Volume 21 Issue 7
Jul.  2023
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HUANG Qian, LIU Deliang, LI Huilin. Research progress on correlations between CD36 and type 2 diabetes mellitus[J]. Chinese Journal of General Practice, 2023, 21(7): 1206-1210. doi: 10.16766/j.cnki.issn.1674-4152.003085
Citation: HUANG Qian, LIU Deliang, LI Huilin. Research progress on correlations between CD36 and type 2 diabetes mellitus[J]. Chinese Journal of General Practice, 2023, 21(7): 1206-1210. doi: 10.16766/j.cnki.issn.1674-4152.003085

Research progress on correlations between CD36 and type 2 diabetes mellitus

doi: 10.16766/j.cnki.issn.1674-4152.003085
Funds:

 81774225

 81704002

 2020A1515010775

  • Received Date: 2022-10-11
    Available Online: 2023-08-28
  • With the rapid development of the global economy, the improvement of people's living standards and the changes of their life style, diabetes has become one of the most severe noncommunicable diseases threatening the life and health of the whole of humanity, among which type 2 diabetes mellitus (T2DM) accounts for the vast majority of cases. Although there are many kinds of drugs targeting different targets of T2DM, their efficacy is not satisfactory, and may be accompanied by some side-effects, such as abdominal bloating, nausea and vomiting, weight gain, urinary tract infection and so on. Therefore, it is urgent and significant to find new therapeutic targets and develop new therapeutic drugs for T2DM. T2DM is primarily caused by insufficient insulin secretion by the pancreatic β cells and/or insulin resistance (IR) in peripheral tissues. Thus, it is important to find new ways to improve IR and regulate insulin secretion of pancreatic β cells for the treatment of T2DM. Cluster of differentiation 36 (CD36) is a multifunctional membrane protein receptor, which is widely expressed in various cells of the body. It participates in the occurrence and progression of T2DM through recognizing and binding different ligands to regulate lipid metabolism, adhesion, apoptosis, inflammatory response and immune response and other physiological and pathological processes. An increased expression of CD36 induced by hyperglycemia in the main insulin target tissues, including liver, fat and skeletal muscle, is involved in IR through various mechanisms. In addition, CD36 also participates in the process of insulin secretion and pancreatic β cell death by mediating oxidative stress, endoplasmic reticulum stress, inflammation and other pathological processes. Furthermore, CD36 also regulates fat preference and feeding behavior by mediating fat perception signal transduction, participating in the occurrence and progression of T2DM. Therefore, regulation of the expression level of CD36 in various tissues and organs may become an important approach for the treatment of T2DM and related metabolic diseases in the future.

     

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