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MST1 deletion protects β-cells in a mouse model of diabetes

Ardestani, Amin; Maedler, Kathrin

Authors

Kathrin Maedler



Abstract

The pro-apoptotic kinase Mammalian Sterile 20-like kinase 1 (MST1), an integral component of the Hippo pathway, is a key regulator of organ size, stress response, and tissue homeostasis; its aberrant hyperactivation is linked to multiple pathological disorders including diabetes. Here we show that MST1 deletion in mice resulted in improved glucose tolerance and insulin secretion, and restored pancreatic β-cell mass as a result of improved β-cell survival and proliferation in the combined high fat/high sucrose and streptozotocin (HFS/STZ) model of β-cell destruction and diabetes. Importantly, the glucose-lowering effects in the MST1-knockout (KO) mice could be accounted to the enhanced β-cell mass and improved insulin secretion without changes in insulin sensitivity. Metabolic and morphological data suggest that normalization of blood glucose and insulin secretion, islet architecture, and β-cell mass by MST1 deletion in response to diabetes-induced injury occurs as a result of improved β-cell survival and proliferation establishing MST1 as potent regulator of physiological β-cell turnover.

Citation

Ardestani, A., & Maedler, K. (2022). MST1 deletion protects β-cells in a mouse model of diabetes. Nutrition and Diabetes, 12(1), Article 7. https://doi.org/10.1038/s41387-022-00186-3

Journal Article Type Article
Acceptance Date Jan 26, 2022
Online Publication Date Feb 8, 2022
Publication Date Dec 1, 2022
Deposit Date Jan 3, 2024
Publicly Available Date Jan 5, 2024
Journal Nutrition and Diabetes
Electronic ISSN 2044-4052
Publisher Springer Nature [academic journals on nature.com]
Peer Reviewed Peer Reviewed
Volume 12
Issue 1
Article Number 7
DOI https://doi.org/10.1038/s41387-022-00186-3
Keywords Diabetes
Public URL https://hull-repository.worktribe.com/output/4461469

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http://creativecommons.org/licenses/by/4.0

Copyright Statement
© The Author(s) 2022.
Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.




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