Fuel-stimulated insulin secretion by clonal hamster beta-cell line HIT T-15.
Insulin secretion by monolayer cultures of HIT T-15 cells was measured in response to various fuel molecules (glucose, dihydroxyacetone, lactate, glutamine, alpha-ketoisocaproic acid, alpha-ketoisovaleric acid) and a nonmetabolized glucose analogue (3-O-methylglucose). HIT cells secreted insulin in response to fuel molecules, but 3-O-methylglucose was ineffective. Stimulation of insulin release by fuels was increased by isobutylmethylxanthine and blocked by antimycin A. Iodoacetate selectively inhibited glucose-stimulated insulin release but had little effect on alpha-ketoisocaproic acid-stimulated insulin secretion. These results indicate that HIT cells retain the capacity of normal beta-cells to act as fuel sensors. Thus, HIT cells may provide a well-defined and relatively abundant tissue source in studies of stimulus-secretion coupling in beta-cells stimulated by fuels.
D019325:3-O-Methylglucose; D000818:Animals; D002460:Cell Line; D006224:Cricetinae; D004098:Dihydroxyacetone / Q000494:pharmacology; D004734:Energy Metabolism / Q000187:drug effects*; D005947:Glucose / Q000494:pharmacology; D005973:Glutamine / Q000494:pharmacology; D045782:Hemiterpenes; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000187:drug effects* / Q000378:metabolism; D007651:Keto Acids / Q000494:pharmacology; D007773:Lactates / Q000494:pharmacology; D019344:Lactic Acid; D008757:Methylglucosides / Q000494:pharmacology
D045782:Hemiterpenes; D007328:Insulin; D007651:Keto Acids; D007773:Lactates; D008757:Methylglucosides; D005973:Glutamine; D019325:3-O-Methylglucose; D019344:Lactic Acid; C001505:alpha-ketoisovalerate; C013082:alpha-ketoisocaproic acid; D005947:Glucose; D004098:Dihydroxyacetone