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PPAR‐α agonist elicits metabolically active brown adipocytes and weight loss in diet‐induced obese mice
Author(s) -
Rachid Tamiris Lima,
PennadeCarvalho Aline,
Bringhenti Isabele,
Aguila Marcia Barbosa,
MandarimdeLacerda Carlos Alberto,
SouzaMello Vanessa
Publication year - 2015
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.3111
Subject(s) - endocrinology , medicine , fenofibrate , thermogenesis , thermogenin , agonist , prdm16 , uncoupling protein , coactivator , peroxisome proliferator activated receptor , brown adipose tissue , adipose tissue , chemistry , receptor , biology , transcription factor , biochemistry , gene
Obesity is considered a public health problem worldwide. Fenofibrate, a selective peroxisome proliferator‐activated receptor α (PPAR‐α) agonist, elicits weight loss in animal models. This study aimed to examine the effects of fenofibrate on energy expenditure, body mass (BM) and gene expression of thermogenic factors in brown adipose tissue of diet‐induced obese mice. Male C57BL/6 mice were fed a standard chow (SC; 10% lipids) diet or a high‐fat (HF; 50% lipids) diet for 10 weeks. Afterwards, groups were subdivided as SC, SC‐F, HF and HF‐F ( n = 10, each). Treatment with fenofibrate (100 mg kg −1 BM mixed into the diet) lasted 5 weeks. Treated groups had reduced final BM compared with their counterparts ( p < 0·05), explained by the increase in energy expenditure, CO 2 production and O 2 consumption after treatment with fenofibrate ( p < 0·05). Similarly, genes involved in thermogenesis as PPAR‐α, PPAR‐γ coactivator 1α, nuclear respiratory factor 1, mitochondrial transcription factor A (Tfam), PR domain containing 16 (PRDM16), β‐3 adrenergic receptor (β3‐AR), bone morphogenetic protein 8B and uncoupling protein 1 were significantly expressed in brown adipocytes after the treatment ( p < 0·05). All observations ensure that selective PPAR‐α agonist can induce thermogenesis by increasing energy expenditure and enhancing the expression of genes involved in the thermogenic pathway. These results suggest fenofibrate as a coadjutant drug for the treatment of obesity. Copyright © 2015 John Wiley & Sons, Ltd.