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Review
. 2018 Aug:58:1-16.
doi: 10.1016/j.jnutbio.2018.02.012. Epub 2018 Feb 27.

Omega-3 fatty acids in obesity and metabolic syndrome: a mechanistic update

Kembra Albracht-Schulte  1 , Nishan Sudheera Kalupahana  2 , Latha Ramalingam  1 , Shu Wang  1 , Shaikh Mizanoor Rahman  1 , Jacalyn Robert-McComb  3 , Naima Moustaid-Moussa  4
Affiliations
Review

Omega-3 fatty acids in obesity and metabolic syndrome: a mechanistic update

Kembra Albracht-Schulte et al. J Nutr Biochem. 2018 Aug.

Abstract

Strategies to reduce obesity have become public health priorities as the prevalence of obesity has risen in the United States and around the world. While the anti-inflammatory and hypotriglyceridemic properties of long-chain omega-3 polyunsaturated fatty acids (n-3 PUFAs) are well known, their antiobesity effects and efficacy against metabolic syndrome, especially in humans, are still under debate. In animal models, evidence consistently suggests a role for n-3 PUFAs in reducing fat mass, particularly in the retroperitoneal and epididymal regions. In humans, however, published research suggests that though n-3 PUFAs may not aid weight loss, they may attenuate further weight gain and could be useful in the diet or as a supplement to help maintain weight loss. Proposed mechanisms by which n-3 PUFAs may work to improve body composition and counteract obesity-related metabolic changes include modulating lipid metabolism; regulating adipokines, such as adiponectin and leptin; alleviating adipose tissue inflammation; promoting adipogenesis and altering epigenetic mechanisms.

Keywords: Adipocytes; Fish oil; Metabolic syndrome; Obesity; Omega-3 polyunsaturated fatty acids; Weight loss.

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Figures

Fig. 1.
Fig. 1.
Adipose tissue, liver and skeletal muscle cross talk in obesity and insulin resistance. The liver maintains normoglycemia during fasting via glycogenolysis and gluconeogenesis. Following a meal, increased glucose delivery to the pancreas stimulates insulin secretion, which acts on the liver, adipose tissue and skeletal muscle. The primary action of insulin on the liver is to suppress hepatic glucose output, while insulin increases glucose uptake by the skeletal muscle and adipose tissue. Insulin additionally inhibits lipolysis in adipose tissue. In obesity, changes in adipokines produced and released from adipose tissue, such as decreased adiponectin and increased TNF-α and other inflammatory cytokines, coupled with increased free fatty acids contribute to hepatic and skeletal muscle insulin resistance.
Fig. 2.
Fig. 2.
Metabolism of omega-6 and omega-3 polyunsaturated fatty acids. LA is an essential n-6 PUFA that is metabolized to AA and further to proinflammatory eicosanoids. ALA is an essential n-3 PUFA that is metabolized to EPA, DPA and DHA. Eicosanoids derived from the metabolism of EPA, DPA and DHA also aid in the regulation of inflammation and are considered more anti-inflammatory. ISOPS, isoprostanes; COX, cyclooxygenases; LOX, lipooxygenases.
Fig. 3.
Fig. 3.
Mechanisms mediating effects of n-3 PUFA on liver, adipose tissue and skeletal muscle metabolism. Omega-3 PUFAs increase fatty acid oxidation in the liver, adipose tissue and skeletal muscle, thus limiting fat storage in these tissues. Omega-3 PUFAs also decrease the production and release of proinflammatory adipokines. In skeletal muscle, n-3 PUFAs promote protein synthesis. All mechanisms depicted here contribute to an improved metabolic profile.
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