Pathomechanism of statins induced increased risk of new onset diabetes:LDLR mediated cholesterol influx induces lipid toxicity in pancreatic β cells
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1.Key Laboratory of Ischemic Cardiovascular Disease in Shaanxi & Institute of Basic and Translational Medicine of Xi'an Medical University, Xi'an, Shaanxi 710021, China;2.Department of Histology and Embryology, Xi'an Medical University, Xi'an, Shaanxi 710021, China)

Clc Number:

R363

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    Abstract:

    Hyperlipidemia is a common risk factor for cardiovascular disease and diabetes. However, the clinical use of statins to control blood lipids increases the risk of new onset diabetes in patients. Conversely, patients with familial hypercholesterolemia (FH) have higher blood lipids and long-term use of statins, which reduce the risk of diabetes. Considering that FH patient is mainly caused by low density lipoprotein receptor (LDLR) mutation, this makes it possible for LDLR mediated cholesterol metabolism to be involved in the onset of diabetes. Statins can upregulate LDLR expression in liver and some tissues and promote cholesterol influx, which may cause some lipotoxicity in some pancreatic islet cells. Pancreatic β cells are more sensitive to cholesterol, and a small amount of cholesterol accumulation can cause cell dysfunction. The purpose of this paper is to discuss the pathological role of LDLR in statins induced diabetes, and to provide new thinking for reducing the adverse reaction of statins and promoting the prevention and treatment of type 2 diabetes.

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YU Qi, WANG Zhang-Li, ZHANG Guang-Wei, XU Cang-Bao. Pathomechanism of statins induced increased risk of new onset diabetes:LDLR mediated cholesterol influx induces lipid toxicity in pancreatic β cells[J]. Editorial Office of Chinese Journal of Arteriosclerosis,2018,26(4):342-346.

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History
  • Received:January 25,2018
  • Revised:February 20,2018
  • Online: May 04,2018
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