutics     Hybrid Journal   (Followers: 8)
Diabetes Therapy     Open Access   (Followers: 13)
Diabetic Foot & Ankle     Open Access   (Followers: 9)
Diabetic Medicine     Hybrid Journal   (Followers: 93)
Diabetologia     Hybrid Journal   (Followers: 107)
Diabetologia Kliniczna     Hybrid Journal  
Diabetologie und Stoffwechsel     Hybrid Journal  
Egyptian Journal of Haematology     Open Access  
Egyptian Journal of Hematology and Bone Marrow Transplantation     Open Access   (Followers: 9)
eJHaem     Open Access   (Followers: 1)
European Journal of Haematology     Hybrid Journal   (Followers: 12)
Experimental Hematology     Hybrid Journal   (Followers: 3)
Experimental Hematology & Oncology     Open Access   (Followers: 6)
Expert Review of Hematology     Hybrid Journal   (Followers: 4)
Fluids and Barriers of the CNS     Open Access   (Followers: 1)
Global Journal of Transfusion Medicine     Open Access   (Followers: 1)
Haematologica - the Hematology journal     Open Access   (Followers: 35)
Haemophilia     Hybrid Journal   (Followers: 15)
Hematologia     Full-text available via subscription   (Followers: 3)
Hematología     Open Access  
Hematology     Open Access   (Followers: 9)
Hematology Reports     Open Access   (Followers: 4)
Hematology, Transfusion and Cell Therapy     Open Access   (Followers: 2)
Hematology/Oncology and Stem Cell Therapy     Open Access   (Followers: 5)
Hemodialysis International     Hybrid Journal   (Followers: 3)
Hepatitis Monthly     Open Access   (Followers: 3)
Immunohematology : Journal of Blood Group Serology and Molecular Genetics     Hybrid Journal   (Followers: 3)
Indian Journal of Hematology and Blood Transfusion     Hybrid Journal   (Followers: 1)
Info Diabetologie     Full-text available via subscription  
InFo Hämatologie + Onkologie : Interdisziplinäre Fortbildung von Ärzten für Ärzte     Full-text available via subscription  
Integrated Blood Pressure Control     Open Access   (Followers: 1)
International Blood Research & Reviews     Open Access  
International Journal of Clinical Transfusion Medicine     Open Access   (Followers: 3)
International Journal of Diabetes in Developing Countries     Hybrid Journal   (Followers: 5)
International Journal of Diabetes Research     Open Access   (Followers: 6)
International Journal of Hematologic Oncology     Open Access   (Followers: 2)
International Journal of Hematology     Hybrid Journal   (Followers: 3)
International Journal of Hematology Research     Open Access   (Followers: 2)
International Journal of Hematology-Oncology and Stem Cell Research     Open Access   (Followers: 2)
International Journal of Laboratory Hematology     Hybrid Journal   (Followers: 24)
Iraqi Journal of Hematology     Open Access  
JMIR Diabetes     Open Access  
Journal of Blood Disorders & Transfusion     Open Access   (Followers: 3)
Journal of Cell Science & Therapy     Open Access   (Followers: 1)
Journal of Applied Hematology     Open Access   (Followers: 2)
Journal of Blood Medicine     Open Access  
Journal of Cerebral Blood Flow & Metabolism     Hybrid Journal   (Followers: 3)
Journal of Diabetes     Open Access   (Followers: 12)
Journal of Diabetes and its Complications     Hybrid Journal   (Followers: 13)
Journal of Diabetes and Metabolic Disorders     Open Access   (Followers: 6)
Journal of Diabetes Investigation     Open Access   (Followers: 6)
Journal of Diabetes Mellitus     Open Access   (Followers: 4)
Journal of Diabetes Research     Open Access   (Followers: 9)
Journal of Diabetes Research     Open Access   (Followers: 4)
Journal of Hematological Malignancies     Open Access  
Journal of Hematology     Open Access   (Followers: 2)
Journal of Hematology and Transfusion Medicine     Open Access   (Followers: 1)
Journal of Hematopathology     Hybrid Journal   (Followers: 3)
Journal of Hypo & Hyperglycemia     Partially Free   (Followers: 1)
Journal of Pediatric Hematology/Oncology     Hybrid Journal   (Followers: 6)
Journal of Social Health and Diabetes     Open Access  
Journal of Thrombosis and Haemostasis     Hybrid Journal   (Followers: 52)
Journal of Thrombosis and Thrombolysis     Hybrid Journal   (Followers: 30)
Journal of Transfusion Medicine     Full-text available via subscription  
Kidney and Blood Pressure Research     Open Access   (Followers: 3)
Leukemia     Hybrid Journal   (Followers: 23)
Leukemia and Lymphoma     Hybrid Journal   (Followers: 13)
Leukemia Research     Hybrid Journal   (Followers: 9)
Leukemia Research Reports     Open Access   (Followers: 1)
Leukemia Supplements     Full-text available via subscription  
Mediterranean Journal of Hematology and Infectious Diseases     Open Access  
Nederlands Tijdschrift voor Diabetologie     Hybrid Journal  
Nutrition & Diabetes     Open Access   (Followers: 18)
Oncohematology     Open Access   (Followers: 1)
Open Diabetes Journal     Open Access  
Open Hematology Journal     Open Access   (Followers: 1)
Open Hypertension Journal     Open Access  
Open Journal of Blood Diseases     Open Access  
Pediatric Blood & Cancer     Hybrid Journal   (Followers: 6)
Pediatric Hematology Oncology Journal     Open Access   (Followers: 3)
Peritoneal Dialysis International     Hybrid Journal  
Plasmatology     Open Access   (Followers: 1)
Platelets     Hybrid Journal   (Followers: 2)
Practical Diabetes     Hybrid Journal   (Followers: 4)
Primary Care Diabetes     Hybrid Journal   (Followers: 16)
Research & Reviews : Journal of Oncology and Hematology     Full-text available via subscription  
Research and Practice in Thrombosis and Haemostasis     Open Access   (Followers: 2)
Revista Cubana de Hematología, Inmunología y Hemoterapia     Open Access  
Seminars in Hematology     Hybrid Journal   (Followers: 9)
Seminars in Thrombosis and Hemostasis     Hybrid Journal   (Followers: 28)
Thalassemia Reports     Open Access   (Followers: 1)
The Lancet Haematology     Full-text available via subscription   (Followers: 43)
Therapeutic Advances in Hematology     Hybrid Journal  
Thrombosis & Haemostasis     Hybrid Journal   (Followers: 106)
Thrombosis Research     Hybrid Journal   (Followers: 30)
Transfusionsmedizin - Immunhämatologie, Hämotherapie, Immungenetik, Zelltherapie     Hybrid Journal  
Transplantation and Cellular Therapy     Hybrid Journal   (Followers: 11)
Veins and Lymphatics     Open Access   (Followers: 1)

           

Similar Journals
Journal Cover
Diabetes
Journal Prestige (SJR): 4.435
Citation Impact (citeScore): 6
Number of Followers: 257  
 
  Full-text available via subscription Subscription journal
ISSN (Print) 0012-1797 - ISSN (Online) 1939-327X
Published by American Diabetes Association Homepage  [4 journals]
  • Comment on Pataky et al. Divergent Skeletal Muscle Metabolomic Signatures
           of Different Exercise Training Modes Independently Predict Cardiometabolic
           Risk Factors. Diabetes 2024;73:23–37

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      Pages: e3 - e3
      Abstract: The recently published article in Diabetes by Pataky et al. (1) delves into the underlying mechanisms of three exercise modalities and their impact on insulin resistance, offering valuable insights into the potential identification of optimal exercises to combat this prevalent health issue. However, while the study presents intriguing findings, I would like to raise some concerns regarding participant characteristics and the study protocol, which I believe warrant further consideration.
      PubDate: Tue, 09 Apr 2024 00:00:00 GMT
      DOI: 10.2337/db24-0033
      Issue No: Vol. 73, No. 6 (2024)
       
  • Response to Comment on Pataky et al. Divergent Skeletal Muscle Metabolomic
           Signatures of Different Exercise Training Modes Independently Predict
           Cardiometabolic Risk Factors. Diabetes 2024;73:23–37

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      Pages: e4 - e5
      Abstract: We appreciate Dr. Astrada’s interest (1) in our recent article (2). Although he raised concern around using BMI as a screening parameter for our study, BMI was not the only defining parameter for screening criteria in our study. Fasting glucose >110 mg/dL was also a critical exclusion criterion for the study, as it limits variation in metabolic characteristics in our study cohort. These and other criteria for participation in the study were reported in the original article (3) from which the samples in our current study (2) were obtained. Furthermore, after participants were screened and included in the study, DEXA scans provide information on body composition, which we reported in the online supplementary material. Within a given age-group, we found no differences in body composition (body fat percentage) between treatment groups at baseline. As for the participants’ daily activities, we did not collect occupation information, but an exclusion criterion for the study was participation in regular exercise (>20 min more than twice per week), which was reported in the original article (3). Thus, none of the participants were regular exercisers, further limiting baseline metabolic variability.
      PubDate: Wed, 20 Mar 2024 00:00:00 GMT
      DOI: 10.2337/dbi24-0017
      Issue No: Vol. 73, No. 6 (2024)
       
  • In This Issue of Diabetes

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      Pages: 821 - 822
      PubDate: Mon, 20 May 2024 00:00:00 GMT
      DOI: 10.2337/db24-ti06
      Issue No: Vol. 73, No. 6 (2024)
       
  • Evidence for C-Peptide as a Validated Surrogate to Predict Clinical
           Benefits in Trials of Disease-Modifying Therapies for Type 1 Diabetes

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      Pages: 823 - 833
      Abstract: Type 1 diabetes is a chronic autoimmune disease in which destruction of pancreatic β-cells causes life-threatening metabolic dysregulation. Numerous approaches are envisioned for new therapies, but limitations of current clinical outcome measures are significant disincentives to development efforts. C-peptide, a direct byproduct of proinsulin processing, is a quantitative biomarker of β-cell function that is not cleared by the liver and can be measured in the peripheral blood. Studies of quantitative measures of β-cell function have established a predictive relationship between stimulated C-peptide as a measure of β-cell function and clinical benefits. C-peptide levels at diagnosis are often high enough to afford glycemic control benefits associated with protection from end-organ complications of diabetes, and even lower levels offer protection from severe hypoglycemia in type 1 diabetes, as observed in large prospective cohort studies and interventional trials of islet transplantation. These observations support consideration of C-peptide not just as a biomarker of β-cell function but also as a specific, sensitive, feasible, and clinically meaningful outcome defining β-cell preservation or restoration for clinical trials of disease-modifying therapies. Regulatory acceptance of C-peptide as a validated surrogate for demonstration of efficacy would greatly facilitate development of disease-modifying therapies for type 1 diabetes.Article HighlightsMixed-meal stimulated C-peptide level has been established as a biomarker of endogenous β-cell function and is used clinically to monitor disease progression in type 1 diabetes.Large prospective cohort studies and interventional trials of islet transplantation demonstrate the relationship between stimulated C-peptide levels and clinical benefits.A recent meta-analysis of interventional clinical trials aimed at preserving β-cell function in those recently diagnosed further supports stimulated C-peptide level as a validated surrogate end point for clinical trials of disease-modifying therapies in type 1 diabetes.
      PubDate: Tue, 13 Feb 2024 00:00:00 GMT
      DOI: 10.2337/dbi23-0012
      Issue No: Vol. 73, No. 6 (2024)
       
  • A Golden Hour and Golden Opportunity for β-Cell Preservation

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      Pages: 834 - 836
      Abstract: Larry M and Leona B Helmsley Charitable TrustRandox LtdU.S. Department of Veterans Affairs Merit AwardI01BX001733Ball Brothers Foundation10.13039/100000989Sigma Beta SororityNational Institute for Health and Care Research (NIHR) Exeter Biomedical Research CentreNational Institute of Diabetes and Digestive and Kidney Diseases10.13039/100000062R01 DK121843-01R01DK093954R01DK127236R01DK127308U01DK127382-01U01DK127786UC4DK104166George and Frances Ball Foundation10.13039/100014159Diabetes UK Harry Keen Fellowship16/0005529JDRF10.13039/1000226902-SRA-2002-1259-S-B2-SRA-2022-1258-M-B2-SRA-2022-1261-S-B3-SRA-2019-827-S-B3-SRA-2022-1241-S-B
      PubDate: Mon, 20 May 2024 00:00:00 GMT
      DOI: 10.2337/dbi24-0019
      Issue No: Vol. 73, No. 6 (2024)
       
  • Insulin Hypersecretion as Promoter of Body Fat Gain and Hyperglycemia

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      Pages: 837 - 843
      Abstract: Graphical Abstract
      PubDate: Mon, 20 May 2024 00:00:00 GMT
      DOI: 10.2337/dbi23-0035
      Issue No: Vol. 73, No. 6 (2024)
       
  • Do We Need a New Hypothesis for K ATP Closure in β-Cells' Distinguishing
           the Baby From the Bathwater

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      Pages: 844 - 848
      Abstract: National Institute of Diabetes and Digestive and Kidney Diseases10.13039/100000062RO1 DK46409U01 DK127747
      PubDate: Fri, 19 Apr 2024 00:00:00 GMT
      DOI: 10.2337/db24-0131
      Issue No: Vol. 73, No. 6 (2024)
       
  • Glucose Regulation of β-Cell K ATP Channels: Is a New Model
           Needed'

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      Pages: 849 - 855
      Abstract: The canonical model of glucose-induced increase in insulin secretion involves the metabolism of glucose via glycolysis and the citrate cycle, resulting in increased ATP synthesis by the respiratory chain and the closure of ATP-sensitive K+ (KATP) channels. The resulting plasma membrane depolarization, followed by Ca2+ influx through L-type Ca2+ channels, then induces insulin granule fusion. Merrins and colleagues have recently proposed an alternative model whereby KATP channels are controlled by pyruvate kinase, using glycolytic and mitochondrial phosphoenolpyruvate (PEP) to generate microdomains of high ATP/ADP immediately adjacent to KATP channels. This model presents several challenges. First, how mitochondrially generated PEP, but not ATP produced abundantly by the mitochondrial F1F0-ATP synthase, can gain access to the proposed microdomains is unclear. Second, ATP/ADP fluctuations imaged immediately beneath the plasma membrane closely resemble those in the bulk cytosol. Third, ADP privation of the respiratory chain at high glucose, suggested to drive alternating, phased-locked generation by mitochondria of ATP or PEP, has yet to be directly demonstrated. Finally, the approaches used to explore these questions may be complicated by off-target effects. We suggest instead that Ca2+ changes, well known to affect both ATP generation and consumption, likely drive cytosolic ATP/ADP oscillations that in turn regulate KATP channels and membrane potential. Thus, it remains to be demonstrated that a new model is required to replace the existing, mitochondrial bioenergetics–based model.
      PubDate: Fri, 19 Apr 2024 00:00:00 GMT
      DOI: 10.2337/dbi23-0031
      Issue No: Vol. 73, No. 6 (2024)
       
  • Glucose Regulation of β-Cell K ATP Channels: It Is Time for a New
           Model!

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      Pages: 856 - 863
      Abstract: An agreed-upon consensus model of glucose-stimulated insulin secretion from healthy β-cells is essential for understanding diabetes pathophysiology. Since the discovery of the KATP channel in 1984, an oxidative phosphorylation (OxPhos)–driven rise in ATP has been assumed to close KATP channels to initiate insulin secretion. This model lacks any evidence, genetic or otherwise, that mitochondria possess the bioenergetics to raise the ATP/ADP ratio to the triggering threshold, and conflicts with genetic evidence demonstrating that OxPhos is dispensable for insulin secretion. It also conflates the stoichiometric yield of OxPhos with thermodynamics, and overestimates OxPhos by failing to account for established features of β-cell metabolism, such as leak, anaplerosis, cataplerosis, and NADPH production that subtract from the efficiency of mitochondrial ATP production. We have proposed an alternative model, based on the spatial and bioenergetic specializations of β-cell metabolism, in which glycolysis initiates insulin secretion. The evidence for this model includes that 1) glycolysis has high control strength over insulin secretion; 2) glycolysis is active at the correct time to explain KATP channel closure; 3) plasma membrane–associated glycolytic enzymes control KATP channels; 4) pyruvate kinase has favorable bioenergetics, relative to OxPhos, for raising ATP/ADP; and 5) OxPhos stalls before membrane depolarization and increases after. Although several key experiments remain to evaluate this model, the 1984 model is based purely on circumstantial evidence and must be rescued by causal, mechanistic experiments if it is to endure.
      PubDate: Fri, 19 Apr 2024 00:00:00 GMT
      DOI: 10.2337/dbi23-0032
      Issue No: Vol. 73, No. 6 (2024)
       
  • Intermittent Fasting–Improved Glucose Homeostasis Is Not Entirely
           Dependent on Caloric Restriction in db/db Male Mice

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      Pages: 864 - 878
      Abstract: Intermittent fasting (IF), which involves prolonged fasting intervals accompanied by caloric restriction (CR), is an effective dietary treatment for obesity and diabetes. Although IF offers many benefits, it is difficult to determine whether these benefits are the consequences of CR. Every-other-day feeding (EODF) is a commonly used IF research model. This study was designed to identify factors, in addition to CR, responsible for the effects of EODF and the possible underlying mechanisms. Diabetic db/db mice were divided into three groups: ad libitum (AL), meal feeding (MF), and EODF. The MF model was used to attain a level of CR comparable to that of EODF, with food distribution evenly divided between 10:00 a.m. and 6:00 p.m., thereby minimizing the fasting interval. EODF yielded greater improvements in glucose homeostasis than MF in db/db mice by reducing fasting glucose levels and enhancing glucose tolerance. However, these effects on glucose metabolism were less pronounced in lean mice. Furthermore, ubiquitination of the liver-specific glucocorticoid (GC) receptor (GR) facilitated its degradation and downregulation of Kruppel-like factor 9 (KLF9), which ultimately suppressed liver gluconeogenesis in diabetic EODF mice. Although GR and KLF9 might mediate the metabolic benefits of EODF, the potential benefits of EODF might be limited by elevated serum GC levels in diabetic EODF mice. Overall, this study suggests that the metabolic benefits of EODF in improving glucose homeostasis are independent of CR, possibly because of the downstream effects of liver-specific GR degradation.Article HighlightsThis study demonstrated that every-other-day feeding (EODF), an intermittent dietary pattern, improved glucose homeostasis in db/db mice, not entirely dependently on calorie restriction.Improvements in glucose metabolism in the EODF group primarily derived from hepatic glucose output suppression mediated by the degradation of liver glucocorticoid (GC) receptor (GR) and Kruppel-like factor 9 as the downstream transcriptional factor.Serum GC levels increased in response to liver GR degradation, whereas GR levels remained unchanged in other metabolic tissues, which can lead to adverse effects associated with high GC levels.
      PubDate: Tue, 19 Mar 2024 00:00:00 GMT
      DOI: 10.2337/db23-0157
      Issue No: Vol. 73, No. 6 (2024)
       
  • CPT1A Protects Podocytes From Lipotoxicity and Apoptosis In Vitro and
           Alleviates Diabetic Nephropathy In Vivo

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      Pages: 879 - 895
      Abstract: Defective fatty acid oxidation (FAO) has been implicated in diabetic kidney disease (DKD), yet little is known about the role of carnitine palmitoyltransferase-1A (CPT1A), a pivotal rate-limiting enzyme of FAO, in the progression of DKD. Here, we investigate whether CPT1A is a reliable therapeutic target for DKD. We first confirmed the downregulation expression of CPT1A in glomeruli from patients with diabetes. We further evaluated the function of CPT1A in diabetic models. Overexpression of CPT1A exhibited protective effects in diabetic conditions, improving albuminuria and glomerular sclerosis as well as mitigating glomerular lipid deposits and podocyte injury in streptozotocin-induced diabetic mice. Mechanistically, CPT1A not only fostered lipid consumption via fatty acid metabolism pathways, thereby reducing lipotoxicity, but also anchored Bcl2 to the mitochondrial membrane, thence preventing cytochrome C release and inhibiting the mitochondrial apoptotic process. Furthermore, a novel transcription factor of CPT1A, FOXA1, was identified. We elucidate the crucial role of CPT1A in mitigating podocyte injury and the progression of DKD, indicating that targeting CPT1A may be a promising avenue for DKD treatment.Article HighlightsFatty acid oxidation has been a critical contributor to podocyte injury and pathological changes in diabetic kidney disease. However, the role of carnitine palmitoyltransferase-1A (CPT1A), which is the initial key rate-limiting enzyme of mitochondrial fatty acid oxidation in diabetic kidney disease, remains largely unknown.We investigate whether CPT1A modulates the progression of diabetic kidney disease.CPT1A ameliorated albuminuria and glomerular sclerosis, and mitigated glomerular lipid deposits and podocyte injury in streptozotocin-induced diabetic mice.Our study reveals a promising avenue for diabetic kidney disease prevention and clarifies a new regulatory mechanism for CPT1A in podocytes.
      PubDate: Wed, 20 Mar 2024 00:00:00 GMT
      DOI: 10.2337/db23-0811
      Issue No: Vol. 73, No. 6 (2024)
       
  • Effect of Dapagliflozin on Renal and Hepatic Glucose Kinetics in T2D and
           NGT Subjects

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      Pages: 896 - 902
      Abstract: Acute and chronic sodium–glucose cotransporter 2 (SGLT-2) inhibition increases endogenous glucose production (EGP). However, the organ—liver versus kidney—responsible for the increase in EGP has not been identified. In this study, 20 subjects with type 2 diabetes (T2D) and 12 subjects with normal glucose tolerance (NGT) received [3-3H]glucose infusion (to measure total EGP) combined with arterial and renal vein catheterization and para-aminohippuric acid infusion for determination of renal blood flow. Total EGP, net renal arteriovenous balance, and renal glucose production were measured before and 4 h after dapagliflozin (DAPA) and placebo administration. Following DAPA, EGP increased in both T2D and NGT from baseline to 240 min, while there was a significant time-related decrease after placebo in T2D. Renal glucose production at baseline was <5% of basal EGP in both groups and did not change significantly following DAPA in NGT or T2D. Renal glucose uptake (sum of tissue glucose uptake plus glucosuria) increased in both T2D and NGT following DAPA (P < 0.05 vs. placebo). The increase in renal glucose uptake was entirely explained by the increase in glucosuria. A single dose of DAPA significantly increased EGP, which primarily is explained by an increase in hepatic glucose production, establishing the existence of a novel renal-hepatic axis.Article HighlightsSodium–glucose cotransporter 2 (SGLT2) inhibitors increase endogenous glucose production (EGP) but the organ—liver versus kidney—responsible for the increase in EGP is unknown.Total EGP ([3-3H]glucose), net renal arteriovenous balance (renal vein catheterization), and renal glucose production were measured in 20 subjects with type 2 diabetes (T2D) and 12 subjects with normal glucose tolerance (NGT) before and 4 h after dapagliflozin and placebo administration.Dapagliflozin increased EGP in both T2D and NGT subjects. All of the increase in EGP was derived from an increase in hepatic glucose output.These results establish the existence of a novel renal-hepatic axis.
      PubDate: Thu, 21 Mar 2024 00:00:00 GMT
      DOI: 10.2337/db23-0457
      Issue No: Vol. 73, No. 6 (2024)
       
  • Metabolic Fluxes in the Renal Cortex Are Dysregulated In Vivo in
           Response to High-Fat Diet

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      Pages: 903 - 908
      Abstract: Diabetes and obesity are risk factors for kidney disease. Whereas renal glucose production increases in diabetes, recent data suggest that gluconeogenic and oxidative capacity decline in kidney disease. Thus, metabolic dysregulation caused by diet-induced insulin resistance may sensitize the kidney for a loss in function. Here, we examined how diet-induced insulin resistance disrupts mitochondrial metabolic fluxes in the renal cortex in vivo. C57BL/6J mice were rendered insulin resistant through high-fat (HF) feeding; anaplerotic, cataplerotic, and oxidative metabolic fluxes in the cortex were quantified through 13C-isotope tracing during a hyperinsulinemic-euglycemic clamp. As expected, HF-fed mice exhibited increased body weight, gluconeogenesis, and systemic insulin resistance compared with chow-fed mice. Relative to the citric acid cycle, HF feeding increased metabolic flux through pyruvate carboxylation (anaplerosis) and phosphoenolpyruvate carboxykinase (cataplerosis) and decreased flux through the pyruvate dehydrogenase complex in the cortex. Furthermore, the relative flux from nonpyruvate sources of acetyl-CoA profoundly increased in the cortex of HF-fed mice, correlating with a marker of oxidative stress. The data demonstrate that HF feeding spares pyruvate from dehydrogenation at the expense of increasing cataplerosis, which may underpin renal gluconeogenesis during insulin resistance; the results also support the hypothesis that dysregulated oxidative metabolism in the kidney contributes to metabolic disease.Article HighlightsDiabetes and obesity are risk factors for kidney disease, yet the impact of diet-induced insulin resistance on renal metabolism is incompletely characterized.In vivo metabolic flux analysis of the renal cortex was performed in mice fed chow or high-fat diet that underwent a hyperinsulinemic-euglycemic clamp.In diet-induced insulin resistance, increased acetyl-CoA flux was derived from nonpyruvate substrates; this switch coincided with increased anaplerosis and accumulation of peroxidized lipid products in the renal cortex.The dysregulation in renal metabolic fluxes observed in diet-induced insulin resistance may instigate oxidative stress that sensitizes the kidney to injury.
      PubDate: Tue, 19 Mar 2024 00:00:00 GMT
      DOI: 10.2337/db23-0710
      Issue No: Vol. 73, No. 6 (2024)
       
  • Inhibition of HSP20 Ameliorates Steatotic Liver Disease by Stimulating
           ERK2-Dependent Autophagy

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      Pages: 909 - 925
      Abstract: HSP20 emerges as a novel regulator of autophagy in the heart. Nonetheless, the detailed function of HSP20 in the liver and its effect on autophagy remain unknown. Here, we observed that HSP20 expression is increased in liver tissues from mice and patients with metabolic dysfunction–associated steatotic liver disease (MASLD), formerly known as nonalcoholic fatty liver disease. Liver-specific downregulation of HSP20 mitigates hepatic steatosis and insulin resistance in obese mice, while upregulating HSP20 promotes lipid deposition and hepatocyte cell death. Mechanistically, liquid chromatography–tandem mass spectrometry revealed that HSP20 interacts with phosphorylated extracellular regulated protein kinase 2 (ERK2) and prevents its dephosphorylation by dual specificity phosphatase 6, leading to ERK2-mediated repression of autophagy and resulting in aggravated saturated fatty acid (SFA)–triggered hepatocyte death. Importantly, such adverse effects could be ameliorated by ERK inhibitor. Our data reveal a framework of how HSP20 increases susceptibility of SFA-induced liver injury through enhancing ERK2 phosphorylation, which represents a plausible therapeutic intervention to combat MASLD.Article HighlightsHSP20 expression was increased in the livers of mice and people living with metabolic dysfunction–associated steatotic liver disease and positively correlated with steatosis grade and body mass.Upregulating HSP20 sensitizes hepatocytes to lipotoxicity by inhibiting autophagy.HSP20 interacts with phosphorylated extracellular regulated protein kinase 2 and prevents its dephosphorylation by phosphatase dual specificity phosphatase 6, leading to aggravation of saturated fatty acid–triggered hepatocyte death by suppressing autophagy function.The HSP20-extracellular regulated protein kinase 2 pathway is an important target to maintain liver homeostasis in patients with metabolic disorders.
      PubDate: Mon, 11 Mar 2024 00:00:00 GMT
      DOI: 10.2337/db23-0688
      Issue No: Vol. 73, No. 6 (2024)
       
  • Gut Microbiota−Tryptophan Metabolism−GLP-1 Axis Participates in
           β-Cell Regeneration Induced by Dapagliflozin

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      Pages: 926 - 940
      Abstract: Sodium–glucose cotransporter 2 inhibitors, efficacious antidiabetic agents that have cardiovascular and renal benefits, can promote pancreatic β-cell regeneration in type 2 diabetic mice. However, the underlying mechanism remains unclear. In this study, we aimed to use multiomics to identify the mediators involved in β-cell regeneration induced by dapagliflozin. We showed that dapagliflozin lowered blood glucose level, upregulated plasma insulin level, and increased islet area in db/db mice. Dapagliflozin reshaped gut microbiota and modulated microbiotic and plasmatic metabolites related to tryptophan metabolism, especially l-tryptophan, in the diabetic mice. Notably, l-tryptophan upregulated the mRNA level of glucagon-like peptide 1 (GLP-1) production–related gene (Gcg and Pcsk1) expression and promoted GLP-1 secretion in cultured mouse intestinal L cells, and it increased the supernatant insulin level in primary human islets, which was eliminated by GPR142 antagonist. Transplant of fecal microbiota from dapagliflozin-treated mice, supplementation of l-tryptophan, or treatment with dapagliflozin upregulated l-tryptophan, GLP-1, and insulin or C-peptide levels and promoted β-cell regeneration in db/db mice. Addition of exendin 9-39, a GLP-1 receptor (GLP-1R) antagonist, or pancreatic Glp1r knockout diminished these beneficial effects. In summary, treatment with dapagliflozin in type 2 diabetic mice promotes β-cell regeneration by upregulating GLP-1 production, which is mediated via gut microbiota and tryptophan metabolism.Article HighlightsSodium–glucose cotransporter 2 inhibitors, novel and efficacious antidiabetic agents, can preserve β-cell mass in type 2 diabetic animals, but the mechanism remains unclear.We find that dapagliflozin reshapes gut microbiota, improves microbiotic and plasmatic metabolites related to tryptophan metabolism, and increases glucagon-like peptide 1 (GLP-1) production mediated via tryptophan metabolism. GLP-1−GLP-1 receptor signaling participates in the dapagliflozin-induced β-cell regeneration.Our study reveals that the gut microbiota–tryptophan metabolism–GLP-1 axis is a novel mechanism of β-cell regeneration induced by dapagliflozin and provides experimental evidence for its β-cell protection in treating type 2 diabetes.
      PubDate: Tue, 12 Mar 2024 00:00:00 GMT
      DOI: 10.2337/db23-0553
      Issue No: Vol. 73, No. 6 (2024)
       
  • Comparison of β-Cell Function and Insulin Sensitivity Between
           Normal-Weight and Obese Chinese With Young-Onset Type 2 Diabetes

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      Pages: 953 - 963
      Abstract: Normal-weight individuals with usual-onset type 2 diabetes have reduced β-cell function and greater insulin sensitivity compared with their obese counterparts. The relative contribution of β-cell dysfunction and insulin resistance to young-onset type 2 diabetes (YOD) among normal-weight individuals is not well established. In 44 individuals with YOD (24 with normal weight and 20 with obesity) and 24 healthy control individuals with normoglycemia (12 with normal weight and 12 with obesity), we conducted 2-h 12 mmol/L hyperglycemic clamps to measure acute (0–10 min) and steady-state (100–120 min) insulin and C-peptide responses, as well as insulin sensitivity index. Normal-weight individuals with YOD had lower acute insulin response, steady-state insulin and C-peptide responses, and a higher insulin sensitivity index compared with their obese counterparts with YOD. Compared with BMI-matched healthy control individuals, normal-weight individuals with YOD had lower acute and steady-state insulin and C-peptide responses but a similar insulin sensitivity index. The impairment of steady-state β-cell response relative to healthy control individuals was more pronounced in normal-weight versus obese individuals with YOD. In conclusion, normal-weight Chinese with YOD exhibited worse β-cell function but preserved insulin sensitivity relative to obese individuals with YOD and BMI-matched healthy individuals with normoglycemia. The selection of glucose-lowering therapy should account for pathophysiological differences underlying YOD between normal-weight and obese individuals.Article HighlightsThe metabolic architecture of normal-weight young-onset type 2 diabetes (YOD) remains unclear.We investigated the relative contribution of β-cell dysfunction and insulin resistance to normal-weight YOD.Normal-weight individuals with YOD had worse β-cell responses and preserved insulin sensitivity than obese counterparts with YOD and normal-weight healthy control individuals.Our results confirm the pivotal role of β-cell defects in normal-weight YOD and emphasize the importance of preserving β-cell function in this group.
      PubDate: Wed, 20 Mar 2024 00:00:00 GMT
      DOI: 10.2337/db23-0966
      Issue No: Vol. 73, No. 6 (2024)
       
  • Adiponectin Reduces Glomerular Endothelial Glycocalyx Disruption and
           Restores Glomerular Barrier Function in a Mouse Model of Type 2 Diabetes

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      Pages: 964 - 976
      Abstract: Adiponectin has vascular anti-inflammatory and protective effects. Although adiponectin protects against the development of albuminuria, historically, the focus has been on podocyte protection within the glomerular filtration barrier (GFB). The first barrier to albumin in the GFB is the endothelial glycocalyx (eGlx), a surface gel-like barrier covering glomerular endothelial cells (GEnCs). In diabetes, eGlx dysfunction occurs before podocyte damage; hence, we hypothesized that adiponectin could protect from eGlx damage to prevent early vascular damage in diabetic kidney disease (DKD). Globular adiponectin (gAd) activated AMPK signaling in human GEnCs through AdipoR1. It significantly reduced eGlx shedding and the tumor necrosis factor-α (TNF-α)–mediated increase in syndecan-4 (SDC4) and MMP2 mRNA expression in GEnCs in vitro. It protected against increased TNF-α mRNA expression in glomeruli isolated from db/db mice and against expression of genes associated with glycocalyx shedding (namely, SDC4, MMP2, and MMP9). In addition, gAd protected against increased glomerular albumin permeability (Ps’alb) in glomeruli isolated from db/db mice when administered intraperitoneally and when applied directly to glomeruli (ex vivo). Ps’alb was inversely correlated with eGlx depth in vivo. In summary, adiponectin restored eGlx depth, which was correlated with improved glomerular barrier function, in diabetes.Article HighlightsAdiponectin protects against diabetic kidney disease (DKD). Understanding its role on glomerular endothelial barrier properties should help formulate a strategic therapeutic approach.This study shows adiponectin protects against endothelial glycocalyx shedding and restores albumin permeability in experimental diabetes.Activation of the glomerular endothelial cell adiponectin signaling pathway may be an early treatment strategy for patients with diabetes who are at risk of DKD.
      PubDate: Tue, 26 Mar 2024 00:00:00 GMT
      DOI: 10.2337/db23-0455
      Issue No: Vol. 73, No. 6 (2024)
       
  • Risk of Diabetic Retinopathy According to Subtype of Type 2 Diabetes

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      Pages: 977 - 982
      Abstract: Type 2 diabetes is a heterogeneous disease that can be subdivided on the basis of β-cell function and insulin sensitivity. We investigated the presence, incidence, and progression of diabetic retinopathy (DR) according to subtypes of type 2 diabetes. In a national cohort, we identified three subtypes of type 2 diabetes: classical, hyperinsulinemic, and insulinopenic type 2 diabetes, based on HOMA2 measurements. From the Danish Registry of Diabetic Retinopathy we extracted information on level of DR. We used several national health registries to link information on comorbidity, medications, and laboratory tests. We found individuals with hyperinsulinemic type 2 diabetes were less likely to have DR at entry date compared with those with classical type 2 diabetes, whereas individuals with insulinopenic type 2 diabetes were more likely to have DR. In multivariable Cox regression analysis, individuals with hyperinsulinemic type 2 diabetes had a decreased risk of both incidence and progression of DR compared to those with classical type 2 diabetes. We did not find any clear difference in risk of incident or progression of DR in individuals with insulinopenic compared to classical type 2 diabetes. These findings indicate that subcategorization of type 2 diabetes is important in evaluating the risk of DR.Article HighlightsType 2 diabetes can be subcategorized on the basis of β-cell function and insulin sensitivity, but little is known about the association of subtypes of type 2 diabetes with risk of diabetic retinopathy (DR).Do individuals with hyperinsulinemic or insulinopenic type 2 diabetes have an increased risk of DR compared with individuals with classical type 2 diabetes'Individuals with hyperinsulinemic type 2 diabetes had almost half the risk of prevalent or incident DR or progression of DR compared with individuals with classical type 2 diabetes.These results suggest that more individualized screening intervals for DR may be possible within subgroups of type 2 diabetes.
      PubDate: Mon, 18 Mar 2024 00:00:00 GMT
      DOI: 10.2337/db24-0016
      Issue No: Vol. 73, No. 6 (2024)
       
  • Genetic Evidence of Causal Relation Between Intestinal Glucose Absorption
           and Early Postprandial Glucose Response: A Mendelian Randomization Study

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      Pages: 983 - 992
      Abstract: The postprandial glucose response is an independent risk factor for type 2 diabetes. Observationally, early glucose response after an oral glucose challenge has been linked to intestinal glucose absorption, largely influenced by the expression of sodium–glucose cotransporter 1 (SGLT1). This study uses Mendelian randomization (MR) to estimate the causal effect of intestinal SGLT1 expression on early glucose response. Involving 1,547 subjects with class II/III obesity from the Atlas Biologique de l’Obésité Sévère cohort, the study uses SGLT1 genotyping, oral glucose tolerance tests, and jejunal biopsies to measure SGLT1 expression. A loss-of-function SGLT1 haplotype serves as the instrumental variable, with intestinal SGLT1 expression as the exposure and the change in 30-min postload glycemia from fasting glycemia (Δ30 glucose) as the outcome. Results show that 12.8% of the 1,342 genotyped patients carried the SGLT1 loss-of-function haplotype, associated with a mean Δ30 glucose reduction of −0.41 mmol/L and a significant decrease in intestinal SGLT1 expression. The observational study links a 1-SD decrease in SGLT1 expression to a Δ30 glucose reduction of −0.097 mmol/L. MR analysis parallels these findings, associating a statistically significant reduction in genetically instrumented intestinal SGLT1 expression with a Δ30 glucose decrease of −0.353. In conclusion, the MR analysis provides genetic evidence that reducing intestinal SGLT1 expression causally lowers early postload glucose response. This finding has a potential translational impact on managing early glucose response to prevent or treat type 2 diabetesArticle HighlightsLoss-of-function variant of SGLT1 is associated with reduced intestinal SGLT1 expression and early postload glucose response.Mendelian randomization supports the causal relationship between intestinal glucose absorption and postprandial glucose.Modulating intestinal SGLT1 expression/function is a promising avenue for the prevention and treatment of type 2 diabetes.
      PubDate: Mon, 18 Mar 2024 00:00:00 GMT
      DOI: 10.2337/db23-0805
      Issue No: Vol. 73, No. 6 (2024)
       
  • Polygenic Risk for Type 2 Diabetes in African Americans

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      Pages: 993 - 1001
      Abstract: African Americans (AAs) have been underrepresented in polygenic risk score (PRS) studies. Here, we integrated genome-wide data from multiple observational studies on type 2 diabetes (T2D), encompassing a total of 101,987 AAs, to train and optimize an AA-focused T2D PRS (PRSAA), using a Bayesian polygenic modeling method. We further tested the score in three independent studies with a total of 7,275 AAs and compared the PRSAA with other published scores. Results show that a 1-SD increase in the PRSAA was associated with 40–60% increase in the odds of T2D (odds ratio [OR] 1.60, 95% CI 1.37–1.88; OR 1.40, 95% CI 1.16–1.70; and OR 1.45, 95% CI 1.30–1.62) across three testing cohorts. These models captured 1.0–2.6% of the variance (R2) in T2D on the liability scale. The positive predictive values for three calculated score thresholds (the top 2%, 5%, and 10%) ranged from 14 to 35%. The PRSAA, in general, performed similarly to existing T2D PRS. The need remains for larger data sets to continue to evaluate the utility of within-ancestry scores in the AA population.Article HighlightsThis study aimed to better understand the performance of existing and a novel polygenic risk scores (PRS) for type 2 diabetes in African American (AA) populations.A PRS was developed using only genetic data from AA populations (PRSAA) and compared with scores developed using genetic data from other ancestral populations.The performance metrics of the PRSAA were comparable to a published multiancestry PRS developed using training data from much larger study samples.The utility of single-ancestry PRS in AAs should be reevaluated when larger AA training data sets are available.
      PubDate: Tue, 12 Mar 2024 00:00:00 GMT
      DOI: 10.2337/db23-0232
      Issue No: Vol. 73, No. 6 (2024)
       
  • Epistasis Between HLA-DRB1*16:02:01 and SLC16A11 T-C-G-T-T Reduces Odds
           for Type 2 Diabetes in Southwest American Indians

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      Pages: 1002 - 1011
      Abstract: We sought to identify genetic/immunologic contributors of type 2 diabetes (T2D) in an indigenous American community by genotyping all study participants for both high-resolution HLA-DRB1 alleles and SLC16A11 to test their risk and/or protection for T2D. These genes were selected based on independent reports that HLA-DRB1*16:02:01 is protective for T2D and that SLC16A11 associates with T2D in individuals with BMI <35 kg/m2. Here, we test the interaction of the two loci with a more complete data set and perform a BMI sensitivity test. We defined the risk protection haplotype of SLC16A11, T-C-G-T-T, as allele 2 of a diallelic genetic model with three genotypes, SLC16A11*11, *12, and *22, where allele 1 is the wild type. Both earlier findings were confirmed. Together in the same logistic model with BMI ≥35 kg/m2, DRB1*16:02:01 remains protective (odds ratio [OR] 0.73), while SLC16A11 switches from risk to protection (OR 0.57 [*22] and 0.78 [*12]); an added interaction term was statistically significant (OR 0.49 [*12]). Bootstrapped (b = 10,000) statistical power of interaction, 0.4801, yielded a mean OR of 0.43. Sensitivity analysis demonstrated that the interaction is significant in the BMI range of 30–41 kg/m2. To investigate the epistasis, we used the primary function of the HLA-DRB1 molecule, peptide binding and presentation, to search the entire array of 15-mer peptides for both the wild-type and ancient human SLC16A11 molecules for a pattern of strong binding that was associated with risk and protection for T2D. Applying computer binding algorithms suggested that the core peptide at SLC16A11 D127G, FSAFASGLL, might be key for moderating risk for T2D with potential implications for type 1 diabetes.Article HighlightsThis study enlarged our sample of high-resolution HLA-DRB1 alleles and 5 individually typed mutations for the SLC16A11 locus and used these to test for protection, risk, and interaction for type 2 diabetes.We confirmed our earlier reports of protection (DRB1*16:02) and risk (SLC16A11) and used all genotypes in a sensitivity analysis for BMI.HLA-DRB1*16:02 was found to be protective, and sensitivity analysis demonstrated that SLC16A11 is a risk in lower BMI strata and protective in higher ones.Epistasis for individuals with DRB1*16:02 and T-C-G-T-T reduces the odds for type 2 diabetes in a BMI range of 30–41 kg/m2, and binding studies implicate core peptide FSAFASGLL.
      PubDate: Tue, 26 Mar 2024 00:00:00 GMT
      DOI: 10.2337/db23-0925
      Issue No: Vol. 73, No. 6 (2024)
       
  • Genetic Evidence for Distinct Biological Mechanisms That Link Adiposity to
           Type 2 Diabetes: Toward Precision Medicine

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      Pages: 1012 - 1025
      Abstract: We aimed to unravel the mechanisms connecting adiposity to type 2 diabetes. We used MR-Clust to cluster independent genetic variants associated with body fat percentage (388 variants) and BMI (540 variants) based on their impact on type 2 diabetes. We identified five clusters of adiposity-increasing alleles associated with higher type 2 diabetes risk (unfavorable adiposity) and three clusters associated with lower risk (favorable adiposity). We then characterized each cluster based on various biomarkers, metabolites, and MRI-based measures of fat distribution and muscle quality. Analyzing the metabolic signatures of these clusters revealed two primary mechanisms connecting higher adiposity to reduced type 2 diabetes risk. The first involves higher adiposity in subcutaneous tissues (abdomen and thigh), lower liver fat, improved insulin sensitivity, and decreased risk of cardiometabolic diseases and diabetes complications. The second mechanism is characterized by increased body size and enhanced muscle quality, with no impact on cardiometabolic outcomes. Furthermore, our findings unveil diverse mechanisms linking higher adiposity to higher disease risk, such as cholesterol pathways or inflammation. These results reinforce the existence of adiposity-related mechanisms that may act as protective factors against type 2 diabetes and its complications, especially when accompanied by reduced ectopic liver fat.Article HighlightsThe relationship between excess adiposity and type 2 diabetes is complex.Can genetic subtypes of adiposity reveal distinct pathways linking adiposity with type 2 diabetes'Higher adiposity increases type 2 diabetes risk via different mechanisms (e.g., cholesterol pathways or inflammation) but decreases risk via other mechanisms (lower liver fat and improved insulin sensitivity, or increased body size and enhanced muscle quality).These insights could improve precision medicine for type 2 diabetes via treating adiposity.
      PubDate: Tue, 26 Mar 2024 00:00:00 GMT
      DOI: 10.2337/db23-1005
      Issue No: Vol. 73, No. 6 (2024)
       
  • Issues and Events

    • Free pre-print version: Loading...

      Pages: 1026 - 1026
      PubDate: Mon, 20 May 2024 00:00:00 GMT
      DOI: 10.2337/db24-ie06
      Issue No: Vol. 73, No. 6 (2024)
       
  • Alterations in Adipose Tissue Distribution, Cell Morphology, and Function
           Mark Primary Insulin Hypersecretion in Youth With Obesity

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      Pages: 941 - 952
      Abstract: Excessive insulin secretion independent of insulin resistance, defined as primary hypersecretion, is associated with obesity and an unfavorable metabolic phenotype. We examined the characteristics of adipose tissue of youth with primary insulin hypersecretion and the longitudinal metabolic alterations influenced by the complex adipo-insular interplay. In a multiethnic cohort of adolescents with obesity but without diabetes, primary insulin hypersecretors had enhanced model-derived β-cell glucose sensitivity and rate sensitivity but worse glucose tolerance, despite similar demographics, adiposity, and insulin resistance measured by both oral glucose tolerance test and euglycemic-hyperinsulinemic clamp. Hypersecretors had greater intrahepatic and visceral fat depots at abdominal MRI, hypertrophic abdominal subcutaneous adipocytes, higher free fatty acid and leptin serum levels per fat mass, and faster in vivo lipid turnover assessed by a long-term 2H2O labeling protocol. At 2-year follow-up, hypersecretors had greater fat accrual and a threefold higher risk for abnormal glucose tolerance, while individuals with hypertrophic adipocytes or higher leptin levels showed enhanced β-cell glucose sensitivity. Primary insulin hypersecretion is associated with marked alterations in adipose tissue distribution, cellularity, and lipid dynamics, independent of whole-body adiposity and insulin resistance. Pathogenetic insight into the metabolic crosstalk between β-cell and adipocyte may help to identify individuals at risk for chronic hyperinsulinemia, body weight gain, and glucose intolerance.Article HighlightsExcessive insulin secretion independent of insulin resistance, named primary hypersecretion, has been associated with obesity and glucose intolerance.We examined whether early alterations in adipose tissue phenotype and function are linked to primary insulin hypersecretion in a complex interplay influencing glucose tolerance, β-cell function, and adiposity.In adolescents with obesity, insulin hypersecretors have greater ectopic fat depots, hypertrophic adipocytes, higher leptin and free fatty acid levels per fat mass, and greater lipid turnover than normosecretors.Hypertrophic adipocytes and hyperleptinemia predict short-term increases in β-cell glucose sensitivity, while the hypersecretory phenotype identifies individuals at risk of glucose intolerance and accruing adiposity over time.
      PubDate: Mon, 23 Oct 2023 00:00:00 GMT
      DOI: 10.2337/db23-0450
      Issue No: Vol. 73, No. 6 (2023)
       
 
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  Subjects -> MEDICAL SCIENCES (Total: 8186 journals)
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HEMATOLOGY (160 journals)                     

Showing 1 - 153 of 153 Journals sorted alphabetically
Acta Angiologica     Open Access   (Followers: 3)
Acta Haematologica     Full-text available via subscription   (Followers: 18)
Acta Haematologica Polonica     Open Access  
Adipocyte     Open Access  
Advances in Hematology     Open Access   (Followers: 13)
Africa Sanguine     Full-text available via subscription  
American Journal of Hematology     Hybrid Journal   (Followers: 46)
Anemia     Open Access   (Followers: 6)
Annals of Hematology     Hybrid Journal   (Followers: 14)
Archives of Hematology Case Reports and Reviews     Open Access  
Arteriosclerosis, Thrombosis and Vascular Biology     Full-text available via subscription   (Followers: 25)
Artery Research     Hybrid Journal   (Followers: 4)
Artificial Cells, Nanomedicine and Biotechnology     Hybrid Journal   (Followers: 3)
ASAIO Journal     Hybrid Journal   (Followers: 2)
Best Practice & Research Clinical Haematology     Hybrid Journal   (Followers: 5)
Blood     Hybrid Journal   (Followers: 291)
Blood Advances     Open Access   (Followers: 9)
Blood and Lymphatic Cancer : Targets and Therapy     Open Access   (Followers: 7)
Blood Cancer Journal     Open Access   (Followers: 21)
Blood Cells, Molecules, and Diseases     Hybrid Journal   (Followers: 5)
Blood Coagulation & Fibrinolysis     Hybrid Journal   (Followers: 27)
Blood Pressure     Open Access   (Followers: 1)
Blood Pressure Monitoring     Hybrid Journal   (Followers: 2)
Blood Purification     Full-text available via subscription   (Followers: 5)
Blood Reviews     Hybrid Journal   (Followers: 20)
BMC Hematology     Open Access   (Followers: 6)
BMJ Open Diabetes Research & Care     Open Access   (Followers: 23)
Bone Marrow Transplantation     Hybrid Journal   (Followers: 15)
British Journal of Diabetes & Vascular Disease     Open Access   (Followers: 14)
British Journal of Haematology     Hybrid Journal   (Followers: 54)
British Journal of Primary Care Nursing - Cardiovascular Disease, Diabetes and Kidney Care     Full-text available via subscription   (Followers: 7)
Canadian Journal of Diabetes     Hybrid Journal   (Followers: 9)
Case Reports in Hematology     Open Access   (Followers: 10)
Clinical and Applied Thrombosis/Hemostasis     Open Access   (Followers: 28)
Clinical Diabetes     Full-text available via subscription   (Followers: 30)
Clinical Diabetes and Endocrinology     Open Access   (Followers: 14)
Clinical Lymphoma & Myeloma     Full-text available via subscription   (Followers: 2)
Clinical Lymphoma Myeloma and Leukemia     Hybrid Journal   (Followers: 6)
Conquest : The Official Journal of Diabetes Australia     Full-text available via subscription   (Followers: 1)
Current Angiogenesis     Hybrid Journal   (Followers: 1)
Current Diabetes Reports     Hybrid Journal   (Followers: 14)
Current Diabetes Reviews     Hybrid Journal   (Followers: 13)
Current Hematologic Malignancy Reports     Hybrid Journal   (Followers: 2)
Current Opinion in Hematology     Hybrid Journal   (Followers: 14)
Cytotherapy     Full-text available via subscription   (Followers: 1)
Der Diabetologe     Hybrid Journal  
Diabetes     Full-text available via subscription   (Followers: 257)
Diabetes aktuell     Hybrid Journal   (Followers: 2)
Diabetes and Vascular Disease Research     Hybrid Journal   (Followers: 8)
Diabetes Care     Full-text available via subscription   (Followers: 283)
Diabetes Case Reports     Open Access  
Diabetes Educator     Hybrid Journal   (Followers: 10)
Diabetes Management     Full-text available via subscription   (Followers: 7)
Diabetes Research and Clinical Practice     Hybrid Journal   (Followers: 18)
Diabetes Spectrum     Full-text available via subscription   (Followers: 14)
Diabetes Technology & Therapeutics     Hybrid Journal   (Followers: 8)
Diabetes Therapy     Open Access   (Followers: 13)
Diabetic Foot & Ankle     Open Access   (Followers: 9)
Diabetic Medicine     Hybrid Journal   (Followers: 93)
Diabetologia     Hybrid Journal   (Followers: 107)
Diabetologia Kliniczna     Hybrid Journal  
Diabetologie und Stoffwechsel     Hybrid Journal  
Egyptian Journal of Haematology     Open Access  
Egyptian Journal of Hematology and Bone Marrow Transplantation     Open Access   (Followers: 9)
eJHaem     Open Access   (Followers: 1)
European Journal of Haematology     Hybrid Journal   (Followers: 12)
Experimental Hematology     Hybrid Journal   (Followers: 3)
Experimental Hematology & Oncology     Open Access   (Followers: 6)
Expert Review of Hematology     Hybrid Journal   (Followers: 4)
Fluids and Barriers of the CNS     Open Access   (Followers: 1)
Global Journal of Transfusion Medicine     Open Access   (Followers: 1)
Haematologica - the Hematology journal     Open Access   (Followers: 35)
Haemophilia     Hybrid Journal   (Followers: 15)
Hematologia     Full-text available via subscription   (Followers: 3)
Hematología     Open Access  
Hematology     Open Access   (Followers: 9)
Hematology Reports     Open Access   (Followers: 4)
Hematology, Transfusion and Cell Therapy     Open Access   (Followers: 2)
Hematology/Oncology and Stem Cell Therapy     Open Access   (Followers: 5)
Hemodialysis International     Hybrid Journal   (Followers: 3)
Hepatitis Monthly     Open Access   (Followers: 3)
Immunohematology : Journal of Blood Group Serology and Molecular Genetics     Hybrid Journal   (Followers: 3)
Indian Journal of Hematology and Blood Transfusion     Hybrid Journal   (Followers: 1)
Info Diabetologie     Full-text available via subscription  
InFo Hämatologie + Onkologie : Interdisziplinäre Fortbildung von Ärzten für Ärzte     Full-text available via subscription  
Integrated Blood Pressure Control     Open Access   (Followers: 1)
International Blood Research & Reviews     Open Access  
International Journal of Clinical Transfusion Medicine     Open Access   (Followers: 3)
International Journal of Diabetes in Developing Countries     Hybrid Journal   (Followers: 5)
International Journal of Diabetes Research     Open Access   (Followers: 6)
International Journal of Hematologic Oncology     Open Access   (Followers: 2)
International Journal of Hematology     Hybrid Journal   (Followers: 3)
International Journal of Hematology Research     Open Access   (Followers: 2)
International Journal of Hematology-Oncology and Stem Cell Research     Open Access   (Followers: 2)
International Journal of Laboratory Hematology     Hybrid Journal   (Followers: 24)
Iraqi Journal of Hematology     Open Access  
JMIR Diabetes     Open Access  
Journal of Blood Disorders & Transfusion     Open Access   (Followers: 3)
Journal of Cell Science & Therapy     Open Access   (Followers: 1)
Journal of Applied Hematology     Open Access   (Followers: 2)
Journal of Blood Medicine     Open Access  
Journal of Cerebral Blood Flow & Metabolism     Hybrid Journal   (Followers: 3)
Journal of Diabetes     Open Access   (Followers: 12)
Journal of Diabetes and its Complications     Hybrid Journal   (Followers: 13)
Journal of Diabetes and Metabolic Disorders     Open Access   (Followers: 6)
Journal of Diabetes Investigation     Open Access   (Followers: 6)
Journal of Diabetes Mellitus     Open Access   (Followers: 4)
Journal of Diabetes Research     Open Access   (Followers: 9)
Journal of Diabetes Research     Open Access   (Followers: 4)
Journal of Hematological Malignancies     Open Access  
Journal of Hematology     Open Access   (Followers: 2)
Journal of Hematology and Transfusion Medicine     Open Access   (Followers: 1)
Journal of Hematopathology     Hybrid Journal   (Followers: 3)
Journal of Hypo & Hyperglycemia     Partially Free   (Followers: 1)
Journal of Pediatric Hematology/Oncology     Hybrid Journal   (Followers: 6)
Journal of Social Health and Diabetes     Open Access  
Journal of Thrombosis and Haemostasis     Hybrid Journal   (Followers: 52)
Journal of Thrombosis and Thrombolysis     Hybrid Journal   (Followers: 30)
Journal of Transfusion Medicine     Full-text available via subscription  
Kidney and Blood Pressure Research     Open Access   (Followers: 3)
Leukemia     Hybrid Journal   (Followers: 23)
Leukemia and Lymphoma     Hybrid Journal   (Followers: 13)
Leukemia Research     Hybrid Journal   (Followers: 9)
Leukemia Research Reports     Open Access   (Followers: 1)
Leukemia Supplements     Full-text available via subscription  
Mediterranean Journal of Hematology and Infectious Diseases     Open Access  
Nederlands Tijdschrift voor Diabetologie     Hybrid Journal  
Nutrition & Diabetes     Open Access   (Followers: 18)
Oncohematology     Open Access   (Followers: 1)
Open Diabetes Journal     Open Access  
Open Hematology Journal     Open Access   (Followers: 1)
Open Hypertension Journal     Open Access  
Open Journal of Blood Diseases     Open Access  
Pediatric Blood & Cancer     Hybrid Journal   (Followers: 6)
Pediatric Hematology Oncology Journal     Open Access   (Followers: 3)
Peritoneal Dialysis International     Hybrid Journal  
Plasmatology     Open Access   (Followers: 1)
Platelets     Hybrid Journal   (Followers: 2)
Practical Diabetes     Hybrid Journal   (Followers: 4)
Primary Care Diabetes     Hybrid Journal   (Followers: 16)
Research & Reviews : Journal of Oncology and Hematology     Full-text available via subscription  
Research and Practice in Thrombosis and Haemostasis     Open Access   (Followers: 2)
Revista Cubana de Hematología, Inmunología y Hemoterapia     Open Access  
Seminars in Hematology     Hybrid Journal   (Followers: 9)
Seminars in Thrombosis and Hemostasis     Hybrid Journal   (Followers: 28)
Thalassemia Reports     Open Access   (Followers: 1)
The Lancet Haematology     Full-text available via subscription   (Followers: 43)
Therapeutic Advances in Hematology     Hybrid Journal  
Thrombosis & Haemostasis     Hybrid Journal   (Followers: 106)
Thrombosis Research     Hybrid Journal   (Followers: 30)
Transfusionsmedizin - Immunhämatologie, Hämotherapie, Immungenetik, Zelltherapie     Hybrid Journal  
Transplantation and Cellular Therapy     Hybrid Journal   (Followers: 11)
Veins and Lymphatics     Open Access   (Followers: 1)

           

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