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Understanding the role of pancreatic β‐cell CD36 in the development of Type 2 Diabetes
Author(s) -
Kolar Elizabeth Anne,
Gajrawala Eshaa,
Deeney Jude,
Hamilton James
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.670.63
Subject(s) - cd36 , scavenger receptor , medicine , chemistry , oil red o , endocrinology , cell culture , type 2 diabetes , fatty acid , lipotoxicity , glucose uptake , foam cell , cell , docosahexaenoic acid , insulin resistance , insulin , diabetes mellitus , biochemistry , biology , receptor , lipoprotein , in vitro , cholesterol , polyunsaturated fatty acid , adipogenesis , genetics
CD36 is a transmembrane scavenger receptor for oxidized LDL (oxLDL). Expression of CD36 and subsequent uptake of oxLDL into macrophages is central to foam cell formation in atherosclerotic plaques. CD36 is also reported to play a pivotal role in glucotoxicity‐induced β‐cell dysfunction in Type 2 Diabetes (T2D). The aim of this study is to investigate mechanistic functions of CD36 that contribute to β‐cell dysfunction and the onset of T2D. For this study, rat INS‐1 pancreatic β‐cells were cultured in either low (5 mM) or high (11 mM) glucose conditions. Cells grown in high glucose exhibited a left shift in glucose stimulated insulin secretion (GSIS), showing that the cells are more sensitive to lower glucose levels. These cells also contained more lipid droplets, as shown by Nile Red staining. Using immunofluorescence and Western blotting, we demonstrated that CD36 expression increased with increasing glucose concentrations. When cells were incubated with DiI‐labeled oxLDL to investigate uptake, cells that were grown in high glucose exhibited increased labeling. Interestingly, oxLDL uptake by INS‐1 cells grown in 11 mM glucose can be suppressed by the addition of the ω‐3 fatty acid, docosahexaenoic acid (DHA). Studies investigating the effect of DHA and additional fatty acids on uptake of oxLDL by INS‐1 cells and effects on GSIS are ongoing. We propose that CD36 plays a role in how β‐cells respond to high glucose levels, similarly found in T2D. The increase in oxLDL uptake via CD36 in these cells may contribute to glucolipotoxic effects in β‐cells that results in aberrant insulin secretion in T2D. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .