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. 2021 May 26;70(8):1717–1728. doi: 10.2337/db21-0037

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© 2021 by the American Diabetes Association

Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. More information is available at https://www.diabetesjournals.org/content/license.

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β-Cell model of mitochondrial metabolism. This model shows the export of TCA-derived citrate and isocitrate via CIC, which has been proposed to regulate insulin secretion following generation of NADPH by Idh1. Our data indicate that CIC is required for NADPH production but not insulin secretion. Furthermore, we suggest that Idh1 conversion of isocitrate to α-ketoglutarate (α-KG) is necessary to prevent a negative feedback of glycolytic flux by (iso)citrate that suppresses insulin secretion. AcCoA, acetyl CoA; ACLY, ATP-citrate lyase; MPC, mitochondrial pyruvate carrier.