One-Time Injection of Parathyrin Increases Glucose Tolerance

Abstract

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.

Calcitonin and Parathyrin are Glucoregulating Hormones

“…It was showed the decreasing of the blood glucose level after onetime injection of parathyroidin (the preparation of bull PTH), which caused by hypercalcaemia, that confirms in tests with the calcium laktat load [57]. Besides, there is a close negative correlation established between glucose and calcium level (r =-0, 813, P>0,02).…”

“…Calcium channels blockers (isoptin and nifedipin) led to much more decreasing of hyperglycemia under glucose-tolerance test against the background of PTH [57]. It indicates the role of L-type Ca2 +channel in the mechanisms of PTH effect on glucose homeostasis and testifies about PTHcapacity to increase glucose tolerance.…”

“…Unlike CT, induced glucose intolerance, PTH, on the contrary, decreasing the blood glucose level, decreased the degree of hyperglycemia, i.e. it increased glucose tolerance [57]. Apparently, PTHdue to hypercalcaemia stimulates insulin secretion, which, in one's turn, normalizes the blood glucose level and the same one doesn't make worse glucose tolerance.…”

“…A special interest is the data of glucose consumption by muscle and adipose tissue in vivo and in vitro. Just like CT, PTHdidn't effect on glucose consumption by these tissues but unlike CT [27] it didn't change insulin-stimulating effect on this process [57]. Thus, it is established the opposite to CT action of PTHon glucose metabolism.…”

Calcitonin and parathyrin are antagonists concerning to the regulation of glucose metabolism

“…However, there are a lot of facts about CT hyperglycemic, contra-insular effect and it participant in the development of insulin resistance [1][2][3][4][5][6] have studied now. More less facts are known about PTH effects on glucose metabolism [7,8]. We thought it appropriate to compare the effects of CT and PTH on glucose metabolism and its interaction to analyze possible mechanisms underlying of its effects on glucose metabolism.…”