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High-density lipoprotein, beta cells, and diabetes
Arnold von Eckardstein1, Christian Widmann2
1Institute of Clinical Chemistry, University Hospital Zurich, Zurich, Switzerland.
Insights
High-density lipoproteins (HDL) protect pancreatic beta cells from stress-induced death and improve insulin secretion, suggesting HDL's importance in preventing diabetes.
Area of Science:
- Endocrinology
- Metabolic Research
- Cell Biology
Background:
- High-density lipoproteins (HDL) offer protective effects on various cell types, including anti-atherogenic actions.
- HDLs demonstrate anti-diabetogenic functions in pancreatic beta cells, inhibiting stress-induced cell death.
- HDL-cholesterol levels inversely correlate with diabetes risk, highlighting HDL's role in metabolic health.
Purpose of the Study:
- To review the beneficial effects of HDLs on pancreatic beta cells.
- To elucidate the mechanisms underlying HDL's actions on beta cells.
- To identify knowledge gaps in HDL signaling pathways within beta cells.
Main Methods:
- Review of existing literature on HDL function in pancreatic beta cells.
- Discussion of HDL's modulation of endoplasmic reticulum stress.
- Analysis of HDL's impact on glucose-stimulated insulin secretion and glucose uptake.
Main Results:
- HDLs inhibit stress-induced cell death in pancreatic beta cells.
- HDLs enhance glucose-stimulated insulin secretion.
- HDLs stimulate glucose uptake in skeletal muscle, adipose tissue, and liver.
Conclusions:
- Maintaining appropriate HDL levels and functionality is crucial for diminishing diabetes risk.
- Further research into HDL signaling pathways in beta cells is needed.
- Understanding these pathways can inform the development of therapeutic strategies for preserving beta cell function.
Abstract:
High-density lipoproteins (HDLs) exert a series of potentially beneficial effects on many cell types including anti-atherogenic actions on the endothelium and macrophage foam cells. HDLs may also exert anti-diabetogenic functions on the beta cells of the endocrine pancreas, notably by potently inhibiting stress-induced cell death and enhancing glucose-stimulated insulin secretion. HDLs have also been found to stimulate insulin-dependent and insulin-independent glucose uptake into skeletal muscle, adipose tissue, and liver. These experimental findings and the inverse association of HDL-cholesterol levels with the risk of diabetes development have generated the notion that appropriate HDL levels and functionality must be maintained in humans to diminish the risks of developing diabetes. In this article, we review our knowledge on the beneficial effects of HDLs in pancreatic beta cells and how these effects are mediated. We discuss the capacity of HDLs to modulate endoplasmic reticulum stress and how this affects beta-cell survival. We also point out the gaps in our understanding on the signalling properties of HDLs in beta cells. Hopefully, this review will foster the interest of scientists in working on beta cells and diabetes to better define the cellular pathways activated by HDLs in beta cells. Such knowledge will be of importance to design therapeutic tools to preserve the proper functioning of the insulin-secreting cells in our body.
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