eleostearic-acid and Dyslipidemias

We previously reported that bitter melon seed oil (BMSO) was an effective anti-steatosis and antiobesity agent. Since the major fatty acid α-eleostearic acid (α-ESA) in BMSO is a peroxisome proliferator-activated receptor α (PPARα) activator, the objective was to investigate the role of PPARα in BMSO-modulated lipid disorders and α-ESA metabolism. C57BL/6J wild (WD) and PPARα 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 PPARα, in vivo reduction of α-ESA into rumenic acid was slightly but significantly lowered, along with remarkable reduction of hepatic retinol saturase (

Topics: Acyl-CoA Oxidase; Adipose Tissue, White; Adiposity; Animals; Cyclic AMP-Dependent Protein Kinases; Diet, High-Fat; Dyslipidemias; Fatty Liver; Linoleic Acids, Conjugated; Linolenic Acids; Liver; Mice; Mice, Inbred C57BL; Mice, Knockout; Momordica charantia; Oxidoreductases Acting on CH-CH Group Donors; Phytotherapy; Plant Oils; PPAR alpha; Signal Transduction; Triglycerides; Tyrosine 3-Monooxygenase; Uncoupling Protein 1