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Review
. 2022 May 4;23(9):5104.
doi: 10.3390/ijms23095104.

Effects of Sodium-Glucose Co-Transporter-2 Inhibitors on Pancreatic β-Cell Mass and Function

Affiliations
Review

Effects of Sodium-Glucose Co-Transporter-2 Inhibitors on Pancreatic β-Cell Mass and Function

Akinobu Nakamura. Int J Mol Sci. .

Abstract

Sodium-glucose co-transporter-2 inhibitors (SGLT2is) not only have antihyperglycemic effects and are associated with a low risk of hypoglycemia but also have protective effects in organs, including the heart and kidneys. The pathophysiology of diabetes involves chronic hyperglycemia, which causes excessive demands on pancreatic β-cells, ultimately leading to decreases in β-cell mass and function. Because SGLT2is ameliorate hyperglycemia without acting directly on β-cells, they are thought to prevent β-cell failure by reducing glucose overload in this cell type. Several studies have shown that treatment with an SGLT2i increases β-cell proliferation and/or reduces β-cell apoptosis, resulting in the preservation of β-cell mass in animal models of diabetes. In addition, many clinical trials have shown that that SGLT2is improve β-cell function in individuals with type 2 diabetes. In this review, the preclinical and clinical data regarding the effects of SGLT2is on pancreatic β-cell mass and function are summarized and the protective effect of SGLT2is in β-cells is discussed.

Keywords: beta-cells; glucokinase; glucose metabolism; insulin secretion.

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Conflict of interest statement

A.N. has obtained research support from Mitsubishi Tanabe Pharma, Nippon Boehringer Ingelheim Co., Kissei Pharmaceutical Co., Ltd., and Taisho Pharmaceutical Co., Ltd. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, or in the decision to publish the results.

Figures

Figure 1
Figure 1
Target organs of the deleterious effects of chronic hyperglycemia.
Figure 2
Figure 2
Basis for the use of sodium-glucose co-transporter-2 inhibitors (SGLT2is) to prevent the progression of pancreatic β-cell failure.

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