Plasma Insulin and Working Dynamics of Calcium Channel Blockers on Thyroid Hormone Impaired Glucose Metabolism

The use of calcium channel blocker as supplementary in thyroid hormone treatment had been strongly proposed but gradually became unpopular after observations that clinical outcomes for angina, or myocardial infarct were not improved by the use of these agents. This study therefore examined the influence of calcium channel blockers on thyroid hormone impaired glucose metabolism. Twenty (20) male albino Wistar rats were randomized into four groups (n= 5 per group). Two groups were respectively pre-treated with verapamil (20 mg/Kg body weight) or nifedipine (20 mg/Kg body weight) 20 mins before oral administration of L- Thyroxine (L-T4) 20 ug/kg body weight twice daily for six (6) days. One group received only L- Thyroxine (L-T4) 20 ug/kg body weight twice daily for six (6) days while the control group received no drug. Glucose concentrations were measured in blood obtained from the tip of tail with one- Touch Basic glucometer on 1st, 4th and 7th days and fasting plasma insulin was measured on the 7th day using ELISA. The results showed raised plasma glucose levels on days 4 that were not significantly different from those of day 1 in all the groups. However, plasma glucose concentrations on day 7 in groups treated with L-T4 and after verapamil or nifedipine pre-treatment were significantly higher than those on day 1 and also significantly higher than those of the control group on day 7. Highest concentration of plasma glucose was observed in the nifedipine pre-treatment group on day 7. Plasma insulin level was not significantly changed. Insulin resistance indices for the levothyroxine group were not significantly higher (p>0.05) than that of the control. However, HOMA- IR values were significantly higher and the QUICKI values lower when levothyroxine was administered to calcium channel blockers pre-treated animals. This suggests that the thyroid hormone induced hyperglycemia was neither due to alterations in insulin concentrations by thyroxine nor can be ameliorated by the blockage of the opening of the L-voltage gated calcium channels but may be associated with increased insulin resistance.