Modulation of human monocyte CD36 by type 2 diabetes mellitus and other atherosclerotic risk factors.
2011, Eur J Clin Invest. 2011 Aug;41(8):854-62. doi: 10.1111/j.1365-2362.2011.02475.x. Epub 2011 Feb 25.
Bernal-Lopez RM, Llorente-Cortes V, López-Carmona D, Mayas DM, Gomez-Huelgas R, Tinahones FJ, Badimon L.
Autors del centre relacionats: Badimon Lina, Llorente Vicenta.
Bernal-Lopez RM, Llorente-Cortes V, López-Carmona D, Mayas DM, Gomez-Huelgas R, Tinahones FJ, Badimon L.
Autors del centre relacionats: Badimon Lina, Llorente Vicenta.
Source
Endocrinology Department, Biomedical Research Laboratory, Hospital Virgen de la Victoria, Málaga, Spain.
Abstract
BACKGROUND:
The pathophysiological role of CD36 in atherosclerosis seems to be largely dependent on its pro-inflammatory function and ability to take up oxidized low-density lipoprotein. Controversy exists concerning the potential beneficial/harmful effects of vascular CD36 inhibition in atherosclerosis. However, as atherosclerosis in murine models does not result in clinical end points such as plaque rupture and thrombotic ischaemia, typical of human disease, clinical studies are required to understand the functional role of CD36 in human atherosclerosis.
MATERIALS AND METHODS:
Our aim was to investigate whether CD36 expression in monocytes is modulated by the presence of an increasing number of atherosclerotic risk factors, and specifically by hyperglycaemia because of diabetes mellitus. The study included 33 patients with advanced atherosclerosis and eight healthy blood donors, as controls. The patients were classified according to the presence of atherosclerotic risk factors. Diabetes mellitus was classified as either well-controlled or poorly controlled. Monocytes were exposed in vitro to low (5·5mM) or high glucose (26mM) concentrations for increasing times.
RESULTS:
Our results demonstrated that protein levels of glycated CD36 were significantly higher in patients with 3-4 atherosclerotic risk factors than in those with 0-2 atherosclerotic risk factors or in subjects with no atherosclerotic symptoms (P=0·04, in both cases). However, when we analysed just the poorly controlled diabetic patients, their glycated CD36 levels were lower. These data were corroborated by in vitro studies demonstrating that increasing glucose concentrations reduced glycated protein levels (P<0·05).
CONCLUSIONS:
Our results demonstrate that CD36 expression is altered by hyperglycaemia in atherosclerotic patients.
Endocrinology Department, Biomedical Research Laboratory, Hospital Virgen de la Victoria, Málaga, Spain.
Abstract
BACKGROUND:
The pathophysiological role of CD36 in atherosclerosis seems to be largely dependent on its pro-inflammatory function and ability to take up oxidized low-density lipoprotein. Controversy exists concerning the potential beneficial/harmful effects of vascular CD36 inhibition in atherosclerosis. However, as atherosclerosis in murine models does not result in clinical end points such as plaque rupture and thrombotic ischaemia, typical of human disease, clinical studies are required to understand the functional role of CD36 in human atherosclerosis.
MATERIALS AND METHODS:
Our aim was to investigate whether CD36 expression in monocytes is modulated by the presence of an increasing number of atherosclerotic risk factors, and specifically by hyperglycaemia because of diabetes mellitus. The study included 33 patients with advanced atherosclerosis and eight healthy blood donors, as controls. The patients were classified according to the presence of atherosclerotic risk factors. Diabetes mellitus was classified as either well-controlled or poorly controlled. Monocytes were exposed in vitro to low (5·5mM) or high glucose (26mM) concentrations for increasing times.
RESULTS:
Our results demonstrated that protein levels of glycated CD36 were significantly higher in patients with 3-4 atherosclerotic risk factors than in those with 0-2 atherosclerotic risk factors or in subjects with no atherosclerotic symptoms (P=0·04, in both cases). However, when we analysed just the poorly controlled diabetic patients, their glycated CD36 levels were lower. These data were corroborated by in vitro studies demonstrating that increasing glucose concentrations reduced glycated protein levels (P<0·05).
CONCLUSIONS:
Our results demonstrate that CD36 expression is altered by hyperglycaemia in atherosclerotic patients.
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