Role of lipoprotein lipase and apolipoprotein E secretion by macrophages in modulating lipoprotein uptake. Possible role in acceleration of atherosclerosis in diabetes.
Because the accumulation of lipid in macrophages is a characteristic feature of atherosclerosis, the mechanisms by which this lipid accumulation occurs have been intensively studied. This paper reviews the receptor- and non-receptor-mediated pathways that promote lipid accumulation in macrophages. Particular emphasis is placed on the contributions of two secretory products of macrophages, lipoprotein lipase and apolipoprotein E, to both receptor- and non-receptor-mediated uptake of triglyceride-rich lipoproteins by macrophages. The hormonal, lipid, and immunological factors that regulate the secretion of LpL and apoE by macrophages are discussed, as are how changes in the secretion of apoE and LpL that can modulate the uptake of triglyceride-rich lipoproteins by macrophages might influence the atherosclerotic process in people with diabetes.
Kraemer
F B
FB
Department of Medicine, Stanford University School of Medicine, Veterans Affairs Medical Center, Palo Alto, California 94304.
D001057:Apolipoproteins E / Q000378:metabolism; D001161:Arteriosclerosis / Q000150:complications / Q000378:metabolism*; D048909:Diabetes Complications; D003920:Diabetes Mellitus / Q000201:enzymology / Q000378:metabolism*; D006801:Humans; D008071:Lipoprotein Lipase / Q000378:metabolism*; D008074:Lipoproteins / Q000378:metabolism*; D008264:Macrophages / Q000201:enzymology / Q000378:metabolism*
D001057:Apolipoproteins E; D008074:Lipoproteins; D008071:Lipoprotein Lipase