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 β-oxidation and lipogenesis in liver and skeletal muscle.
Rabbits are considered as appropriate animal models to study some obesity-associated abnormalities because of the similarity of their blood lipid profile and metabolism to humans. The current study was focused on comparison of adipose differentiation ability in rabbit adipose-derived stem cells (ADSC) in vitro. Subcutaneous and visceral stromal vascular fractions (SVF) were isolated from three 28-d-old New Zealand rabbits by collagenase digestion. Supernatants from both isolates were collected 24 h after the initial plating. On the fourth passage, all isolated cell types undergo triplicate adipogenic induction. The adipose induction potential was calculated as percentage of increasing optical density (OD) values. The data revealed that with increasing the number of induction cycles, the induction tendency in visceral ADSC decreased in contrast to the subcutaneous ones. Although the supernatants did not reach induction levels of their relevant precursors, they follow the same pattern in both subcutaneous and visceral ADSC. All cell types successfully passed osteogenic and chondrogenic differentiation. In conclusion, the best adipose induction ability was observed in directly plated subcutaneous cell population. The increase of induction numbers depressed adipose induction ability in cell populations derived from visceral fat depots.
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 β‐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‐β‐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 β‐oxidation.
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