title: Quantitative and qualitative derangement of apolipoprotein B-containing lipoproteins as a risk factor for diabetic macroangiopathy in nonobese NIDDM subjects.
abstract: Cholesterol, triglyceride (TG), and apolipoprotein (apo) B were determined in plasma and in lipoprotein subfractions (VLDL, intermediate-density lipoproteins [IDL], LDL, and HDL) in nonobese NIDDM subjects, who were classified into well-controlled, fairly controlled, or poorly controlled states with or without macrovascular complications (macroangiopathy [MA]). The same analyses were also performed on subjects who had coronary artery disease (CAD) with stable angina pectoris (SA) or unstable angina pectoris (UA) and acute myocardial infarction, cerebrovascular disease (CVD) with atherothrombotic or lacunar infarction, and arteriosclerosis obliterans (ASO). In nonobese NIDDM subjects, the number of apoB-containing lipoproteins (VLDL, IDL, and LDL) increased. This alteration was more prominent in subjects with poorly or fairly controlled disease as well as in subjects with MA, but not in those with well-controlled NIDDM. Cholesterol/apoB in LDL decreased in subjects with poorly or fairly controlled diabetes or with MA and was correlated with low HDL cholesterol. The disorder is characterized by hyperbetalipoproteinemia with elevated LDL cholesterol and small dense LDL. In obese NIDDM subjects, the similar disorder was more pronounced. Glycemic control had less effect and hyperinsulinemia, if present, aggravated the lipid disorder. In those with CAD, the number of IDLs increased and the LDL fraction had the properties of small dense LDL. HDL cholesterol decreased. In those with UA, the LDL number increased without elevation of LDL cholesterol, indicating typical hyperbetalipoproteinemia. The subjects with atherothrombotic brain infarction, an increased number of small-sized LDLs was noted. In those with ASO, the number of VLDL and IDL increased with small LDL. HDL cholesterol decreased in those with CAD, cerebrovascular disease, and ASO. Since similar quantitative and qualitative alterations of apoB-containing lipoprotein have been observed in NIDDM patients as well as in those with macrovascular diseases, diabetic patients are thought to be more susceptible to the initiation and progression of atheromatous lesions in coronary, brain, and peripheral arteries.
authors.affiliation: Division of Atherosclerosis, Metabolism, and Clinical Nutrition, National Cardiovascular Center, Suita, Osaka, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Harano
authors.forename: A
authors.initials: A
authors.lastname: Kageyama
authors.forename: Y
authors.initials: Y
authors.lastname: Nakao
authors.forename: Y
authors.initials: Y
authors.lastname: Hara
authors.forename: M
authors.initials: M
authors.lastname: Suzuki
authors.forename: A
authors.initials: A
authors.lastname: Sato
authors.forename: M
authors.initials: M
authors.lastname: Ikebuchi
authors.forename: K
authors.initials: K
authors.lastname: Shinozaki
authors.forename: M
authors.initials: M
authors.lastname: Tsushima
mesh_terms: D000328:Adult; D000368:Aged; D001055:Apolipoproteins B / Q000097:blood*; D001162:Arteriosclerosis Obliterans / Q000097:blood; D002784:Cholesterol / Q000097:blood; D003327:Coronary Disease / Q000097:blood; D003924:Diabetes Mellitus, Type 2 / Q000378:metabolism*; D003925:Diabetic Angiopathies / Q000097:blood*; D005260:Female; D006801:Humans; D008074:Lipoproteins / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009765:Obesity; D012307:Risk Factors; D014280:Triglycerides / Q000097:blood
chemical_list: D001055:Apolipoproteins B; D008074:Lipoproteins; D014280:Triglycerides; D002784:Cholesterol