title: Effects of ALA, EPA and DHA in high-carbohydrate, high-fat diet-induced metabolic syndrome in rats.
abstract: We compared the cardiovascular, hepatic and metabolic responses to individual dietary n-3 fatty acids (α-linolenic acid, ALA; eicosapentaenoic acid, EPA; and docosahexaenoic acid, DHA) in a high-carbohydrate, high-fat diet-induced model of metabolic syndrome in rats. Additionally, we measured fatty acid composition of plasma, adipose tissue, liver, heart and skeletal muscle in these rats. The same dosages of ALA and EPA/DHA produced different physiological responses to decrease the risk factors for metabolic syndrome. ALA did not reduce total body fat but induced lipid redistribution away from the abdominal area and favorably improved glucose tolerance, insulin sensitivity, dyslipidemia, hypertension and left ventricular dimensions, contractility, volumes and stiffness. EPA and DHA increased sympathetic activation, reduced the abdominal adiposity and total body fat and attenuated insulin sensitivity, dyslipidemia, hypertension and left ventricular stiffness but not glucose tolerance. However, ALA, EPA and DHA all reduced inflammation in both the heart and the liver, cardiac fibrosis and hepatic steatosis. These effects were associated with complete suppression of stearoyl-CoA desaturase 1 activity. Since the physiological responses to EPA and DHA were similar, it is likely that the effects are mediated by DHA with EPA serving as a precursor. Also, ALA supplementation increased DHA concentrations but induced different physiological responses to EPA and DHA. This result strongly suggests that ALA has independent effects in metabolic syndrome, not relying on its metabolism to DHA.
authors.affiliation: School of Biomedical Sciences, The University of Queensland, Brisbane, 4072, Australia.
authors.forename: Hemant
authors.initials: H
authors.lastname: Poudyal
authors.forename: Sunil K
authors.initials: SK
authors.lastname: Panchal
authors.forename: Leigh C
authors.initials: LC
authors.lastname: Ward
authors.forename: Lindsay
authors.initials: L
authors.lastname: Brown
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism; D000818:Animals; D059305:Diet, High-Fat; D004040:Dietary Carbohydrates / Q000008:administration & dosage*; D004281:Docosahexaenoic Acids / Q000494:pharmacology*; D015118:Eicosapentaenoic Acid / Q000494:pharmacology*; D005395:Fish Oils / Q000008:administration & dosage; D006321:Heart / Q000503:physiopathology; D007333:Insulin Resistance; D008099:Liver / Q000378:metabolism / Q000473:pathology; D008297:Male; D024821:Metabolic Syndrome / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control; D018482:Muscle, Skeletal / Q000378:metabolism; D009206:Myocardium / Q000473:pathology; D009765:Obesity / Q000378:metabolism; D010938:Plant Oils / Q000008:administration & dosage; D051381:Rats; D013230:Stearoyl-CoA Desaturase / Q000378:metabolism; D017962:alpha-Linolenic Acid / Q000494:pharmacology*
chemical_list: D004040:Dietary Carbohydrates; D005395:Fish Oils; D010938:Plant Oils; D017962:alpha-Linolenic Acid; D004281:Docosahexaenoic Acids; D015118:Eicosapentaenoic Acid; D013230:Stearoyl-CoA Desaturase