FSH promotes fat accumulation by activating PPARγ signaling in surgically castrated, but not immunocastrated, male pigs

Abstract

Follicle-stimulating hormone (FSH) was recently implicated as a novel regulator of fat accumulation. Surgical castration causes high FSH concentrations and increases fat accumulation, whereas immunocastration results in low FSH concentrations and less fat in immunocastrated boars versus barrows. However, detailed information regarding the role of FSH in regulation of fat accumulation in male pigs is unclear. First, expression of FSH receptor was confirmed (real-time quantitative PCR) in subcutaneous and visceral adipose tissues (SAT and VAT, respectively) of boars. Then, surgical castration (high FSH model) was compared to immunocastration (low FSH model) to investigate potential roles of FSH in adipogenesis and fat accumulation. High FSH concentrations after surgical castration activated PPARγ signaling by upregulating expression of CREB (P < 0.05), and then recruited an array of PPARγ target adipogenic genes, including transcription factor (C/EBPα), long-chain fatty acid uptake (LPL), fatty acid de novo synthesis (FASN, ACACA) and lipid droplet formation (PLIN1) in both SAT and VAT, promoting fat accumulation in barrows. In contrast, much lower serum FSH concentrations in immunocastrates attenuated (P < 0.05) expressions of PPARγ and PPARγ target genes in both SAT and VAT, resulting in less fat accumulation in immunocastrated boars versus barrows. We concluded that the substantially elevated FSH concentrations in barrows promoted fat accumulation by activating the PPARγ signaling pathway in adipose tissues, whereas immunocastrates accumulated less fat due to low FSH.