Effect of acute hypercalcaemia on glucose tolerance and insulin release in human beings

Abstract

Insulin secretion in response to an oral glucose challenge during acute hypercalcaemia was studied. Oral glucose tolerance tests (OGTT) were performed in 12 non-diabetic, non-obese human volunteers, aged 20\p=n-\28 years. Blood samples were collected for calcium, glucose and insulin determination. The next day the same volunteers received a 4 h infusion of calcium gluconate (15 mg/kg/4 h) and were administered glucose 1 h after starting the infusion. Serum calcium, glucose and insulin concentrations were measured again.Infusion of calcium gluconate resulted in an increase in serum calcium concentration of 5 mg/100 ml over 4 h. During these infusions no significant changes in glucose concentrations were noted. On the other hand, the total mean insulin concentration, expressed as the area under the 3 h glucose tolerance curve, and the insulin peak at 30 min were significantly increased during hypercalcaemia (P < 0.001).These data indicate that acute hypercalcaemia does not affect carbohydrate tolerance but increases insulin secretion in human beings.

One-Time Injection of Parathyrin Increases Glucose Tolerance

“…Evidently, parathyrin due to hypercalcaemia stimulates insulin secretion which normalizes the blood glucose level and the same one doesn't make worse glucose tolerance. Analogous data were received under acute hypercalcaemia [17].…”

The Effect of Acute Hypercalcemia on the Insulin Response to OGTT

“…How- were probably caused by the too short duration of hypercalcemia and too low concentration of extra-cellular calcium. Recently, Gedic, Akalin and Koray (1980) gave 15 mg/kg calcium intravenously during OGTT and were able to produce a significant increase in insulin release as expressed by increment in insulin areas. In the present study we tried to repeat their experiment using 25 mg Ca/kg, but instead of the expected rise of insulin, a significant decrease of insulin output was found.…”

“…Chronic hypercalcemia due to parathyroid hyperfunction caused an increase in insulin secretion during glucose stimulation (Kim, Kalkhoff, Cerllety and Jacobson 1971;Yasuda, Hurukawa, Okuyama, Kikuchi and Yoshinaga 1975;Pento, Kagan and Glick 1974). Acute hypercalcemia induced in vivo in healthy volunteers revealed no clear change in the insulin response (Gaeke, Kaplan, Rubinstein, Starr and Burke 1975;Gero, Szalay, Steczek and Tamas 1976) except for a recent paper (Gedic, Akalin and Koray 1980) which showed a significant increase in insulin release. Because of these conflicting reports, it was decided to reinvestigate the influence of high serum levels of calcium on insulin levels, during OGTT.…”

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

“…Apparently, PTH due 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. Analogues data were received under acute hypercalcaemia [17].…”