n-3 PUFA: bioavailability and modulation of adipose tissue function
Language English Country England, Great Britain Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't, Review
PubMed
19698199
DOI
10.1017/s0029665109990231
PII: S0029665109990231
Knihovny.cz E-resources
- MeSH
- Adiponectin metabolism MeSH
- Dietary Fats pharmacology therapeutic use MeSH
- Insulin Resistance * MeSH
- Rats MeSH
- Fatty Acids, Omega-3 pharmacology therapeutic use MeSH
- Humans MeSH
- Metabolic Syndrome metabolism prevention & control MeSH
- Lipid Metabolism * MeSH
- Mitochondria metabolism MeSH
- Mice MeSH
- Signal Transduction MeSH
- Adipose Tissue metabolism MeSH
- Inflammation diet therapy MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Humans MeSH
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Review MeSH
- Names of Substances
- Adiponectin MeSH
- Dietary Fats MeSH
- Fatty Acids, Omega-3 MeSH
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.
References provided by Crossref.org
The inhibition of fat cell proliferation by n-3 fatty acids in dietary obese mice