title: n-3 PUFA: bioavailability and modulation of adipose tissue function.
abstract: Adipose tissue has a key role in the development of metabolic syndrome (MS), which includes obesity, type 2 diabetes, dyslipidaemia, hypertension and other disorders. Systemic insulin resistance represents a major factor contributing to the development of MS in obesity. The resistance is precipitated by impaired adipose tissue glucose and lipid metabolism, linked to a low-grade inflammation of adipose tissue and secretion of pro-inflammatory adipokines. Development of MS could be delayed by lifestyle modifications, while both dietary and pharmacological interventions are required for the successful therapy of MS. The n-3 long-chain (LC) PUFA, EPA and DHA, which are abundant in marine fish, act as hypolipidaemic factors, reduce cardiac events and decrease the progression of atherosclerosis. Thus, n-3 LC PUFA represent healthy constituents of diets for patients with MS. In rodents n-3 LC PUFA prevent the development of obesity and impaired glucose tolerance. The effects of n-3 LC PUFA are mediated transcriptionally by AMP-activated protein kinase and by other mechanisms. n-3 LC PUFA activate a metabolic switch toward lipid catabolism and suppression of lipogenesis, i.e. in the liver, adipose tissue and small intestine. This metabolic switch improves dyslipidaemia and reduces ectopic deposition of lipids, resulting in improved insulin signalling. Despite a relatively low accumulation of n-3 LC PUFA in adipose tissue lipids, adipose tissue is specifically linked to the beneficial effects of n-3 LC PUFA, as indicated by (1) the prevention of adipose tissue hyperplasia and hypertrophy, (2) the induction of mitochondrial biogenesis in adipocytes, (3) the induction of adiponectin and (4) the amelioration of adipose tissue inflammation by n-3 LC PUFA.
authors.affiliation: Department of Adipose Tissue Biology, Institute of Physiology of the Academy of Sciences of the Czech Republic, Videnska 1083, 142 20 Prague, Czech Republic. kopecky@biomed.cas.cz
authors.forename: Jan
authors.initials: J
authors.lastname: Kopecky
authors.forename: Martin
authors.initials: M
authors.lastname: Rossmeisl
authors.forename: Pavel
authors.initials: P
authors.lastname: Flachs
authors.forename: Ondrej
authors.initials: O
authors.lastname: Kuda
authors.forename: Petr
authors.initials: P
authors.lastname: Brauner
authors.forename: Zuzana
authors.initials: Z
authors.lastname: Jilkova
authors.forename: Barbora
authors.initials: B
authors.lastname: Stankova
authors.forename: Eva
authors.initials: E
authors.lastname: Tvrzicka
authors.forename: Morten
authors.initials: M
authors.lastname: Bryhn
mesh_terms: D052242:Adiponectin / Q000378:metabolism; D000273:Adipose Tissue / Q000378:metabolism*; D000818:Animals; D004041:Dietary Fats / Q000494:pharmacology / Q000627:therapeutic use*; D015525:Fatty Acids, Omega-3 / Q000494:pharmacology / Q000627:therapeutic use*; D006801:Humans; D007249:Inflammation / Q000178:diet therapy; D007333:Insulin Resistance; D050356:Lipid Metabolism; D024821:Metabolic Syndrome / Q000378:metabolism / Q000517:prevention & control*; D051379:Mice; D008928:Mitochondria / Q000378:metabolism; D051381:Rats; D015398:Signal Transduction
chemical_list: D052242:Adiponectin; D004041:Dietary Fats; D015525:Fatty Acids, Omega-3