Open AccessApolipoprotein A‐I possesses an anti‐obesity effect associated with increase of energy expenditure and up‐regulation of UCP1 in brown fat
Author(s) -
Ruan Xiangbo,
Li Zhenghu,
Zhang Yixuan,
Yang Ling,
Pan Yi,
Wang Zhenzhen,
Feng GenSheng,
Chen Yan
Publication year - 2011
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/j.1582-4934.2010.01045.x
Subject(s) - endocrinology , medicine , brown adipose tissue , white adipose tissue , thermogenin , ampk , adipose tissue , uncoupling protein , genetically modified mouse , apolipoprotein b , obesity , transgene , protein kinase a , phosphorylation , chemistry , biology , cholesterol , biochemistry , gene
Abstract Apolipoprotein A‐I (ApoA‐I) is the most abundant protein constituent of high‐density lipoprotein (HDL). Reduced plasma HDL and ApoA‐I levels have been found to be associated with obesity and metabolic syndrome in human beings. However, whether or not ApoA‐I has a direct effect on obesity is largely unknown. Here we analysed the anti‐obesity effect of ApoA‐I using two mouse models, a transgenic mouse with overexpression of ApoA‐I and the mice administered with an ApoA‐I mimetic peptide D‐4F. The mice were induced to develop obesity by feeding with high fat diet. Both ApoA‐I overexpression and D‐4F treatment could significantly reduce white fat mass and slightly improve insulin sensitivity in the mice. Metabolic analyses revealed that ApoA‐I overexpression and D‐4F treatment enhanced energy expenditure in the mice. The mRNA level of uncoupling protein (UCP)1 in brown fat tissue was elevated by ApoA‐I transgenic mice. ApoA‐I and D‐4F treatment was able to increase UCP1 mRNA and protein levels as well as to stimulate AMP‐activated protein kinase (AMPK) phosphorylation in brown adipocytes in culture. Taken together, our results reveal that ApoA‐I has an anti‐obesity effect in the mouse and such effect is associated with increases in energy expenditure and UCP1 expression in the brown fat tissue.