Effect of Glucose Stimulation on 45Calcium Uptake and Total Calcium Content of Pancreatic Islets of Fed and Fasted Rats and Obese Hyperglycemic Mice

Abstract

Effects of fasting on glucose-induced changes of various calcium parameters were investigated. The total calcium content of islets of fed rats and obese mice, determined by fluorometric microanalysis, amounted to 575 +/- 25 and 600 +/- 75 pmol/microgram DNA, respectively. Fasting for 24 or 72 h had no effect on the calcium content of rat islets, but increased that of mice by 30%. Glucose stimulation did not alter their total calcium content. The amount of 45Ca (as percentage of total islet calcium content) taken up over 30 min by fed mouse islets at 2.5, 10, and 15 mM glucose was equivalent to 32%, 41%, and 44% and by fed rat islets to 25%, 31%, and 34%, respectively. The net uptake of fed rat islets over 60 min at 2.5 and 15 mM glucose amounted to 36% and 61%. Fasting for 24 h inhibited insulin secretion over 30 min but not 45Ca uptake, whereas both parameters were inhibited after fasting for 72 h. Insulin secretion of mouse islets, was inhibited after 24 and 72 h of fasting, but 45Ca uptake was not significantly affected. Since glucose stimulates 45Ca uptake without changing the total islet calcium content, it must represent 45Ca- 40Ca exchange. Stimulation of insulin secretion of rat islets is associated with an increased calcium influx rate and increased exchangeable calcium pool(s) size. Calcium pool(s) size seems not to be altered by 24 h of fasting; however, 72 h of fasting tends to decrease the pool(s) size. The inhibition of insulin secretion induced by 24 h of fasting is not due to an altered calcium uptake, but it may be due to a modification of intracellular handling of calcium.

Lack of glucose-induced priming of insulin release in the perfused mouse pancreas

“…Differences in the mobilization of cytosolic calcium could accordingly be a critical event for establishing the difference in the priming and shape of dynamic insulin secretion between mice and rats. Discrepancies between mice and rats in the handling of the calcium ion have been shown (Levy, Herchuelz, Sener & Malaisse, 1976;Hellman, Idahl, Lenzen et al 1978;Wolters, Wiegman & Konijnendijk, 1983).…”

Islet Insulin Release and Net Calcium Retention In Vitro in Vitamin D–Deficient Rats

“…The reason for the difference in net 45 Ca retention in islets of pair-fed rats at 5.6 and 16.7 mM glucose is not known. Studies of fasting rats and mice show either decreased, 20 unchanged, 20 or increased 21 retention of calcium, depending on the duration of fasting, the concentration of glucose in the medium, and the duration of islet incubation. Because the experimental protocols in our studies were identical except for the glucose concentration, the difference in calcium retention at 16.7 and 5.6 mM glucose in islets of pairfed rats must be due to the decrease in glucose concentration.…”

Involvement of Ca2+ in the Impaired Glucose-induced Insulin Release from Islets Cultured at Low Glucose

“…This was also found when Ca was measured by atomic absorption albeit in a small number of observations, 15 but not in another report 16 or when a fluorometric method was used. 17 The effect of glucose to increase islet Ca content was shown to be rapid by either using the present method (islets cultured for 24 h) 3 or by the use of energy dispersive x-ray analysis of perifused islets. 18 As in other cell types, 1920 an increase in the concentration of ionized Ca 2+ in the p-cell cytosol is believed to be the important event mediating cell activation, i.e., insulin release.…”

“…35 Interestingly, islets from starved mice show a clear dissociation between insulin release and Ca content. 17 IBMX, a substance believed to act on islet cell Ca stores via cAMP 2829 overcame the inhibition of glucose-induced insulin release ( Table 2). This may also point to a defective action of glucose on cellular Ca stores.…”