PuSH - Publication Server of Helmholtz Zentrum München: TRPM7 kinase is required for insulin production and compensatory islet responses during obesity.

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Khajavi, N.* ; Beck, A.* ; Ricku, K.* ; Beyerle, P.* ; Jacob, K.* ; Syamsul, S.F.* ; Belkacemi, A.* ; Reinach, P.S.* ; Schreier, P.C.* ; Salah, H.* ; Popp, T.* ; Novikoff, A. ; Breit, A.* ; Chubanov, V.* ; Müller, T.D. ; Zierler, S.* ; Gudermann, T.*

TRPM7 kinase is required for insulin production and compensatory islet responses during obesity.

JCI insight 8:e163397 (2023)

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Most overweight individuals do not develop diabetes due to compensatory islet responses to restore glucose homeostasis. Therefore, regulatory pathways that promote β-cell compensation are potential targets for treatment of diabetes. The melastatin transient receptor potential 7 protein (TRPM7), harboring a cation channel and a serine/threonine kinase, has been implicated in controlling cell growth and proliferation. Here, we report that selective deletion of Trpm7 in β-cells disrupts insulin secretion and leads to progressive glucose intolerance. We indicate that the diminished insulinotropic response in β-cell-specific Trpm7 knockout mice is caused by decreased insulin production due to an impaired enzymatic activity of this protein. Accordingly, high-fat fed mice with a genetic loss of TRPM7 kinase activity (Trpm7R/R) display a marked glucose intolerance accompanied by hyperglycemia. These detrimental glucoregulatory effects are engendered by reduced compensatory β-cell responses due to mitigated AKT/ERK signaling. Collectively, our data identify TRPM7 kinase as a novel regulator of insulin synthesis, β-cell dynamics, and glucose homeostasis under obesogenic diet.

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