Weight cycling enhances adipose tissue inflammatory responses in male mice

• Published in: PloS one 2012-07, Vol.7 (7), p.e39837-e39837
• Main Authors: Barbosa-da-Silva, Sandra, Fraulob-Aquino, Julio C, Lopes, Jessica R, Mandarim-de-Lacerda, Carlos A, Aguila, Marcia B
• Format: Article
• Language: English
• Subjects: Adipokines - blood; Adipose tissue; Adipose Tissue - metabolism; Adipose Tissue - pathology; Animals; Bioindicators; Biology; Blood; Blood lipids; Body fat; Body mass; Body weight loss; Carbohydrate Metabolism; Carbohydrates; Cycles; Cytokines; Diet; Dyslipidemia; Feed conversion; Feed efficiency; Feeding; Glucose; Glucose tolerance; Glucose Tolerance Test; Homeostasis; House mouse; Inflammation; Inflammation - blood; Insulin; Insulin resistance; Lipid metabolism; Lipids; Lipids - blood; Male; Medicine; Metabolism; Mice; Obesity; Panniculitis - blood; Reduction; Rodents; Tumor necrosis factor-TNF; Weight Gain; Weight Loss
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0039837

Obesity is associated with low-grade chronic inflammation attributed to dysregulated production, release of cytokines and adipokines and to dysregulated glucose-insulin homeostasis and dyslipidemia. Nutritional interventions such as dieting are often accompanied by repeated bouts of weight loss and regain, a phenomenon known as weight cycling (WC). In this work we studied the effects of WC on the feed efficiency, blood lipids, carbohydrate metabolism, adiposity and inflammatory markers in C57BL/6 male mice that WC two or three consecutive times by alternation of a high-fat (HF) diet with standard chow (SC). The body mass (BM) grew up in each cycle of HF feeding, and decreased after each cycle of SC feeding. The alterations observed in the animals feeding HF diet in the oral glucose tolerance test, in blood lipids, and in serum and adipose tissue expression of adipokines were not recuperated after WC. Moreover, the longer the HF feeding was (two, four and six months), more severe the adiposity was. After three consecutive WC, less marked was the BM reduction during SC feeding, while more severe was the BM increase during HF feeding. In conclusion, the results of the present study showed that both the HF diet and WC are relevant to BM evolution and fat pad remodeling in mice, with repercussion in blood lipids, homeostasis of glucose-insulin and adipokine levels. The simple reduction of the BM during a WC is not able to recover the high levels of adipokines in the serum and adipose tissue as well as the pro-inflammatory cytokines enhanced during a cycle of HF diet. These findings are significant because a milieu with altered adipokines in association with WC potentially aggravates the chronic inflammation attributed to dysregulated production and release of adipokines in mice.