Context: Excess hepatic and pancreatic fat may contribute to hyperglycemia.
Objective: The objective of this study was to examine the effect of dapagliflozin (an SGLT2 inhibitor) on anthropometric profile, liver, and pancreatic fat in patients with type 2 diabetes mellitus (T2DM).
Methods: This is an observational interventional paired study design without a control group. Patients (n = 30) were given dapagliflozin 10 mg/day (on top of stable dose of metformin and/or sulfonylureas) for 120 days. Changes in anthropometry (circumferences and skinfold thickness), surrogate markers of insulin resistance, body composition, liver, and pancreatic fat (as measured by magnetic resonance imaging (MRI)-derived proton density fat fraction [FF]) were evaluated.
Results: After 120 days of treatment with dapagliflozin, a statistically significant reduction in weight, body mass index (BMI), body fat, circumferences, and all skinfold thickness was seen. A statistically significant reduction in blood glucose, glycated hemoglobin A1c, hepatic transaminases, fasting insulin, homeostatic model assessment of insulin resistance (HOMA-IR), and postprandial C-peptide was noted, while HOMA-β, postprandial insulin sensitivity, and fasting adiponectin were statistically significantly increased. There was no change in lean body mass. Compared to baseline there was a statistically significant decrease in mean liver FF (from 15.2% to 10.1%, P < .0001) and mean pancreatic FF (from 7.5% to 5.99%, P < .0083). Reduction in liver fat was statistically significant after adjustment for change in body weight.
Conclusion: Dapagliflozin, after 120 days of use, reduced pancreatic and liver fat and increased insulin sensitivity in Asian Indian patients with T2DM.
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http://dx.doi.org/10.1210/clinem/dgac138 | DOI Listing |
Nutrients
December 2024
Department of Cardiology, University Medical Centre Groningen, University of Groningen, 9713 GZ Groningen, The Netherlands.
Background: Micronutrient deficiencies are common and play a significant role in the prognosis of many chronic diseases, including heart failure (HF), but their prevalence in HF is not well known. As studies have traditionally focused on causes originating within the intestines, exocrine pancreatic insufficiency (EPI) has been overlooked as a potential contributor. The exocrine pancreas enables the absorption of various (fat-soluble) micronutrients and may be insufficient in HF.
View Article and Find Full Text PDFMol Metab
January 2025
Arthur Riggs Diabetes and Metabolism Research Institute, City of Hope, Duarte, CA 91010, USA; Department of Translational Research and Cellular Therapeutics, City of Hope, Duarte, CA 91010, USA. Electronic address:
Objective: Loss of functional β-cell mass is a major cause of diabetes. Thus, identifying regulators of β-cell health is crucial for treating this disease. The Leucine-rich repeat-containing G-protein-coupled receptor (GPCR) 4 (LGR4) is expressed in β-cells and is the fourth most abundant GPCR in human islets.
View Article and Find Full Text PDFRev Esp Enferm Dig
January 2025
Gastroenterología. Unidad de Endoscopia, Hospital Universitario Donostia.
The pancreatitis, panniculitis, polyarthritis (PPP) syndrome involves the association of pancreatic pathology, panniculitis of pancreatic origin, and polyarthritis secondary to intra-articular fat necrosis. The incidence is unknown, and the mortality rate is as high as 24%. Treatment targets the underlying pancreatic pathology.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Department of Internal Medicine, Erasmus Medical Center (Erasmus MC), Dr. Molewaterplein 40, 3015 GD Rotterdam, The Netherlands.
Consuming a "modern" Western diet and overnutrition may increase insulin secretion. Additionally, nutrition-mediated hyperinsulinemia is a major driver of ectopic fat deposition. The global prevalence of metabolic syndrome is high and growing.
View Article and Find Full Text PDFFront Endocrinol (Lausanne)
January 2025
Department of Psychology, University of Miami, Coral Gables, FL, United States.
The neuropeptide oxytocin (OXT) and its receptor (OXTR) have been shown to play an important role in glucose metabolism, and pancreatic islets express this ligand and receptor. In the current study, OXTR expression was identified in α-, β-, and δ-cells of the pancreatic islet by RNA hybridization, and OXT protein expression was observed only in β-cells. In order to examine the contribution of islet OXT/OXTR in glycemic control and islet β-cell heath, we developed a β-cell specific OXTR knock-out (β-KO) mouse.
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