Decreased Dietary n‐6/n‐3 PUFA Ratio by Supplementing 18:3 and long chain n‐3 PUFA Protected Rats from Fructose‐Induced Adipose Tissue Dysfunction and Insulin Resistance
Authors: Sakamuri Anil , Jeyapal Sugeedha , Kona Suryam Reddy , Pothana Sailaja , Ibrahim Ahamed 
Published: June 2021

Impact of dietary n‐6/n‐3 polyunsaturated fatty acids (PUFA) ratio on the fructose‐induced visceral obesity and adipose tissue dysfunction was not studied previously. Here we studied the effect of diets containing n‐6 PUFA & α‐linolenic acid (ALA, 18:3 n‐3 PUFA) and n‐6 PUFA & long chain n‐3 PUFA (docosahexanoic acid and eicosapentaenoic acid, DHA and EPA) in the ratio of 2:1 and 5:1 respectively on fructose‐induced metabolic syndrome in the rats.

Weanling Wister rats were divided in to four groups and fed with diets containing starch (n‐6/n‐3 PUFA ratio 215:1), fructose (n‐6/n‐3 PUFA ratio 215:1) and fructose‐with n‐6/n‐3 PUFA ratio 2:1 (18:3 n‐3 PUFA) and 5:1 (long chain n‐3 PUFA) diets for twenty‐four weeks. Body composition, adiposity index and adipocyte size were determined along with macrophage infiltration by immunofluorescence. Gene expression of proteins related to pro‐ and anti‐inflammatory cytokines, and pre‐receptor metabolism of glucocorticoids were quantified by quantitative PCR. Plasma fatty acid profile was determined gas chromatography and, circulatory .0lipids and adipokines were measured by kit‐based methods. Insulin resistance was determined by homeostatic measurement of insulin resistance (HOMA‐IR) and oral glucose tolerance test.

Both n‐3 PUFA treatments significantly reduced the fructose‐induced visceral obesity and hyperuricemia. ALA and long chain (LC) n‐3 PUFA feeding significantly reduced fructose‐induced macrophage infiltration in adipose tissue, proinflammatory gene expression including monocyte chemoattractant protein 1, E‐selectin, tumor necrosis factor‐α, toll like receptor 2, 4 and corrected circulatory monocyte chemoattractant protein 1 and interleukin‐10 levels. Both n‐3 PUFA treatments significantly reduced fructose‐induced insulin resistance during fasting (HOMA‐IR) and corrected the elevated circulatory adiponectin levels. Interestingly, only LC n‐3 PUFA corrected the insulin resistance after the oral glucose challenge indicated by decreased area under curve for insulin (AUC). Both n‐3 PUFA treatments significantly reduced fructose‐induced gene expression of 11β‐hydroxysteroid dehydrogenase 1, an enzyme involved in pre‐receptor generation of glucocorticoids.

We conclude that replacement of dietary n‐6 PUFA with ALA and LC n‐3 PUFA ameliorates fructose‐induced visceral obesity, adipocyte dysfunction and insulin resistance. Though both ALA and LC n‐3 PUFA supplementation significantly reduced fructose‐induced adipose tissue dysfunction, considering beneficial effects LC n‐3 PUFA on insulin resistance and as LC n‐3 PUFA exhibited protective nature at less quantity than ALA, we propose that diets with LC n‐3 PUFA gives better protection against fructose‐induced adipose tissue dysfunction and insulin resistance than the diets with ALA.

Support or Funding Information

The present study was carried out with the financial support of Department of Biotechnology (DBT), Ministry of Science and Technology, Government of India, and Indian Council of Medical Research (ICMR), Government of India. AS was supported by Council of Scientific and Industrial Research (CSIR).

This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.