Abstract
We studied the effects of calcitonin, parathyrin, and Ca(2+) channel antagonist isoptin and agonist Bay-K-8644 on glucose consumption by muscle (diaphragm) and adipose (epididymal) tissues and insulin-stimulated glucose consumption in vivo and in vitro. Calcitonin and parathyrin did not alter glucose consumption; parathyrin did not affect, while calcitonin completely abolished the stimulating effect of insulin in vivo and in vitro. Isoptin significantly increased glucose consumption in vivo and in vitro, while Bay-K-8644 in vitro had no effect glucose consumption. Isoptin did not affect, while Bay-K-8644 significantly reduced the stimulating effect of insulin on glucose consumption by the muscle and adipose tissues. Isoptin did not affect the stimulating effect of insulin against the background of parathyrin administration and completely blocked the inhibitory effect of calcitonin on insulin-stimulated glucose consumption by the muscle and adipose tissues in vivo and in vitro, while Bay-K-8644 potentiated this effect of calcitonin in vitro.
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