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cafeteria 饮食诱导肥胖合并慢性应激改变血清瘦素水平。

Cafeteria diet-induced obesity plus chronic stress alter serum leptin levels.

机构信息

Department of Pharmacology, Universidade Federal do Rio Grande do Sul Institute of Basic Health Sciences, Porto Alegre, RS, Brazil.

出版信息

Peptides. 2012 Nov;38(1):189-96. doi: 10.1016/j.peptides.2012.08.007. Epub 2012 Aug 21.

DOI:10.1016/j.peptides.2012.08.007
PMID:22940203
Abstract

Obesity is a disease that has become a serious public health issue worldwide, and chronic stressors, which are a problem for modern society, cause neuroendocrine changes with alterations in food intake. Obesity and chronic stress are associated with the development of cardiovascular diseases and metabolic disorders. In this study, a rat model was used to evaluate the effects of a hypercaloric diet plus chronic restraint stress on the serum leptin and lipids levels and on the weight of specific adipose tissue (mesenteric, MAT; subcutaneous, SAT and visceral, VAT). Wistar rats were divided into the following 4 groups: standard chow (C), hypercaloric diet (HD), stress plus standard chow (S), and stress plus hypercaloric diet (SHD). The animals in the stress groups were subjected to chronic stress (placed inside a 25 cm × 7 cm plastic tube for 1h per day, 5 days per week for 6 weeks). The following parameters were evaluated: the weight of the liver, adrenal glands and specific adipose tissue; the delta weight; the Lee index; and the serum levels of leptin, corticosterone, glucose, total cholesterol, and triglycerides. The hypercaloric diet induced obesity in rats, increasing the Lee index, weight, leptin, triglycerides, and cholesterol levels. The stress decreased weight gain even in animals fed a hypercaloric diet but did not prevent a significant increase in the Lee index. However, an interaction between the independent factors (hypercaloric diet and stress) was observed, which is demonstrated by the increased serum leptin levels in the animals exposed to both protocols.

摘要

肥胖是一种全球性的严重公共卫生问题,而慢性应激源是现代社会的一个问题,它会导致神经内分泌变化,从而改变食物摄入。肥胖和慢性应激与心血管疾病和代谢紊乱的发展有关。在这项研究中,使用大鼠模型评估了高热量饮食加慢性束缚应激对血清瘦素和血脂水平以及特定脂肪组织(肠系膜、MAT;皮下、SAT 和内脏、VAT)重量的影响。Wistar 大鼠分为以下 4 组:标准饲料(C)、高热量饮食(HD)、应激加标准饲料(S)和应激加高热量饮食(SHD)。应激组的动物接受慢性应激(每天在一个 25cm×7cm 的塑料管中放置 1 小时,每周 5 天,持续 6 周)。评估了以下参数:肝脏、肾上腺和特定脂肪组织的重量;差值体重;Lee 指数;以及血清瘦素、皮质酮、葡萄糖、总胆固醇和甘油三酯水平。高热量饮食导致大鼠肥胖,增加了 Lee 指数、体重、瘦素、甘油三酯和胆固醇水平。应激即使在给予高热量饮食的动物中也会降低体重增加,但不能防止 Lee 指数的显著增加。然而,独立因素(高热量饮食和应激)之间存在相互作用,这表现为暴露于两种方案的动物血清瘦素水平增加。

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