Diet restriction alone improves glucose tolerance and insulin sensitivity than its coadministration with krill or fish oil in a rabbit model of castration-induced obesity.

This study investigated the effect of 50% diet restriction and its coadministration with krill oil (KO) or fish oil (FO) on glucose tolerance and insulin sensitivity in a rabbit model of obesity. Castrated male rabbits were 50% restricted fed and supplemented with KO or FO (600 mg omega-3 polyunsaturated fatty acids/daily) for 2 months. Simultaneously, two control groups were used: castrated, full-diet-fed and castrated, 50% restricted fed rabbits without additives restricted group (RG). The energy-restricted diet decreased final body weight in castrated male rabbits and improved most insulin sensitivity and ß-cell function indexes. Combining the same diet and KO or FO, further reduced fasting blood glucose levels. However, this feed regime significantly accelerated insulin secretion and reduced gene expression of insulin receptor substrate-1, pyruvate kinase and 3-hydroxy-3-methylglutaryl-CoA synthase 2. This was manifested by reduced dynamic insulin sensitivity, assessment homoeostasis-ß-cell function indices and increased glucose elimination rate to levels comparable to or above the obese animals. Aspartate and alanine aminotransferases enzyme activities were raised more than those in the obese group. Surprisingly, KO and FO administration downregulated acetyl-coenzyme A oxidase and carnitine palmitoyltransferase 2 messenger RNA gene expression compared to the RG. In conclusion, we can assume that a better effect on insulin sensitivity and glucose tolerance was observed in the diet restriction alone than in the coadministration of KO or FO when animals are exposed to highly obesity predisposing factors. These effects could be at least in part ascribed to the modified gene expression levels of some critical enzymes and factors involved in liver glucose metabolism and ß-oxidation.

Effect of fish and krill oil supplementation on glucose tolerance in rabbits with experimentally induced obesity.

PURPOSE: This study was conducted to investigate the effect of fish oil (FO) and krill oil (KO) supplementation on glucose tolerance in obese New Zealand white rabbits. METHODS: The experiments were carried out with 24 male rabbits randomly divided into four groups: KO-castrated, treated with KO; FO-castrated, treated with FO; C-castrated, non-treated; NC-non-castrated, non-treated. At the end of treatment period (2 months), an intravenous glucose tolerance test (IVGTT) was performed in all rabbits. RESULTS: Fasting blood glucose concentrations in FO and KO animals were significantly lower than in group C. The blood glucose concentrations in FO- and KO-treated animals returned to initial values after 30 and 60 min of IVGTT, respectively. In liver, carnitine palmitoyltransferase 2 (Cpt2) and 3-hydroxy-3-methyl-glutaryl-CoA synthase 2 (Hmgcs2) genes were significantly increased in FO-fed rabbits compared with the C group. Acetyl-CoA carboxylase alpha (Acaca) expression was significantly reduced in both KO- and FO-fed rabbits. In skeletal muscle, Hmgcs2 and Cd36 were significantly higher in KO-fed rabbits compared with the C group. Acaca expression was significantly lower in KO- and FO-fed rabbits compared with the C group. CONCLUSION: The present results indicate that FO and KO supplementation decreases fasting blood glucose and improves glucose tolerance in obese New Zealand white rabbits. This could be ascribed to the ameliorated insulin sensitivity and insulin secretion and modified gene expressions of some key enzymes involved in ß-oxidation and lipogenesis in liver and skeletal muscle.