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Diet‐induced obesity regulates the galanin‐mediated signaling cascade in the adipose tissue of mice
Author(s) -
Kim Ahreum,
Park Taesun
Publication year - 2010
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.200900317
Subject(s) - endocrinology , medicine , galanin , adipose tissue , adipocyte , biology , receptor , signal transduction , thermogenesis , protein kinase a , phosphorylation , coactivator , prdm16 , brown adipose tissue , microbiology and biotechnology , neuropeptide , biochemistry , transcription factor , gene
Galanin is a neuropeptide that regulates the food intake, neurogenesis, memory, and gut secretion. This study was conducted to evaluate the high‐fat diet (HFD)‐induced regulation of the galanin receptors (GalRs) and the associated signaling molecules in the adipose tissues of mice. Twenty C57BL/6J mice were given either an HFD or a normal diet for 12 wk. The results of the semiquantitative RT‐PCR analyses indicated that the HFD upregulated the expression of GalR1, GalR2, GalR3, resistance to audiogenic seizures, peroxisome proliferator‐activated receptorγ2, adipocyte protein 2, and protein kinase Cδ and downregulated the expression of peroxisome proliferative activated receptor γ coactivator 1α and uncoupling protein 1 in the adipose tissues. The immunoblot results showed that the protein levels of peroxisome proliferator‐activated receptorγ2 and adipocyte protein 2, and the phosphorylation of c‐Raf and extracellular signal‐regulated kinase 1/2 were increased, while the phosphorylation of cyclic adenosine monophosphate‐responsive element‐binding protein, which regulates peroxisome proliferative activated receptor γ coactivator 1α and uncoupling protein 1, was decreased in the epididymal adipose tissues of the HFD‐fed mice. These results suggest the possible association of the galanin‐mediated signaling pathways in the manifestation of the HFD‐induced activation of adipogenesis along with the suppression of thermogenesis in the adipose tissues of mice.