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- W4236068065 abstract "Type 2 diabetes mellitus (T2DM) is characterized by β cell dysfunction due to impaired glucose-stimulated insulin secretion (GSIS). Studies show that β cell circadian clocks are important regulators of GSIS and glucose homeostasis. These observations raise the question whether enhancement of the circadian clock in β cells will confer protection against β cell dysfunction under diabetogenic conditions. To test this we employed an approach by first generating mice with β cell-specific inducible overexpression of <i>Bmal1</i> (core circadian transcription factor; <i>β-Bmal1<sup>OV</sup></i>). We subsequently examined the effects of <i>β-Bmal1<sup>OV</sup> </i>on the circadian clock, GSIS, islet transcriptome, and glucose metabolism in context of diet-induced obesity. We additionally tested the effects of circadian clock-enhancing small molecule Nobiletin on GSIS in mouse and human control and T2DM islets. We report that <i>β-Bmal1<sup>OV</sup> </i>mice display<i> </i>enhanced islet circadian clock amplitude, augmented <i>in vivo</i> and <i>in vitro</i> GSIS and are protected against obesity-induced glucose intolerance. These effects were associated with increased expression of purported BMAL1-target genes mediating insulin secretion, processing, and lipid metabolism. Furthermore, exposure of isolated islets to Nobiletin enhanced β cell secretory function in <i>Bmal1</i>-dependent manner. This work suggests therapeutic targeting of the circadian system as a potential strategy to counteract β cell failure under diabetogenic conditions." @default.
- W4236068065 created "2022-05-12" @default.
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- W4236068065 date "2020-10-21" @default.
- W4236068065 modified "2023-09-29" @default.
- W4236068065 title "Induction of core circadian clock transcription factor Bmal1 enhances β cell function and protects against obesity-induced glucose intolerance" @default.
- W4236068065 doi "https://doi.org/10.2337/figshare.13103045.v1" @default.
- W4236068065 hasPublicationYear "2020" @default.
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