PDF(Pubmed)
Abstract：
BACKGROUND: High-fat diet (HFD) consumption and being exposed to daily psychological stress, common environmental factors in modern lifestyle, play an important role on metabolic disorders such as glucose homeostasis impairment. The aim of this study was to investigate the effects of high-fat diet (HFD) and psychological stress combination on metabolic response to chronic psychological stress in male rats.
METHODS: Male Wistar rats were divided into HFD, and normal diet (ND) groups and then into stress and nonstress subgroups. The diets were applied for 5 weeks, and psychological stress was induced for 7 consecutive days. Then, blood samples were taken to measure glucose, insulin, free fatty acids (FFA), and leptin and corticosterone concentrations. Subsequently, glucose-stimulated insulin release from pancreatic isolated islets was assessed.
RESULTS: HFD did not significantly change fasting plasma glucose, insulin and corticosterone levels, whereas increased plasma leptin (7.05 ± 0.33) and FFA (p < 0.01) levels and impaired glucose tolerance. Additionally, HFD and stress combination induced more profound glucose intolerance associated with increased plasma corticosterone (p < 0.01) and leptin (8.63 ± 0.38) levels. However, insulin secretion from isolated islets did not change in the presence of high-fat diet and/or stress.
CONCLUSIONS: HFD should be considered as an intensified factor of metabolic impairments caused by chronic psychological stress.
METHODS: Male Wistar rats were divided into HFD, and normal diet (ND) groups and then into stress and nonstress subgroups. The diets were applied for 5 weeks, and psychological stress was induced for 7 consecutive days. Then, blood samples were taken to measure glucose, insulin, free fatty acids (FFA), and leptin and corticosterone concentrations. Subsequently, glucose-stimulated insulin release from pancreatic isolated islets was assessed.
RESULTS: HFD did not significantly change fasting plasma glucose, insulin and corticosterone levels, whereas increased plasma leptin (7.05 ± 0.33) and FFA (p < 0.01) levels and impaired glucose tolerance. Additionally, HFD and stress combination induced more profound glucose intolerance associated with increased plasma corticosterone (p < 0.01) and leptin (8.63 ± 0.38) levels. However, insulin secretion from isolated islets did not change in the presence of high-fat diet and/or stress.
CONCLUSIONS: HFD should be considered as an intensified factor of metabolic impairments caused by chronic psychological stress.
摘要：
背景：高脂肪饮食（HFD）的消耗和日常心理压力，现代生活方式中常见的环境因素，在代谢紊乱如葡萄糖稳态损害中起重要作用。本研究旨在探讨高脂饮食(HFD)与心理应激组合对雄性大鼠慢性心理应激代谢反应的影响。
方法：雄性Wistar大鼠分为HFD,和正常饮食（ND）组，然后进入压力和非压力亚组。饮食应用5周，并连续7天诱发心理应激。然后，采集血样来测量葡萄糖，胰岛素，游离脂肪酸（FFA），以及瘦素和皮质酮的浓度。随后，评估了葡萄糖刺激的胰腺分离胰岛的胰岛素释放。
结果：HFD没有显著改变空腹血糖，胰岛素和皮质酮水平，而血浆瘦素（7.05±0.33）和FFA（p<0.01）水平升高，糖耐量受损。此外,HFD和应激组合引起更严重的葡萄糖耐受不良，与血浆皮质酮（p<0.01）和瘦素（8.63±0.38）水平升高有关。然而,在高脂饮食和/或应激存在的情况下,离体胰岛的胰岛素分泌没有变化.
结论：HFD应被视为慢性心理应激引起的代谢障碍的加剧因素。
方法：雄性Wistar大鼠分为HFD,和正常饮食（ND）组，然后进入压力和非压力亚组。饮食应用5周，并连续7天诱发心理应激。然后，采集血样来测量葡萄糖，胰岛素，游离脂肪酸（FFA），以及瘦素和皮质酮的浓度。随后，评估了葡萄糖刺激的胰腺分离胰岛的胰岛素释放。
结果：HFD没有显著改变空腹血糖，胰岛素和皮质酮水平，而血浆瘦素（7.05±0.33）和FFA（p<0.01）水平升高，糖耐量受损。此外,HFD和应激组合引起更严重的葡萄糖耐受不良，与血浆皮质酮（p<0.01）和瘦素（8.63±0.38）水平升高有关。然而,在高脂饮食和/或应激存在的情况下,离体胰岛的胰岛素分泌没有变化.
结论：HFD应被视为慢性心理应激引起的代谢障碍的加剧因素。
