eleostearic-acid and 9-11-linoleic-acid

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

The presence of a significant amount of 9,11-conjugated linoleic acid (CLA, 9,11-18:2) was confirmed in the liver and plasma lipids of rats fed a 1% (w/w % of diet) eleostearic acid (ESA, 9,11,13-18:3) diet for 4 wk. The chemical structure of the 9,11-CLA apparent in the tissue lipids was identified by gas chromatography-electron impact mass spectrometry after its conversion to a 4,4-dimethyloxazoline derivative. The concentration of CLA in the total fatty acids of the liver and plasma lipids reached to about 1%, for each in the CLA-supplemented rats, while reaching 3.2% and 2.5%, respectively, in the ESA-supplemented rats. The results suggest that alpha-ESA is metabolized partially to CLA via a delta 13-saturation reaction in the rat. Some biological activities observed in alpha-ESA-fed animals may be ascribed also to CLA that is formed from ESA in the body.

Topics: Animals; Chromatography, Gas; Linoleic Acids, Conjugated; Linolenic Acids; Liver; Male; Mass Spectrometry; Oxazoles; Rats; Rats, Sprague-Dawley

We investigated the cytotoxic effect of conjugated trienoic fatty acids on various human tumor cell lines: DLD- 1, colorectal; HepG2, hepatoma; A549, lung; MCF-7, breast; and MKN-7, stomach. Conjugated linoleic acid (CLA) and conjugated linolenic acid were prepared from linoleic acid (18:2, n-6) and alpha-linolenic acid (18:3, n-3), respectively, by treatment with 6.6% or 21% potassium hydroxide. Spectrophotometric readings at 235 nm for the conjugated diene formation, and at 268 nm for the conjugated triene, were confirmed for the respective conjugated fatty acids. In addition, tung oil (Aleurites fordii) fatty acids consisting principally of a conjugated triene (eleostearic acid, approximately 80% of total fatty acids) were prepared using an alkaline saponification procedure. All tumor cells were incubated for 24 h with 5-100 microM of the conjugated fatty acids, and MTT dye reduction was measured to verify the cell viability. Among the conjugated fatty acids examined, conjugated linolenic acid and tung oil fatty acids exhibited the most intense cytotoxic effects on DLD-1, HepG2, A549, MCF-7 and MKN-7 cells, while CLA was not cytotoxic to the tumor cells. These results demonstrate that conjugated trienoic fatty acids are more cytotoxic to human tumor cells than the conjugated dienoic fatty acid, CLA.

Topics: Antineoplastic Agents; Cell Survival; Coloring Agents; Drug Screening Assays, Antitumor; Humans; Linoleic Acids; Linoleic Acids, Conjugated; Linolenic Acids; Oxidation-Reduction; Plant Oils; Tetrazolium Salts; Tumor Cells, Cultured