Dietary omega-3 fatty acid supply influences mechanisms controlling body weight and glucose metabolism.

Abstract:

Background - Omega-3 polyunsaturated fatty acids are known to influence crucial membrane functions, eicosanoid metabolism and gene expression mechanisms. Objective - To determine the influence of dietary omega-3 fatty acid supply on ingestive behaviour, body weight, adiposity and glucose tolerance. Design - Female rats were fed with a alpha-linolenic acid (ALA) sufficient (CON) or deficient (DEF) diet throughout gestation and lactation. Three groups of male offspring were studied: (1) pups maintained on CON diet, from mothers on CON diet, CON (n=11); (2) pups maintained on DEF diet, from mothers on DEF diet, DEF (n=11); (3) pups maintained on CON diet from weaning (3 weeks of age), from mothers on DEF diet, DEF-CON (n=11). Food intake, body weight, fat and oral glucose tolerance were assessed in adult offspring. Brain gene expression of 3-week old and adult offspring was evaluated. Fatty acid profile of mothers' milk was also analyzed. Statistical analysis by ANOVA; P<0.05 was considered significant. Outcomes - CON-mothers showed a 15-fold increase of ALA content in milk compared with DEF-mothers. Relative to CON offspring, adult DEF-CON offspring consumed more food (P<0.05), were heavier, had a greater proportion of body fat and showed impairment in glucose tolerance; adult DEF animals had similar food intake, body weight, proportion of body fat, but showed impaired glucose tolerance. Two genes coding for proteins involved in glucose homeostasis (Pttg1; Pituitary tumor-transforming 1, Exoc7; exocyst complex component 7) were under-expressed in DEF weanlings but not in adult animals. The expression of genes coding for glucose transporter 4, insulin and leptin receptors and neuropeptide Y were not altered due to omega-3 deficiency. Conclusions - Deficiency of omega-3 fatty acids from conception adversely affected glucose tolerance, assessed in adulthood. Exposure of DEF offspring to CON diet from weaning, however, caused more severe disruption of physio-logical mechanisms, possibly initiated by changes in the mechanisms controlling food intake.