Long-term High-fat High-sucrose Diet Promotes Enlarged Islets and beta-Cell Damage by Oxidative Stress in Bama Minipigs

文献类型： 外文期刊

第一作者： Zhao, Zhan-zhao

作者： Zhao, Zhan-zhao;Xin, Lei-lei;Xia, Ji-han;Yang, Shu-lin;Li, Kui;Zhao, Zhan-zhao;Chen, Yao-xing

作者机构：

关键词： Bama minipigs;pancreas;steatosis;apoptosis;oxidative stress

期刊名称：PANCREAS （ 影响因子：3.327； 五年影响因子：3.417 ）

ISSN： 0885-3177

年卷期： 2015 年 44 卷 6 期

页码：

收录情况： SCI

摘要： Objectives The effect of a long-term high-fat, high-caloric diet on the dysfunction of pancreas has not been clarified. We investigated the pancreatic histopathology and -cell apoptosis in Bama minipigs after 23 months on a high-fat high-sucrose diet (HFHSD). Methods Bama minipigs were randomly assigned to control (n = 6) and HFHSD groups (n = 6) for 23 months, and biochemical parameters were measured. Pancreata were subjected to histological analysis, followed by assessment with transmission electron microscopy. Lipid peroxidation was determined by the malondialdehyde concentration and antioxidant enzyme activity. B-cell apoptosis was measured by an immunohistochemical method. Results In the HFHSD group, the islets were enlarged, and the pancreatic tissue had observed significant fatty infiltration. Moreover, the feeding program damaged the normal pancreatic tissue structure. The level of lipid peroxidation was increased, and the activities of pancreatic antioxidant enzymes were significantly decreased. The expression levels of caspase-3, Bax, and insulin were significantly increased (P < 0.05), and the expression levels of proliferating cell nuclear antigen and Bcl-2 were decreased (P < 0.05). Conclusions The long-term HFHSD promotes pancreatic steatosis and oxidative stress, which increases -cell apoptosis as indicated by the activation of caspase-3 through the mitochondrial pathway (Bcl-2/Bax).

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