Chemerin as an Inducer of β Cell Proliferation Mediates Mitochondrial Homeostasis and Promotes β Cell Mass Expansion

Loss of the beta cell population is a crucial feature of type 2 diabetes. Restoring the beta cell mass by stimulating beta cell proliferation and preventing its apoptosis was proposed as a therapeutic approach to treating diabetes. Therefore, researchers have been increasingly interested in identifying exogenous factors that can stimulate beta cell proliferation in situ and in vitro. Adipokine chemerin, which is secreted from adipose tissue and the liver, has been identified as a chemokine that plays a critical role in the regulation of metabolism. In this study, we demonstrate that chemerin as a circulating adipokine promotes beta cell proliferation in vivo and in vitro. Chemerin serum levels and the expression of the main receptors within islets are highly regulated under a variety of challenging conditions, including obesity and type 2 diabetes. As compared to their littermates, mice overexpressing chemerin had a larger islet area and increased beta cell mass with both a normal and high-fat diet. Moreover, in chemerin-overexpressed mice, we observed improved mitochondrial homeostasis and increased insulin synthesis. In summary, our findings confirm the potential role of chemerin as an inducer of beta cell proliferation, and they provide novel insights into the helpful strategy to expand beta cell population.

Automated summary

Loss of beta cell population is a key factor in type 2 diabetes, and restoring beta cell mass through proliferation and preventing apoptosis offers a potential therapeutic approach. Chemerin, an adipokine, has been identified as a promoter of beta cell proliferation both in vivo and in vitro. Overexpression of chemerin in mice resulted in larger islet area, increased beta cell mass, improved mitochondrial homeostasis, and increased insulin synthesis.