Abstract
Aging may be a risk factor for type 2 diabetes in the elderly. Dietary intervention can affect glucose tolerance in adults, which may be due to body composition and islet cell autophagy. The aim of this study was to determine the effects of various dietary interventions on islet cell autophagy. Pancreatic tissue and blood samples were collected from Sprague Dawley rats (14–16 months old, n = 15 for each group) that received a normal diet (ND), a high-fat diet (HFD), or a calorie-restricted diet (CRD). The body weight (BW), visceral fat, serum lipid levels, fasting serum glucose, insulin levels, and β/α cell area were determined in 14-16-(0-w), 16-18-(8-w), and 18-20(16-w)-month-old rats. Pancreatic islet autophagy (LC3B and LAMP2), AP (Acid Phosphatase) and apoptosis (apoptosis index, AI (TUNEL assay) and cleaved caspase-3) were detected using immunohistochemistry, ELISA and western blot. At 16 weeks, the expressions of LC3B, LAMP2 and AP markedly increased in both the HFD (P<0.01) and CRD (P<0.05) groups; however, an increase in the AI (P<0.05), cleaved caspase-3 and Beclin1 expression and a decrease in the expressions of BCL2 and BCLXL (P<0.05) were observed in only the HFD group. FFA, triglyceride levels, HOMA-IR, insulin levels and glucagon levels were significantly increased in the HFD group but decreased in the CRD group at 16 weeks (P<0.05). The degree of islet cell autophagy was potentially regulated by the levels of FFA and islet cell insulin and glucagon, which may have been due to the effects of Beclin1/BCL2.
Highlights
Glucose metabolism reduces with age, resulting in impaired glucose tolerance and a high prevalence of type 2 diabetes (T2DM) in the elderly population[1]
Pancreatic islet cell autophagy was determined by analyzing the levels of the autophagy-specific proteins (LC3B and LAMP2) using both immunohistochemistry and western blot analyses, and Acid phosphatase (AP) was determined via ELISA assay
We previously demonstrated that from 2 to 20–24 months of age, the appearance of autophagosomes and increased LC3B and LAMP2 expression in pancreatic islet cells coincided with a significant decrease in insulin secretion and elevated fasting blood glucose in aged rats without observable levels of apoptosis[14]
Summary
Glucose metabolism reduces with age, resulting in impaired glucose tolerance and a high prevalence of type 2 diabetes (T2DM) in the elderly population[1]. Age-related increases in visceral adiposity and decreases in insulin sensitivity (IS) may promote the degeneration of islet cell function, which leads to a diabetic condition[2, 3]. A high-fat diet has been proven to increase insulin resistance and thereby promote the prevalence of T2DM[9, 10], and HFD intervention in young mice (8 weeks old) was shown to increase autophagic flux in pancreatic β cells both in and ex vivo[11]. Our study evaluated the expression of autophagic proteins and changes in body composition, insulin and glucagon in islet cells after dietary intake intervention, including CRD and HFD, from mid to late adulthood in rats
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