EFFECTS OF CALCITRIOL ADMINISTRATION ON GLYCATION AND SERUM INSULIN LEVEL IN FRUCTOSE-INDUCED INSULIN RESISTANCE IN WISTAR RATS
Keywords:
Calcitriol, Diabetes mellitus, Glycated Haemoglobin, HyperglycaemiaAbstract
High fructose diet induces adverse metabolic alterations including insulin resistance, diabetes mellitus,
dyslipidaemia and liver steatosis. The study was designed to evaluate the role of calcitriol administration on
metabolic alterations induced by 10% fructose solution in Wistar rats. Twenty five (25) male Wistar rats were
used in this research work. The rats were divided into 5 groups of 5 animals each: Group I: Control; received
grower’s mash + Distilled water Group II: Received grower’s mash + 125 μg/Kg body weight of Calcitriol
daily; Group III: Received grower’s mash + 10% fructose solution + 125 μg/Kg body weight of calcitriol daily;
Group IV: Received grower’s mash + 10% fructose solution Group V: Received grower’s mash + 10% fructose
diet + 0.3 mg / Kg body weight of glibenclamide daily. For the induction of hyperglycaemia and lipidaemia rats
were given 10% fructose solution as drinking water for eight (8) weeks. Calcitriol was administered 5 weeks
after the beginning of fructose drinking. The result of the study shows that, Group IV exhibited significant
change in body weights compared with the control rats (219.1 ± 17.36 vs 189.2 ± 6.37). Groups II, III and V
compared with the control rats, revealed no significant change in body weight. Calcitriol administration
produced no significant change in plasma glucose level and HbA1c in group II rats compared to control rats
(5.12 ± 0.39 vs 5.20 ± 0.15 mmol/L), (4.43 ± 0.28 vs 4.29 ± 0.31 %). Glibenclamide administration group V
effectively abolished the fructose-induced hyperglycaemia and glycated haemoglobin. Oral calcitriol treatment
ameliorated serum insulin levels and HOMA-IR in fructose-fed rats. In conclusion calcitriol treatment did not
produce significant effect on body weight, fasting glucose levels and HbA1c but alleviated fructose-induced
hyperinsulinemia as well as insulin resistance.