Abstract
Results obtained from studies on the effect of vitamin D supplementation with or without calcium on glucose homeostasis and hematological parameters have been inconsistent. This experimentally-controlled designed study investigated the combined effects of Ca2+ and Vit.D-fortified diet on body weight, glycemic profile, biochemical, haemostatic and haematological parameters in 2 groups (n=8, each) of experimental male diabetic and healthy albino rats following treatment with Ca2+ and Vit.D-fortified diet for 6 weeks. 2 similar groups of rats (n=8, each) on normal diets served as normal and diabetic controls respectively to allow comparison between groups. Induction of diabetes (100mg/dL, intraperitoneally) was achieved with freshly prepared alloxan monohydrate solution after 15 hours overnight fast while oral glucose tolerance test, biochemical and hematological analysis were performed on blood samples. Fasting blood glucose (FBG) was taken at study baseline and 6 weeks after feeding. Mean weights were significantly (p < 0.05) lower in calcium/vitamin D-fortifed diet-fed diabetic and normal rats compared with their respective controls. Actual percentage numerical weight gain at 6 weeks of study includes: diabetic rats on treatment diet (15.50%); diabetic controlled rats (18.70%); normal rats on treatment diet (20.40%); normal controlled rats (25.10%). At 6 weeks of study, experimental diabetic rats showed significant (p < 0.05) reduction (22.83%) in mean FBG concentration compared with the diabetic control rats. Experimental rats fed on calcium and vitamin D-fortified diet displayed improved glycemic tolerance over their respective controls. Hematological analysis revealed insignificant (p > 0.05) difference in hematological and hemostatic indices between the experimental and controlled rats. In diabetic rats, Ca2+ and Vit.D-fortified diet reduced body weight with beneficial hypoglycemic and remarkable glycemic tolerant effects on glycemic profile without significant impact on hemostatic and hematological indices.
Highlights
Obesity is a well-defined epidemic in Westernized cultures and increasing prevalence is being seen in developing countries too
The hallmarks of impaired insulin sensitivity in these three tissues are decreased insulin-stimulated glucose uptake into skeletal muscle, impaired insulin-mediated inhibition of hepatic glucose production in liver, and a reduced ability of insulin to inhibit lipolysis in adipose tissue.insulin resistance is a major predictor for the development of various metabolic sequelae, including type 2 diabetes and is a defining feature of syndrome X, which is known as the metabolic syndrome
This syndrome encompasses a constellation of conditions, including insulin resistance, dyslipidemia, hypertension, and obesity, and is often accompanied by hyperinsulinemia, sleep apnea, and other disorders[2].MetS increases the risk developing CVD by 2-fold .Obesity (BMI > 30 kg/m2), which presents with dyslipidemia and elevated cholesterol levels, plays a major role in the development of MetS, which increases the risk of type II diabetes .Because of the exploding obesity epidemic, research efforts have escalated to better understand all aspects of the pathophysiology, including how obesity affects lipid and lipoprotein metabolism
Summary
Obesity is a well-defined epidemic in Westernized cultures and increasing prevalence is being seen in developing countries too. The hallmarks of impaired insulin sensitivity in these three tissues are decreased insulin-stimulated glucose uptake into skeletal muscle, impaired insulin-mediated inhibition of hepatic glucose production in liver, and a reduced ability of insulin to inhibit lipolysis in adipose tissue.insulin resistance is a major predictor for the development of various metabolic sequelae, including type 2 diabetes and is a defining feature of syndrome X, which is known as the metabolic syndrome This syndrome encompasses a constellation of conditions, including insulin resistance, dyslipidemia, hypertension, and obesity, and is often accompanied by hyperinsulinemia, sleep apnea, and other disorders[2].MetS increases the risk developing CVD by 2-fold .Obesity (BMI > 30 kg/m2), which presents with dyslipidemia and elevated cholesterol levels, plays a major role in the development of MetS, which increases the risk of type II diabetes .Because of the exploding obesity epidemic, research efforts have escalated to better understand all aspects of the pathophysiology, including how obesity affects lipid and lipoprotein metabolism
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