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Most type 2 diabetes mellitus patients are obese and have obesity related vascular complications. Exenatide treatment is well known for both decreasing glycated hemoglobin levels and reduction in body weight. So, this study aimed to determine the effects of exenatide on body composition, glycated hemoglobin levels, and vascular stiffness in obese type 2 diabetes mellitus patients.
For 1 month, 32 obese type 2 diabetes mellitus patients were administered 5 µg of exenatide twice daily. The dosage was then increased to 10 µg. Patients' height, body weight, glycated hemoglobin levels, lipid profile, pulse wave velocity (PWV), body mass index, fat mass, and muscle mass were measured by using Inbody at baseline and after 3 months of treatment.
After 3 months of treatment, glycated hemoglobin levels decreased significantly (
Effects of short term exenatide use in obese type 2 diabetes mellitus with cardiometabolic high risk patients not only reduced body weight without muscle mass loss, body fat mass, and glycated hemoglobin levels but also improved aortic PWV in accordance with waist to hip ratio.
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Inflammatory factors and β-cell dysfunction due to high-fat diets aggravate chronic diseases and their complications. However, omega-3 dietary fats have anti-inflammatory effects, and the involvement of autophagy in the etiology of diabetes has been reported. Therefore, we examined the protective effects of autophagy on diabetes using fat-1 transgenic mice with omega-3 self-synthesis capability.
Streptozotocin (STZ) administration induced β-cell dysfunction in mice; blood glucose levels and water consumption were subsequently measured. Using hematoxylin and eosin (H&E) and Masson's trichrome staining, we quantitatively assessed STZ-induced changes in the number, mass, and fibrosis of pancreatic islets in fat-1 and control mice. We identified the microtubule-associated protein 1A/1B light chain 3-immunoreactive puncta in β-cells and quantified p62 levels in the pancreas of fat-1 and control mice.
STZ-induced diabetic phenotypes, including hyperglycemia and polydipsia, were attenuated in fat-1 mice. Histological determination using H&E and Masson's trichrome staining revealed the protective effects of the fat-1 expression on cell death and the scarring of pancreatic islets after STZ injection. In the β-cells of control mice, autophagy was abruptly activated after STZ treatment. Basal autophagy levels were elevated in fat-1 mice β-cells, and this persisted after STZ treatment. Together with autophagosome detection, these results revealed that n-3 polyunsaturated fatty acid (PUFA) enrichment might partly prevent the STZ-related pancreatic islet damage by upregulating the basal activity of autophagy and improving autophagic flux disturbance.
Fat-1 transgenic mice with a n-3 PUFA self-synthesis capability exert protective effects against STZ-induced β-cell death by activating autophagy in β-cells.
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