The review contains contemporary literature data about calcitonin role in the development of insulin resistance and its potential role in the pathogenesis of carbohydrate metabolism disturbances. Analogues disturbances revealed under diabetes mellitus and under calcitonin treatment are considered. Literature data about hormone diabetogenicity are discussed. The analysis of experimental and literature data testifies that calcitonin under unfavorable conditions (age, obesity, stress) against the background of the decreasing of functional activity of insular apparatus can lead to the development of metabolic syndrome and diabetes mellitus. It is shown that calcium channel blockers inhibit calcitonin effect leads to glucose intolerance and decreases tissue insulin sensitivity. In this connection a question about direct influence on calcium mechanisms of endocrine system as possible method of drug therapy is discussed.
We studied the effects of Russian preparation of porcine calcitonin (Calcitrinum, 1 U/100 g) on the level of glucose and total calcium, glycogen concentration in the liver, and glucose consumption by the muscle and adipose tissues in vivo and in vitro. The basal level of insulin and secretion of insulin in the dynamics of glucose tolerance test were studied after treatment with calcitonin. In addition to hypocalcemic effect, this substance produced significant hyperglycemic effects, decreased glycogen amount in the liver, inhibited insulin-induced glucose consumption by muscular and adipose tissues in vivo and in vitro, slowed down insulin secretion during glucose load, and impaired glucose tolerance. Thus, calcitonin had contra-insular effects on glucose metabolism.
The effect of a 100-300-fold attenuated geomagnetic field on the embryonic development of great ramshorn Planorbarius corneus and oxidation-reduction properties in water environment were studied in a hypomagnetic chamber. Mainly the hypomagnetic field effected beneficial influence on the development of mollusks: teratogenic effects were less massive, i.e. embryos that first occurred in hypomagnetic conditions were characterized by low death rate. The mobility index increased in embryos on the stage of late veliger and post-metamorphosis. Under the sharp increasing of the magnetic field to the normal level the embryos and juvenile mollusks rapidly perished (practically, their growth was stopped). Type of induction was dependent on adaptation of juvenile P. corneus to a magnetic field. Mollusks growth in the normal geomagnetic field would prefer the conditions with maximal induction, whereas mollusks developed in the hypomagnetic chamber, on the contrary, chose the conditions with minimal induction. It was revealed that the oxidation-reduction potential of water increased as magnetic induction attenuated pointing to a natural decline that testifies about the regular decreasing of internal energy of water molecules, which, in our opinion, is caused the inhibition of the mollusk embryonic development.
One-time injection of domestic preparation of bull parathyrin-parathyreoidin (1 U/100g body weight, intramuscular) leads to a significant decrease of the blood glucose level and an increase of the serum calcium level in rats. There is a close negative correlation established between glucose and calcium level (r = −0.813, P > 0.02). The calcium laktat load (9 mg) per os induces the same changes. There is a functional negative correlation established between glucose levels and total calcium content (r = −0.997, P < 0.01). It proves that the decrease of the blood glucose level under parathyrin injection is connected with hypercalcaemia. Parathyrin causes the reduction of the dynamics of hyperglycemia under the glucose load per os (30% solution, 1 ml/100g), i.e. parathyrin increases glucose tolerance. Glucose consumption by muscle (diaphragm) and adipose (epididymal) tissues in vivo and in vitro does not alter under parathyrin and it does not affect the stimulating effect of insulin on the process. The combinative effect of parathyrin and calcium channel blockers-isoptin (5 mg/kg, intraperitoneal) or nifedipin (1 mg/kg, intraperitoneal) reveals more intensive and lasting decrease of the blood glucose level in comparison with only parathyrin effect and more reduction of the dynamics of hyperglycemia under the glucose load. Thus, parathyrin decreases the blood glucose level, increases glucose tolerance and does not effect insulin resistance.
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