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krebs-ringer bicarbonate-hepes buffer hong tao & yingsheng zhou caloric-restricted ob/ob mice high-fat diet-induced hyperglycemia reverse β-cell dysfunction low-calorie diet mimics hf → nc group achieved suggesting β-cell dysfunction induced β-cell autophagy glucose-stimulated insulin secretion diet-induced weight loss indicating β-cell autophagy hf → nc mice showed observe β-cell morphology early-phase insulin secretion cellular degradation-recycling system dylight-labeled secondary antibodies reflect β-cell function restoring β-cell function pancreatic β-cell damage article download pdf diet-induced obese mice uranyl acetate/lead citrate reduced beta-cell mass high-fat-fed mice activated β-cell autophagy increased β-cell autophagy increased β-cell area reduced atp/ca2+ signaling β-cell autophagy activity endoplasmic reticulum stress improve β-cell function dietary-induced obese mice β-cell autophagy level found β-cell autophagy showed glucose intolerance hf → nc cr group beta-cell failure hf → nc cr mice β-cell dysfunction low–calorie diet low-calorie diet achieve normal weight hf → nc cr islets hf → nc cr groups acid-ethanol solution [18] rebound weight gain fat cell size positive staining area high-fat diet

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         headline:Moderate calorie restriction to achieve normal weight reverses β-cell dysfunction in diet-induced obese mice: involvement of autophagy
         description:Severe calorie restriction (CR) is shown to improve or even reverse β-cell dysfunction in patients with obesity and type 2 diabetes mellitus. However, whether mild to moderate CR can reverse β-cell dysfunction induced by obesity and the underlying mechanism remain unclear. Autophagy plays an important role in maintaining mass, architecture and function of β-cells. While the impact of CR on β-cell autophagy is unknown. This study aims to investigate the effects of moderate CR on β-cell function and autophagy activity in diet-induced obese (DIO) mice. DIO C57BL/6 mice were subjected to 3 weeks of switching to normal chow (HF → NC group) or normal chow with 40 % CR (HF → NC CR group). Then hematoxylin-eosin and immunohistochemistry staining were performed to observe β-cell morphology. β-cell function was evaluated by intraperitoneal glucose tolerance test in vivo and static GSIS (glucose-stimulated insulin secretion) in isolated islets. β-cell autophagy activity was determined by transmission electron microscope and western blot. In the HF → NC CR group, CR normalized body weights, completely restored glucose tolerance, early-phase and second-phase insulin secretion, insulin sensitivity, and islet size. CR also normalized insulin content and glucose-stimulated insulin secretion in isolated islets in vitro. Furthermore, β-cell autophagy level was increased in the HF → NC CR group, but AMPK phosphorylation remained unchanged. Although HF → NC mice achieved moderate weight loss and normal glucose tolerance, their insulin secretion was not improved compared with obese control mice, and additionally, β-cell autophagy was not activated in these mice. Moderate (40 %) CR to achieve normal weight reversed β-cell dysfunction and insulin resistance, and restored glucose homeostasis in DIO mice. Furthermore, the up-regulation of β-cell autophagy may play a role in this process, independent of AMPK activation.
         datePublished:2015-10-06T00:00:00Z
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      headline:Moderate calorie restriction to achieve normal weight reverses β-cell dysfunction in diet-induced obese mice: involvement of autophagy
      description:Severe calorie restriction (CR) is shown to improve or even reverse β-cell dysfunction in patients with obesity and type 2 diabetes mellitus. However, whether mild to moderate CR can reverse β-cell dysfunction induced by obesity and the underlying mechanism remain unclear. Autophagy plays an important role in maintaining mass, architecture and function of β-cells. While the impact of CR on β-cell autophagy is unknown. This study aims to investigate the effects of moderate CR on β-cell function and autophagy activity in diet-induced obese (DIO) mice. DIO C57BL/6 mice were subjected to 3 weeks of switching to normal chow (HF → NC group) or normal chow with 40 % CR (HF → NC CR group). Then hematoxylin-eosin and immunohistochemistry staining were performed to observe β-cell morphology. β-cell function was evaluated by intraperitoneal glucose tolerance test in vivo and static GSIS (glucose-stimulated insulin secretion) in isolated islets. β-cell autophagy activity was determined by transmission electron microscope and western blot. In the HF → NC CR group, CR normalized body weights, completely restored glucose tolerance, early-phase and second-phase insulin secretion, insulin sensitivity, and islet size. CR also normalized insulin content and glucose-stimulated insulin secretion in isolated islets in vitro. Furthermore, β-cell autophagy level was increased in the HF → NC CR group, but AMPK phosphorylation remained unchanged. Although HF → NC mice achieved moderate weight loss and normal glucose tolerance, their insulin secretion was not improved compared with obese control mice, and additionally, β-cell autophagy was not activated in these mice. Moderate (40 %) CR to achieve normal weight reversed β-cell dysfunction and insulin resistance, and restored glucose homeostasis in DIO mice. Furthermore, the up-regulation of β-cell autophagy may play a role in this process, independent of AMPK activation.
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         β-cell function
         Autophagy
         Clinical Nutrition
         Metabolic Diseases
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