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Long‐term in vitro treatment of INS‐1 rat pancreatic β‐cells by unsaturated free fatty acids protects cells against gluco‐ and lipotoxicities via activation of GPR40 receptors

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Summary

G‐Protein coupled receptor 40 (GPR40) is a membrane‐bound G‐protein‐coupled receptor with high binding affinity to medium‐ and long‐chain free fatty acids (FFAs). Acute activation of GPR40 on pancreatic β‐cells causes insulin secretion, whereas prolonged activation may contribute to a deterioration of the effect of saturated FFAs on β‐cells. It has been documented that different types of FFAs produce various effects on insulin secretion; however, little information is available regarding the expression of GPR40 and its function after long‐term exposure of β‐cells to unsaturated FFAs. In the present study, GPR40 expression and function were assessed in INS‐1 β‐cells after 48 h exposure to different types of unsaturated FFAs. The mRNA and protein expression of GPR40 was increased significantly by long‐term exposure of cells to polyunsaturated α‐linolenic acid, but not to either oleic acid or linoleic acid. Immunocytochemistry revealed a reduction in the number of insulin‐containing granules in cells treated with α‐linolenic acid, which was correlated with an increase in cellular expression of GPR40. Basal and glucose‐stimulated insulin secretion were markedly suppressed by 48 h treatment of cells with saturated palmitic acid, but not unsaturated α‐linolenic acid. By testing various FFAs, it was found that FFA‐induced suppression of basal and glucose‐stimulated insulin secretion was attenuated by an increase in the degree of unsaturation of the FFAs and GPR40 expression in response to FFA treatment in INS‐1 cells. The results of the present study indicate that long‐term in vitro treatment of INS‐1 rat pancreatic β‐cells by unsaturated FFAs protects the cells against from gluco‐ and lipotoxicities and that this coincides with an increase in GPR40 expression.
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Document Type: Research Article

Publication date: May 1, 2012

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