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O304 ameliorates hyperglycemia in mice by dually promoting muscle glucose effectiveness and preserving β-cell function

ABSTRACT: In Type 2 diabetes, insulin resistance elicits compensatory insulin hypersecretion, provoking β-cell stress and eventually compensatory failure. In insulin deficient STZ treated diabetic mice the dual AMPK activator and mitochondrial uncoupler O304 stimulates insulin independent glucose uptake and utilization in skeletal muscle and heart in vivo, thus improving glucose homeostasis. In obese In type 2 diabetic db/db mice, O304 additionally preserves β-cell function by preventing decline in insulin secretion, β-cell mass, and pancreatic insulin content. It remains however unclear whether these effects of O304 is mediated by a direct protective effect on β-cells, or indirectly by improving glucose homeostasis thereby inducing β-cell rest. To investigate the ability of O304 to directly mitigate the detrimental effect of hyperglycemia on β-cell function, we exposed isolated islets ex vivo to normoglycemic and hyperglycemic comdition in the abscence or prescene of O304.

ORGANISM(S): Mus musculus

PROVIDER: GSE240298 | GEO | 2023/08/17

REPOSITORIES: GEO

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MicroRNA-21 Promotes Pancreatic β cell Function through Modulating Glucose Uptake

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2022-05-16 | GSE191194 | GEO

Paired box 6 gene delivery preserves beta cells and improves islet transplantation efficacy

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Expression analysis in pancreatic and liver tissues of diabetic db/db mice in response to dietary supplementation with selenate

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Expression analysis in pancreatic and liver tissues of diabetic db/db mice in response to dietary supplementation with selenate

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2016-12-13 | PXD003349 | Pride

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