title: Supplementation with alpha-linolenic acid-rich diacylglycerol suppresses fatty liver formation accompanied by an up-regulation of beta-oxidation in Zucker fatty rats.
abstract: Insulin resistance-related obesity and diabetes mellitus are the predominant causes of fatty liver disease. Here we examine the effects of dietary diacylglycerol (DG), which is a minor component of plant oils, on lipid accumulation and the expression of genes involved in lipid metabolism in the liver. The animals were fed diets containing either 10% triacylglycerol (TG), 10% TG + 4% alpha-linolenic acid-rich TG (ALATG) or 10% TG + 4% alpha-linolenic acid-rich diacylglycerol (ALADG) for a period of 1 month. Supplementation with ALADG significantly inhibited hepatic triglyceride accumulation; this was accompanied by the up-regulation of beta-oxidation activity, and acyl-CoA oxidase (ACO) and medium-chain acyl-CoA dehydrogenase (MCAD) mRNA levels. By contrast, no significant changes were observed in the levels of peroxisome proliferator-activated receptor-alpha (PPARalpha) and sterol regulatory element-binding protein-1 (SREBP-1) mRNAs. These results indicate that ALADG might be useful in the prevention of fatty liver formation; this effect could be closely related to the stimulation of lipid catabolism in the liver. In addition, our findings suggest that both acylglycerol structure (that is, the structural difference between TG and DG) and fatty-acid species affect the nutritional behaviour of dietary lipids.
authors.affiliation: Biological Science Laboratories, Kao Corporation, Ichikai-machi, Haga-gun, Tochigi, Japan. murase.takatoshi@kao.co.jp
authors.forename: Takatoshi
authors.initials: T
authors.lastname: Murase
authors.forename: Masafumi
authors.initials: M
authors.lastname: Aoki
authors.forename: Ichiro
authors.initials: I
authors.lastname: Tokimitsu
mesh_terms: D015094:3-Hydroxyacyl CoA Dehydrogenases / Q000037:antagonists & inhibitors; D000102:Acetyl-CoA C-Acyltransferase / Q000037:antagonists & inhibitors; D000818:Animals; D001835:Body Weight / Q000187:drug effects; D019748:Carbon-Carbon Double Bond Isomerases / Q000037:antagonists & inhibitors; D002784:Cholesterol / Q000097:blood / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000188:drug therapy* / Q000378:metabolism; D004032:Diet; D004075:Diglycerides / Q000008:administration & dosage / Q000737:chemistry / Q000494:pharmacology*; D004746:Enoyl-CoA Hydratase / Q000037:antagonists & inhibitors; D005234:Fatty Liver / Q000097:blood / Q000378:metabolism / Q000517:prevention & control*; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008297:Male; D009929:Organ Size / Q000187:drug effects; D019998:Racemases and Epimerases / Q000037:antagonists & inhibitors; D051381:Rats; D011924:Rats, Zucker; D014280:Triglycerides / Q000097:blood / Q000378:metabolism; D017962:alpha-Linolenic Acid / Q000008:administration & dosage / Q000737:chemistry / Q000494:pharmacology*
chemical_list: D004075:Diglycerides; D014280:Triglycerides; C038784:fatty acid oxidation complex; D017962:alpha-Linolenic Acid; D002784:Cholesterol; D015094:3-Hydroxyacyl CoA Dehydrogenases; D000102:Acetyl-CoA C-Acyltransferase; D004746:Enoyl-CoA Hydratase; D019998:Racemases and Epimerases; D019748:Carbon-Carbon Double Bond Isomerases