Abstract

The increasing secretion of calcitonin and hypocalcemia under insulin hypoglycemia, induced with insulin injection (1 IU/100g), was established. Physiological mechanisms of the stimulating effect of insulin hypoglycemia on calcitonin secretion were studied in double-side adrenalectomized and pancreatectomized rats and under the blocking synaptic transmission in sympathetic ganglions or via peripheral cholino- and adreno-receptor structures. Insulin hypoglycemia didn’t expose the increasing secretion of calcitonin in rats under adrenalectomy and pancreatectomy. Ganglion-blocker pentamin (2.5 mg/100g body weight), blocker of M-cholino-receptors atropine (0.2 ml), α-adreno-blocker tropaphen (0.1 mg/100g), and β-adreno-blocker obzidan (0.1 mg/100g) evoked the inhibiting effect on calcitonin secretion in spite of simultaneously increasing of hypog-lycemia. Corticosteroids and, obviously, glucagon and also the tone of autonomic nervous system via peripheral M-cholinoreactive and α- and β-adrenoreactive structures take part in the activation of calcitonin secretion under insulin hypoglycemia.

Highlights

  • The calcitonin (CT) effect on carbohydrate metabolism is well-known

  • Insulin injection led to the decreasing of the blood glucose level to 2.4 ± 0.2 m∙mol/l (P1 < 0.001) and increasing of serum CT-activity to 23.1 ± 3.5 IU/ml

  • There is a close negative correlation established between calcium level and 11-OCS content in the blood serum (r = −0.89, P < 0.05), and between glucose level and 11-OCS content (r = −0.87, P < 0.05) that testifies about interaction of regulating effects of calcium and carbohydrate metabolism

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Summary

Introduction

The calcitonin (CT) effect on carbohydrate metabolism is well-known. In part, it possesses hyperglycemic action [1]-[8]. For CT secretion, it is indifferent and is the state of carbohydrate metabolism. Hypocalcaemia and increasing of CT secretion under insulin hypoglycemia (IH) [9] [10] were established. The mechanisms of the hypoglycemia stimulating effects on CT secretion have yet been stu-. How to cite this paper: Moisa, S.S. and Nozdrachev, A.D. Open Journal of Endocrine and Metabolic Diseases, 4, 231-237.

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