- Clinical Study
- Effects of Short-Term Exenatide Treatment on Regional Fat Distribution, Glycated Hemoglobin Levels, and Aortic Pulse Wave Velocity of Obese Type 2 Diabetes Mellitus Patients
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Ju-Young Hong, Keun-Young Park, Byung-Joon Kim, Won-Min Hwang, Dong-Ho Kim, Dong-Mee Lim
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Endocrinol Metab. 2016;31(1):80-85. Published online March 16, 2016
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DOI: https://doi.org/10.3803/EnM.2016.31.1.80
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Abstract
PDFPubReader
- Background
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. MethodsFor 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. ResultsAfter 3 months of treatment, glycated hemoglobin levels decreased significantly (P=0.007). Triglyceride, total cholesterol, and low density lipoprotein levels decreased, while aspartate aminotransferase and alanine aminotransferase levels were no change. Body weight, and fat mass decreased significantly (P=0.002 and P=0.001, respectively), while interestingly, muscle mass did not decrease (P=0.289). In addition to, Waist-to-hip ratio and aortic PWV decreased significantly (P=0.006 and P=0.001, respectively). ConclusionEffects 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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Citations
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Daniel de Luis Román, Juana Carretero Gómez, José Manuel García-Almeida, Fernando Garrachón Vallo, German Guzmán Rolo, Juan José López Gómez, Francisco José Tarazona-Santabalbina, Alejandro Sanz-Paris Reviews in Endocrine and Metabolic Disorders.2024; 25(4): 651. CrossRef - The Current Landscape of Pharmacotherapies for Sarcopenia
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- Endocrine Research
- Omega-3 Polyunsaturated Fatty Acids May Attenuate Streptozotocin-Induced Pancreatic β-Cell Death via Autophagy Activation in Fat1 Transgenic Mice
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Won-Min Hwang, Dong-Ho Bak, Dong Ho Kim, Ju Young Hong, Seung-Yun Han, Keun-Young Park, Kyu Lim, Dong-Mee Lim, Jae Gu Kang
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Endocrinol Metab. 2015;30(4):569-575. Published online December 31, 2015
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DOI: https://doi.org/10.3803/EnM.2015.30.4.569
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4,908
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Abstract
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- Background
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. MethodsStreptozotocin (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. ResultsSTZ-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. ConclusionFat-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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