Roles of Peroxisome Proliferator-Activated Receptor ? in Bitter Melon Seed Oil-Corrected Lipid Disorders and Conversion of ?-Eleostearic Acid into Rumenic Acid in C57BL/6J Mice.

ABSTRACT: We previously reported that bitter melon seed oil (BMSO) was an effective anti-steatosis and antiobesity agent. Since the major fatty acid ?-eleostearic acid (?-ESA) in BMSO is a peroxisome proliferator-activated receptor ? (PPAR?) activator, the objective was to investigate the role of PPAR? in BMSO-modulated lipid disorders and ?-ESA metabolism. C57BL/6J wild (WD) and PPAR? knockout (KO) mice were fed a high-fat diet containing BMSO (15% soybean oil + 15% BMSO, HB) or not (30% soybean oil, HS) for 5 weeks. The HB diet significantly reduced hepatic triglyceride concentrations and increased acyl-CoA oxidase activity in WD, but not in KO mice. However, regardless of genotype, body fat percentage was lowered along with upregulated protein levels of uncoupling protein 1 (UCP1) and tyrosine hydroxylase, as well as signaling pathway of cAMP-dependent protein kinase and AMP-activated protein kinase in the white adipose tissue of HB-treated groups compared to HS cohorts. In WD-HB and KO-HB groups, white adipose tissue had autophagy, apoptosis, inflammation, and browning characteristics. Without PPAR?, in vivo reduction of ?-ESA into rumenic acid was slightly but significantly lowered, along with remarkable reduction of hepatic retinol saturase (RetSat) expression. We concluded that BMSO-mediated anti-steatosis depended on PPAR?, whereas the anti-adiposity effect was PPAR?-independent. In addition, PPAR?-dependent enzymes may participate in ?-ESA conversion, but only have a minor role.

SUBMITTER: Chang YY 

PROVIDER: S-EPMC5188460 | biostudies-literature | 2016 Dec

REPOSITORIES: biostudies-literature