Proceedings of the Nutrition Society

Research Article

n-3 PUFA: bioavailability and modulation of adipose tissue function

Symposium on ‘Frontiers in adipose tissue biology’

on 7 and 8 April 2009, A Meeting of the Nutrition Society, was held at the Royal Society of Edinburgh, Edinburgh, hosted by the Scottish Section.

Jan Kopeckya1 c1, Martin Rossmeisla1, Pavel Flachsa1, Ondrej Kudaa1, Petr Braunera1, Zuzana Jilkovaa1, Barbora Stankovaa2, Eva Tvrzickaa2 and Morten Bryhna3

a1 Department of Adipose Tissue Biology, Institute of Physiology of the Academy of Sciences of the Czech Republic, Videnska 1083, 142 20 Prague, Czech Republic

a2 Charles University in Prague, 1st Faculty of Medicine, 4th Department of Medicine, U Nemocnice 2, 128 08 Prague, Czech Republic

a3 Silentia AS, Svelvik, Norway

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.

(Online publication August 24 2009)

Correspondence:

c1 Corresponding author: Professor Jan Kopecky, fax +420 241062599, email kopecky@biomed.cas.cz