The Protective Effect of Vitamin D on Cerebral Infarction in Rats Received High Fructose Diet

Background and aim: The relationship between insulin resistance (IR), hypovitamine D and cerebral infarction and its exact mechanism are not fully understood. However, oxidative stress and pro-inflammatory mediators may be involved. Thus, the aim of the present study was to investigate the effects of vitamin D on cerebral infarction, insulin resistance and inflammatory mediators in rats received high-fructose-diet. Material and methods: Eight four adult albino rats were divided randomly into 3 groups, normal control group, diabetic group rats received high fructose diet for 2 months without no treatment, diabetic rats received alphacalcidol (10?g//kg/day, orally), which was continued daily throughout the experiment, After 2 months, fasting blood glucose level and insulin, IR was evaluated by the homeostasis model assessment method (HOMA-IR). Some cerebrovascular risk markers as lipid profile (total cholesterol, HDL-C and triglycerides), as well as inflammatory biomarker interleukin-6 and cerebral infarction size were measured. Results: Rats had high fructose diet showed low 1, 25 (OH)2 D, with a significant (p <0.05) increase in fasting blood glucose level and higher HOMA-IR index, total cholesterol, low-density lipoprotein cholesterol (LDL-C), triglyceride and IL-6 as compared to control group. There were significant correlations between 1, 25 (OH)2 D levels and HOMA-IR index (r=-0.47; p <0.01), 1, 25 (OH)2 D, total cholesterol (r=-0.34; p <0.01); HDL-C (r=0.54; p <0.01), LDL-C(R=-0.34; P <0.01), IL-6 (r=-0.33; p <0.05). A two month oral alphacalcidol (10 ug/kg/day, orally) treatment markedly decreased HOMA-IR index (p <0.001), LDL, triglycereides and IL-6 and significantly reduced total cholesterol and cerebral infarction size. Conclusions: Our data showed that, low 1, 25(OH)2 D3 values are related to IR and associated with chronic inflammatory state and dyslipidemia, all of them can increase cerebrovascular risk. Vitamin D analogue significantly ameliorated the deleterious biochemical impact of diabetes mellitus protects against cerebral injury by its anti-inflammatory and decreasing insulin resistance in diabetic rats.