AI Article Synopsis
- β-cell dysfunction is a key feature of both type 1 and type 2 diabetes, with type 2 being linked to age-related changes in these cells.
- Research shows that mice lacking microsomal prostaglandin E synthase-2 (mPGES-2) demonstrate improved β-cell function, including enhanced insulin secretion and better blood sugar control, especially under high-fat diet conditions.
- The study suggests that targeting mPGES-2 may offer a new therapeutic approach to combat age-related β-cell dysfunction and diabetes by disrupting harmful signaling pathways associated with cell aging.
Article Abstract
β-cell dysfunction is a hallmark of type 1 and type 2 diabetes. Type 2 diabetes is strongly associated with ageing-related β-cell abnormalities that arise through unknown mechanisms. Here we show better β-cell identity, less β-cell senescence, enhanced glucose-stimulated insulin secretion and improved glucose homeostasis in global microsomal prostaglandin E synthase-2 (mPGES-2)-deficient mice challenged with a high-fat diet or bred with a genetic model of type 2 diabetes (db/db mice). Furthermore, the function of mPGES-2 in β-cells is validated using mice with β-cell-specific mPGES-2 deficiency or overexpression. Mechanistically, the protective role of mPGES-2 deletion is induced by antagonizing β-cell senescence via interference of the PGE-EP3-NR4A1 signalling axis. We also discover an inhibitor of mPGES-2, SZ0232, which protects against β-cell dysfunction and diabetes, similar to mPGES-2 deletion. We conclude that mPGES-2 contributes to ageing-associated β-cell senescence and dysfunction via the PGE-EP3-NR4A1 signalling axis. Pharmacologic blockade of mPGES-2 might be effective for treating ageing-associated β-cell dysfunction and diabetes.
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| http://dx.doi.org/10.1038/s42255-022-00536-6 | DOI Listing |
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