de Oliveira Carla, Scarabelot Vanessa Leal, de Souza Andressa, de Oliveira Cleverson Moraes, Medeiros Liciane Fernandes, de Macedo Isabel Cristina, Marques Filho Paulo Ricardo, Cioato Stefania Giotti, Caumo Wolnei, Torres Iraci L S
Pain Pharmacology and Neuromodulation, Animal Models Laboratory, Department of Pharmacology, Universidade Federal do Rio Grande do Sul Institute of Basic Health Sciences, Porto Alegre, RS 90050-170, Brazil; Post Graduate Program in Medicine: Medical Sciences, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS 90035-003, Brazil; Animal Experimentation Unit and Graduate Research Group, Hospital de Clínicas de Porto Alegre, Porto Alegre, RS 90035-003, Brazil.
Pain Pharmacology and Neuromodulation, Animal Models Laboratory, Department of Pharmacology, Universidade Federal do Rio Grande do Sul Institute of Basic Health Sciences, Porto Alegre, RS 90050-170, Brazil; Animal Experimentation Unit and Graduate Research Group, Hospital de Clínicas de Porto Alegre, Porto Alegre, RS 90035-003, Brazil; Post Graduate Program in Biological Sciences - Physiology, Universidade Federal do Rio Grande do Sul Institute of Basic Health Sciences, Porto Alegre, RS 90050-170, Brazil.
Peptides. 2014 Jan;51:46-53. doi: 10.1016/j.peptides.2013.10.024. Epub 2013 Nov 1.
Disruption of the circadian system can lead to metabolic dysfunction as a response to environmental alterations. This study assessed the effects of the association between obesity and chronic stress on the temporal pattern of serum levels of adipogenic markers and corticosterone in rats. We evaluated weekly weight, delta weight, Lee index, and weight fractions of adipose tissue (mesenteric, MAT; subcutaneous, SAT; and pericardial, PAT) to control for hypercaloric diet-induced obesity model efficacy. Wistar rats were divided into four groups: standard chow (C), hypercaloric diet (HD), stress plus standard chow (S), and stress plus hypercaloric diet (SHD), and analyzed at three time points: ZT0, ZT12, and ZT18. Stressed animals were subjected to chronic stress for 1h per day, 5 days per week, during 80 days. The chronic exposure to a hypercaloric diet was an effective model for the induction of obesity and metabolic syndrome, increasing delta weight, Lee index, weight fractions of adipose tissue, and triglycerides and leptin levels. We confirmed the presence of a temporal pattern in the release of triglycerides, corticosterone, leptin, and adiponectin in naïve animals. Chronic stress reduced delta weight, MAT weight, and levels of triglycerides, total cholesterol, and leptin. There were interactions between chronic stress and obesity and serum total cholesterol levels, between time points and obesity and adiponectin and corticosterone levels, and between time points and chronic stress and serum leptin levels. In conclusion, both parameters were able to desynchronize the temporal pattern of leptin and triglyceride release, which could contribute to the development of metabolic diseases such as obesity and metabolic syndrome.
昼夜节律系统的紊乱可导致代谢功能障碍，作为对环境变化的一种反应。本研究评估了肥胖与慢性应激之间的关联对大鼠血清脂肪生成标志物和皮质酮水平的时间模式的影响。我们每周评估体重、体重增量、李氏指数以及脂肪组织（肠系膜脂肪组织，MAT；皮下脂肪组织，SAT；心包脂肪组织，PAT）的重量分数，以控制高热量饮食诱导的肥胖模型的有效性。将Wistar大鼠分为四组：标准饲料组（C）、高热量饮食组（HD）、应激加标准饲料组（S）和应激加高热量饮食组（SHD），并在三个时间点进行分析：ZT0、ZT12和ZT18。应激动物每天接受1小时的慢性应激，每周5天，持续80天。长期暴露于高热量饮食是诱导肥胖和代谢综合征的有效模型，可增加体重增量、李氏指数、脂肪组织重量分数以及甘油三酯和瘦素水平。我们证实了在未受处理的动物中甘油三酯、皮质酮、瘦素和脂联素的释放存在时间模式。慢性应激降低了体重增量、MAT重量以及甘油三酯、总胆固醇和瘦素水平。慢性应激与肥胖以及血清总胆固醇水平之间、时间点与肥胖以及脂联素和皮质酮水平之间、时间点与慢性应激以及血清瘦素水平之间存在相互作用。总之，这两个参数均能够使瘦素和甘油三酯释放的时间模式不同步，这可能有助于肥胖和代谢综合征等代谢疾病的发展。
