title: Flax oil-mediated activation of PPAR-γ correlates with reduction of hepatic lipid accumulation in obese spontaneously hypertensive/NDmcr-cp rats, a model of the metabolic syndrome.
abstract: Flax oil feeding has been proposed to have beneficial effects on the outcome of the metabolic syndrome due to the high n-3 fatty acid content of flax oil; however, the mechanisms of its action remain largely unknown. We investigated the effects of flax oil feeding on hyperlipidaemia, hyperglycaemia, hepatic steatosis and oxidative stress in the spontaneously hypertensive (SHR)/NDmcr-cp rats, a genetic model of the metabolic syndrome. Hepatic gene expression of PPAR-α, PPAR-γ and sterol-regulatory element-binding protein-1c was also assessed in order to investigate the possible underlying mechanisms. Obese and lean SHR/NDmcr-cp rats were fed high-fat diets enriched with either lard or flax oil for a period of 4 weeks. Obese rats exhibited higher body weight, liver weight and mesenteric fat-, epididymal fat- and renal fat-pad weights, and also TAG and cholesterol concentrations in serum and VLDL, LDL and HDL fractions, when compared with the lean rats (P < 0·001), irrespective of the diets. Concentrations of fasting serum insulin and urinary thiobarbituric acid reactive substances were lower in flax oil-fed obese (FO) rats compared with the lard-fed obese (LO) rats (P < 0·01). Flax oil feeding also revealed a significant reduction in hepatic TAG and cholesterol concentrations in obese rats compared with the LO rats (P < 0·05). In addition, FO rats exhibited significantly higher hepatic mRNA expression of PPAR-γ, which negatively correlated (r - 0·98, P < 0·05) with their hepatic lipid levels. These findings suggest that flax oil feeding may activate PPAR-γ-dependent pathways to alter the hepatic lipid metabolism and to increase insulin sensitivity in the obese SHR/NDmcr-cp rats.
authors.affiliation: Department of Pharmacy, School of Pharmacy and Pharmaceutical Sciences, Mukogawa Women's University, Nishinomiya 663-8179, Japan.
authors.forename: Kanta
authors.initials: K
authors.lastname: Chechi
authors.forename: Naomi
authors.initials: N
authors.lastname: Yasui
authors.forename: Katsumi
authors.initials: K
authors.lastname: Ikeda
authors.forename: Yukio
authors.initials: Y
authors.lastname: Yamori
authors.forename: Sukhinder
authors.initials: S
authors.lastname: K Cheema
mesh_terms: D000818:Animals; D004041:Dietary Fats / Q000378:metabolism; D004195:Disease Models, Animal; D019597:Flax / Q000737:chemistry*; D000960:Hypolipidemic Agents / Q000494:pharmacology* / Q000627:therapeutic use; D007328:Insulin / Q000097:blood; D050356:Lipid Metabolism; D008099:Liver / Q000378:metabolism; D024821:Metabolic Syndrome / Q000188:drug therapy* / Q000378:metabolism; D009765:Obesity / Q000188:drug therapy* / Q000378:metabolism; D047495:PPAR gamma / Q000235:genetics / Q000378:metabolism*; D008517:Phytotherapy; D010938:Plant Oils / Q000494:pharmacology* / Q000627:therapeutic use; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D011918:Rats, Inbred SHR; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: D004041:Dietary Fats; D000960:Hypolipidemic Agents; D007328:Insulin; D047495:PPAR gamma; D010938:Plant Oils; D012333:RNA, Messenger; D017392:Thiobarbituric Acid Reactive Substances; C029310:lard