Disease relevance of Hyperlipoproteinemia Type IV

• In a long-term, double-blind study of halofenate or clofibrate treatment of patients with Type IV hyperlipoproteinemia, diabetic patients receiving a sulfonylurea and halofenate either required a reduction in the dose of the sulfonylurea or demonstrated significantly improved control of hyperglycemia (P less than 0.05) or both [1].
• Bile acid metabolism in hereditary forms of hypertriglyceridemia: evidence for an increased synthesis rate in monogenic familial hypertriglyceridemia [2].
• Interactions of obesity and glucose-stimulated insulin secretion in familial hypertriglyceridemia [3].
• The drug caused a significant reduction in very-low-density lipoprotein cholesterol in patients with non-insulin-dependent diabetes mellitus and type IV hyperlipoproteinemia, along with a variable change in high-density lipoprotein cholesterol, independent of its effect on plasma glucose [4].
• VLDL triglyceride was inversely related to HDL cholesterol in familial hypertriglyceridemia (r = -0.74, P < 0.005), but not in familial combined hyperlipidemia [5].

High impact information on Hyperlipoproteinemia Type IV

• We therefore used dietary therapy to lower the triglyceride levels of 29 men with Type IV hyperlipoproteinemia and evaluated the effects on HDL-cholesterol levels [6].
• The persistently low HDL-cholesterol level in the presence of normalization of triglycerides suggests that depressed HDL cholesterol may be an independent metabolic abnormality in Type IV hyperlipoproteinemia [6].
• Thus heterozygous lipoprotein lipase deficiency, together with age-related influences, may account for a form of familial hypertriglyceridemia [7].
• Carriers were prone to the expression of a form of familial hypertriglyceridemia characterized by increased plasma triglyceride, VLDL cholesterol and apolipoprotein B, and decreased LDL and HDL cholesterol concentrations [7].
• Does familial hypertriglyceridemia predispose to NIDDM [8]?

Chemical compound and disease context of Hyperlipoproteinemia Type IV

• The hypolipidemic as well as other laboratory and clinical effects of halofenate, clofibrate, and placebo were compared in 29 patients with type IV hyperlipoproteinemia in a double-blind, controlled, therapeutic trial of 1 yr duration [9].
• Dose-response to tibric acid: a new hypolipidemic drug in type IV hyperlipoproteinemia [10].
• Carnitine, which is necessary for fatty acid oxidation, has been recently reported to lower serum triglycerides in patients with type IV hyperlipoproteinemia [11].
• Effects of fenofibrate on biliary lipids and bile acid pool size in patients with type IV hyperlipoproteinemia [12].
• The present investigation was designed to examine the influence of genetic Type IV hyperlipoproteinemia on the metabolism of lipids in response to estrogen exposure [13].

Biological context of Hyperlipoproteinemia Type IV

• Plasma triglyceride lowering by exercise despite increased food intake in patients with type IV hyperlipoproteinemia [14].
• Serum lipids, plasma insulin and glucagon, aerobic capacity, and body composition were examined in middle-aged men (X age = 44.2 years) with type IV hyperlipoproteinemia to determine the relative effectiveness of a caloric restricted type IV hyperlipoproteinemia diet (group A) versus physical training plus an isocaloric type IV diet (group B) [15].
• Bile acid kinetics were determined with an isotope dilution technique using 14C-labeled C and CD under steady state conditions in control subjects and patients with type IIa and type IV hyperlipoproteinemia [16].
• Cultures of human diploid fibroblasts were shown to accumulate elevated levels of intracellular triglyceride when grown in medium supplemented with sera from patients with endogenous hypertriglyceridemia (Type IV hyperlipoproteinemia) [17].
• In hyperlipidemic CAPD patients, there was no difference in serum albumin concentrations or HTGL activities among lipoprotein phenotypes, whereas LPL activities were significantly higher in the patients with type II than those with type IV hyperlipoproteinemia [18].

Anatomical context of Hyperlipoproteinemia Type IV

• We have previously shown that very low density lipoproteins (VLDL, Sf 60-400) from subjects with type IV hyperlipoproteinemia (HTG-VLDL) will induce appreciable cholesteryl ester accumulation in cultured macrophages (J774A.1) [19].
• In order to see whether or not fenofibrate, a clofibrate analogue, has any influence on biliary cholesterol saturation, we determined the lipid composition of gallbladder bile and the bile acid pool size in 15 patients with type IV hyperlipoproteinemia before and after 6-8 weeks of treatment with a daily dose of 300 mg of the drug [12].

Gene context of Hyperlipoproteinemia Type IV

• Analysis of the ileal bile acid transporter gene, SLC10A2, in subjects with familial hypertriglyceridemia [20].
• No evidence for linkage between familial hypertriglyceridemia and apolipoprotein B, apolipoprotein C-III or lipoprotein lipase genes [21].
• Platelet function in patients with familial hypertriglyceridemia: evidence that platelet reactivity is modulated by apolipoprotein E content of very-low-density lipoprotein particles [22].
• Type IV hyperlipoproteinemia and moderate instability of CAG triplet expansion in the androgen-receptor gene. Lipid, sex hormone and molecular study in a Chinese family with Kennedy-Alter-Sung disease [23].
• Apolipoprotein AI and AII metabolism in patients with primary high-density lipoprotein deficiency associated with familial hypertriglyceridemia [24].

Analytical, diagnostic and therapeutic context of Hyperlipoproteinemia Type IV

• Gas-liquid chromatography profiling of intact lipids. Observation of differences between triglyceride structure of lipoproteins in type III and type IV hyperlipoproteinemia [25].
• Triglyceride-rich lipoproteins (TRLs) separated by ultracentrifugation (d < 1.006 g/dL) and chylomicrons and chylomicron remnants (quantified by apolipoprotein [apo] B-48 determination) were determined after a fat load in 10 patients with familial hypertriglyceridemia before and after therapy with gemfibrozil (900 mg daily) [26].
• Our specific aim was to assess severe hypertriglyceridemia and pancreatitis that occurred when postmenopausal estrogen replacement therapy (ERT) or tamoxifen had been given by their physicians to women with preexisting, usually covert, primary familial hypertriglyceridemia [27].

References