Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0154251 (lipid disorder)
 795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Quantitative and qualitative derangement of apolipoprotein B-containing lipoproteins as a risk factor for diabetic macroangiopathy in nonobese NIDDM subjects. 867 86

Atherosclerotic cardiovascular disease is the major cause of morbidity and mortality in NIDDM patients. But the exact pathophysiology of accelerated atherosclerosis seen in NIDDM is not completely understood. Hyperinsulinemia and hyperlipidemia frequently coexist in these subjects. Present study was undertaken to demonstrate relationship of serum insulin with atherogenic lipids in 92 (male = 62, female = 30) newly diagnosed, middle-aged, nonsmoking, uncomplicated and untreated NIDDM patients with normal body mass index (BMI). Fourty (male = 20, female = 20) non-diabetic healthy subjects with a negative family history of diabetes served as control. After an overnight fasting, venous blood was collected for plasma glucose, serum insulin and lipid profile. ECG and oral glucose tolerance test (OGTT) were done in all subjects. Diabetes mellitus was diagnosed by WHO criteria. Total cholesterol, LDL-c, LDL/HDL ratio, TG (p always < 0.001) and fasting serum insulin (p = 0.033) were significantly higher and HDL-c was significantly lower (p = 0.001) in NIDDM than control subjects. Fasting serum insulin was inversely related to the degree of hyperglycemia in NIDDM subjects (r = -0.1867; p = 0.037). NIDDM with hyperinsulinemia (n = 18) had a strong negative correlation (r = -0.449, p = 0.031) with HDL-c. Neither total cholesterol nor LDL-c had any significant correlation with insulin. The results indicate that diabetic state itself is associated with atherogenic lipid disorder.
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PMID:Lipid profile and its relation to fasting insulin level in non-insulin dependent diabetes mellitus (NIDDM). 881 64

Hyperlipoproteinemia is one of the main coronary risk factors. Lipid metabolism disorders occur in about 40-60% of patients with NIDDM. Hyperlipidemia in diabetics is related to diabetes control, presence of diabetic nephropathy, diet, some drugs and genetic factors. Lipid metabolism disorders in NIDDM comprise qualitative changes--usually increase of serum triglyceride concentration and decrease of HDL--cholesterol, and qualitative changes of lipoprotein composition, glycation and oxidation. The first steps of hypolipemic therapy are good control of diabetes, reduction of overweight, hypolipidemic diet, and if a goal level is not achieved--farmacotherapy. Hypolipidemic treatment should be relevant in reduction of cardiovascular diseases in diabetic patients.
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PMID:[Lipid disorders in non-insulin dependent diabetes--principles of treatment]. 899 31