AIM: The purpose of this study was to investigate the relationship between -174 G>C IL-6 polymorphism gene on the level of IL-6 and CRP in the population of western Indonesia obese who are obese.
METHODS: In this study, we examined 178 subjects consisting of 89 who are obese with BMI> 25, and controls with BMI between 18.5 and 23. Fasting blood was taken from each subject for the examination of IL-6 and CRP levels by the ELISA method. Determination of genotype -174 G>C IL-6 gene was examined by Polymerase Chain reaction- Restriction Fragment Length Polymorphism (PCR-RFLP) methods.
RESULTS: The results of this study showed increased levels of IL-6 and CRP in the obese group compared to the controls. In the obese group, CC genotype had higher CRP and lower IL-6 levels than the GC and GG genotypes. The frequency of CC genotype in the obese group was 47.2% compared with 28.1% in controls and this genotype was considered a risk factor for obesity. Carriers of the C genotype as a dominant or a recessive model had greater risk of obesity.
CONCLUSION: It was concluded that the polymorphism - 174G>C IL-6 gene is a risk factor for obesity and is associated with increased levels of IL-6 and CRP in an obese group of the Western Indonesian ethnic population.
AIM: To investigate the beneficial effects of fish oil consumption on the progression of insulin resistance and pancreatic islet dysfunction in a rat model of diabetes.
METHODS: Diabetic rats model (n = 30) were divided into five groups and received; 1) NS injection + NS oral (normal control); 2) NS injection + 3 g/kg fish oil (fish oil control); 3) streptozotocin (STZ) injection + NS oral [diabetes control (DC)]; 4) STZ injection + 1 g/kg fish oil (DFO1); and 5) STZ injection + 3 g/kg fish oil (DFO3). Fasting blood insulin was analyzed by commercial rat insulin enzyme-linked immunosorbent assay; meanwhile, the determination of insulin sensitivity was calculated by homeostatic model assessment of insulin resistance (HOMA-IR) and homeostatic model assessment of beta-cell function. A histological study was conducted on pancreas tissue using H and E staining.
RESULTS: Fish oil supplementation reduced hyperglycemia and ameliorated HOMA-IR in STZ-induced animal models indicating that fish oil supplementation improved insulin sensitivity. Furthermore, animals treated with fish oil at a dose of 3 g/kg (DFO3) showed an enhancement in pancreatic islets, which was displayed by less abnormal structures than DC animals. This could imply that the administration of fish oil, especially rich in bioactive omega-3 fatty acids effectively inhibits insulin resistance and restore islet of Langerhans alteration in rats injected with STZ.
CONCLUSION: Thus, the current study suggested that fish oil supplementation could support the treatment of diabetes but should not be considered as an alternative therapy.
METHODS: Human umbilical vein endothelial (HUVEC), fibroblast (CCD-18) and retinal ganglion (RGC-5) cells were cultured in medium containing different concentrations of FVCO. The proliferation, migration and morphological changes of cells were determined. The angiogenic effect of FVCO was evaluated by rat aortic assay. The therapeutic effect of FVCO on wound healing was further assessed in a wound excision model in Sprague Dawley rats. The expression of phospho-VEGFR2 (vascular endothelial growth factor receptor 2) in HUVECs was detected by Western blot.
RESULTS: FVCO (6 and 12 µg/mL) significantly improved the proliferation of HUVEC, CCD-18 and RGC-5 cells (P < 0.05 or 0.01). FVCO (25 µg/mL) markedly increased the migration ability of CCD-18 and RGC-5 cells (P < 0.05). FVCO did not affect cell morphology as indicated by fluorescein diacetate (FDA), rhodamine 123 and Hoechst staining. FVCO (25, 50 and 100 µg/mL) significantly stimulated the ex vivo blood vessel formation as compared with negative control (P < 0.05). Rats in FVCO group had significantly smaller wound size, higher wound healing percentage, and shorter wound closure time when compared with control group since day 8 (P < 0.05), suggesting that oral FVCO administration notably promoted the wound healing process. FVCO treatment (6 and 12 µg/mL) significantly enhanced the phospho-VEGFR2 expression in HUVECs (P = 0.006 and 0.000, respectively).
CONCLUSION: Our study confirms a high angiogenic and wound healing potency of FVCO that might be mediated by the regulation of VEGF signing pathway.