Nutrient-induced intracellular calcium movement in rat pancreatic B cell.
Several insulin secretagogues increase 45Ca efflux from islets prelabeled with the tracer in the presence of glucose, an effect attributable to stimulation of 40Ca entry into islet cells. When the islets are prelabeled in the absence instead of presence of glucose, the 45Ca becomes more readily releasable, and the secretory response to nutrient or ionic secretagogues is decreased. Such a decrease is more marked in response to glucose than other secretagogues because the prior nutrient deprivation also impairs the metabolism of glucose in islet cells. In the islets prelabeled in the absence of glucose, both glyceraldehyde and 2-ketoisocaprote dramatically stimulated 45Ca efflux. This effect persists in the absence of extracellular Ca2+ or presence of the calmodulin-antagonist trifluoperazine. It may correspond to a nutrient-induced intracellular Ca2+ movement, the existence of which would be unmasked in islets prelabeled in the absence of glucose. This so-far-undetected Ca2+ movement may play a role in the secretory response to nutrient secretagogues.
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D005947:Glucose / Q000494:pharmacology*; D005985:Glyceraldehyde / Q000494:pharmacology; D007328:Insulin / Q000378:metabolism; D007515:Islets of Langerhans / Q000378:metabolism*; D007651:Keto Acids / Q000494:pharmacology; D010084:Oxidation-Reduction; D011188:Potassium / Q000494:pharmacology; D051381:Rats; D012964:Sodium / Q000378:metabolism; D013806:Theophylline / Q000494:pharmacology
D007328:Insulin; D007651:Keto Acids; D005985:Glyceraldehyde; C013082:alpha-ketoisocaproic acid; D012964:Sodium; D013806:Theophylline; D005947:Glucose; D011188:Potassium; D002118:Calcium