1999
DOI: 10.1152/ajpendo.1999.277.3.e521
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Lipid rather than glucose metabolism is implicated in altered insulin secretion caused by oleate in INS-1 cells

Abstract: A comprehensive metabolic study was carried out to understand how chronic exposure of pancreatic β-cells to fatty acids causes high basal secretion and impairs glucose-induced insulin release. INS-1 β-cells were exposed to 0.4 mM oleate for 3 days and subsequently incubated at 5 or 25 mM glucose, after which various parameters were measured. Chronic oleate promoted triglyceride deposition, increased fatty acid oxidation and esterification, and reduced malonyl-CoA at low glucose in association with elevated bas… Show more

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Cited by 69 publications
(83 citation statements)
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“…Long-term exposure of the beta cell to high glucose induces glucose desensitisation, depletion of the readily releasable pool of insulin and may cause apoptosis [55]. Long-term exposure of beta cells to NEFA increases basal insulin release but inhibits glucose-induced insulin secretion [56]. NEFA also reduces glucose-induced insulin gene expression [57] and induces beta cell apoptosis [58].…”
Section: Discussionmentioning
confidence: 99%
“…Long-term exposure of the beta cell to high glucose induces glucose desensitisation, depletion of the readily releasable pool of insulin and may cause apoptosis [55]. Long-term exposure of beta cells to NEFA increases basal insulin release but inhibits glucose-induced insulin secretion [56]. NEFA also reduces glucose-induced insulin gene expression [57] and induces beta cell apoptosis [58].…”
Section: Discussionmentioning
confidence: 99%
“…Sustained elevated lipid concentrations result in impaired insulin action and secretion in vivo and in vitro; this has implications for obesity-related diabetes [1][2][3]. It is known that increased plasma NEFA concentrations reduce insulinmediated glucose uptake and metabolism in muscles-the Randle effect [4]-but the exact mechanism of action of NEFA on the beta cell to modulate glucose-stimulated insulin secretion (GSIS) [5,6] is not known.…”
Section: Introductionmentioning
confidence: 99%
“…To a large part at least, the effects of activated AMPK can be attributed to a suppression of glucose oxidation [52,56,57] and consequently Ca 2+ influx. The mechanisms through which AMPK inhibits glucose metabolism have yet to be fully elucidated, but the activation of fatty acid oxidation and also a Randle effect [66] may be involved (though see [67] for a contrary view).…”
Section: Introductionmentioning
confidence: 99%