Are marine n-3 fatty acids protective towards insulin resistance? From cell to human

• Published in: Proceedings of the Nutrition Society Vol. 79; no. 4; pp. 417 - 427
• Main Author: Delarue, Jacques
• Format: Journal Article
• Language: English
• Published: Cambridge, UK Cambridge University Press 01.11.2020
• Subjects: Acid resistance; Adipocytes; Animal models; Cell adhesion & migration; Clinical trials; Conference on ‘Malnutrition in an Obese World: European Perspectives’; Cytokines; Dexamethasone; Diabetes; Diabetes mellitus; Diet; Endoplasmic reticulum; Fatty acids; FENS 2019; Food; Gene expression; Genotype & phenotype; Heterogeneity; Human subjects; humans; Inflammation; Insulin; Insulin resistance; Kinases; Lipids; meta-analysis; noninsulin-dependent diabetes mellitus; Phosphorylation; Population studies; protective effect; Proteins; Risk; Risk reduction; Rodents; Sucrose; Sugar; Symposium 3B: Omega-3 fatty acids: from lab to clinic; Traditional foods; Western diets; Type-2 diabetes; Inflammation; Adipose tissue; n-3 Fatty acids
• ISSN: 0029-6651; 1475-2719; 1475-2719
• DOI: 10.1017/S0029665120000087

Marine n-3 fatty acids improve most of the biochemical alterations associated with insulin resistance (IR). Experimental models of dietary-induced IR in rodents have shown their ability (often at a very high dose) to prevent IR, but with sometimes a tissue specific effect. However, in a high sucrose diet-induced IR rat model, they are unable to reverse IR once installed; in other rodent models (dexamethasone, Zucker rats), they are inefficacious perhaps because of the severity of IR. The very low incidence of type-2 diabetes (T2D) in Inuits in the 1960s, which largely increased over the following decades in parallel to the replacement of their traditional marine food for a western diet strongly suggests a protective effect of marine n-3 towards the risk of T2D; this was confirmed by reversal of its incidence in intervention studies reintroducing their traditional food. In healthy subjects and insulin-resistant non-diabetic patients, most trials and meta-analyses conclude to an insulin-sensitising effect and to a very probable preventive or alleviating effect towards IR. Concerning the risk of T2D, concordant data allow us to conclude the protective effect of marine n-3 in Asians while suspicion exists of an aggravation of risk in Westerners, but with the possibility that it could be explained by a high heterogeneity of studies performed in this population. Some longitudinal cohorts in US/European people showed no association or a decreased risk. Further studies using more homogeneous doses, sources of n-3 and assessment of insulin sensitivity methods are required to better delineate their effects in Westerners.