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pubmed:abstractText |
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.
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