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. 2016 Mar 8;65(6):1534–1555. doi: 10.2337/db15-1323

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© 2016 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.

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A: The mechanistic action of mitoNEET in MIP-MitoN β-cells. MitoNEET lowers ΔΨ_m. This depolarization of ΔΨ_m activates PINK1 and recruitment of Parkin to the OMM to trigger mitophagy, as observed by the formation of mitophagosomes and autophagic vacuoles. Such effects impair the ability of the MIP-MitoN β-cell to secrete insulin and, under increasing concentrations of Dox, promote β-cell death. At the whole-body level, MIP-MitoN mice exhibit hyperglycemia and severe glucose intolerance. Parkin is also known to polyubiquitinate (Ub) mitoNEET; however, the functional implications of this modification are currently unknown. B: Proposed model of mitoNEET-driven cellular and whole-body action in MIP-MitoN mice (β-cell induction of mitoNEET), PPG-MitoN mice (α-cell induction), and MIP-PPG-MitoN mice (β- and α-cell induction).

A: The mechanistic action of mitoNEET in MIP-MitoN β-cells. MitoNEET lowers ΔΨ_m. This depolarization of ΔΨ_m activates PINK1 and recruitment of Parkin to the OMM to trigger mitophagy, as observed by the formation of mitophagosomes and autophagic vacuoles. Such effects impair the ability of the MIP-MitoN β-cell to secrete insulin and, under increasing concentrations of Dox, promote β-cell death. At the whole-body level, MIP-MitoN mice exhibit hyperglycemia and severe glucose intolerance. Parkin is also known to polyubiquitinate (Ub) mitoNEET; however, the functional implications of this modification are currently unknown. B: Proposed model of mitoNEET-driven cellular and whole-body action in MIP-MitoN mice (β-cell induction of mitoNEET), PPG-MitoN mice (α-cell induction), and MIP-PPG-MitoN mice (β- and α-cell induction).