Matches in SemOpenAlex for { <https://semopenalex.org/work/W4312211874> ?p ?o ?g. }
- W4312211874 abstract "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 transient receptor potential cation channel subfamily M member 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 disrupted insulin secretion and led to progressive glucose intolerance. We indicate that the diminished insulinotropic response in β cell–specific Trpm7-knockout mice was caused by decreased insulin production because of impaired enzymatic activity of this protein. Accordingly, high-fat–fed mice with a genetic loss of TRPM7 kinase activity displayed a marked glucose intolerance accompanied by hyperglycemia. These detrimental glucoregulatory effects were engendered by reduced compensatory β cell responses because of mitigated protein kinase B (AKT)/ERK signaling. Collectively, our data identify TRPM7 kinase as a potentially novel regulator of insulin synthesis, β cell dynamics, and glucose homeostasis under obesogenic diet." @default.
- W4312211874 created "2023-01-04" @default.
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- W4312211874 date "2023-02-08" @default.
- W4312211874 modified "2023-10-06" @default.
- W4312211874 title "TRPM7 kinase is required for insulin production and compensatory islet responses during obesity" @default.
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- W4312211874 doi "https://doi.org/10.1172/jci.insight.163397" @default.
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- W4312211874 hasPublicationYear "2023" @default.
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