Topic
Clofibrate
About: Clofibrate is a research topic. Over the lifetime, 1853 publications have been published within this topic receiving 44665 citations. The topic is also known as: Atromid-S® & AY-61123.
Papers published on a yearly basis
1 / 2
Papers
TL;DR: Purified rat liver peroxisomes contain a cyanide-insensitive fatty acyl-CoA oxidizing system that uses O2 and NAD as electron acceptors, and the activity of this system is increased approximately one order of magnitude in rats treated with clofibrate.
Abstract: Purified rat liver peroxisomes contain a cyanide-insensitive fatty acyl-CoA oxidizing system that uses O2 and NAD as electron acceptors. The system was detected by the ability of added palmitoyl-CoA to elicit O2 consumption, H2O2 production, and O2-dependent NAD reduction. The activity of this system is increased approximately one order of magnitude in rats treated with clofibrate, a hypolipidemic drug known to cause peroxisomal proliferation.
1,152 citations
TL;DR: Treatment of NASH with UDCA for 12 months resulted in significant improvement in alkaline phosphatase, ALT, GGT, and hepatic steatosis, but despite the known lipid‐lowering effects of clofibrate, it did not appear to be of clinical benefit in the treatment ofNASH in this 1‐year pilot study.
625 citations
TL;DR: It was calculated that the contribution of the peroxisomes to fatty acid oxidation was less than 10% both in cells from control and clofibrate-treated animals and remained unchanged in starvation and diabetes.
447 citations
TL;DR: The data indicate that homozygous familial apolipoprotein (apo) E deficiency is a cause of type III HLP, is associated with markedly decreased apoE production, and that ApoE is essential for the normal catabolism of triglyceride-rich lipoprotein constituents.
Abstract: A unique kindred with premature cardiovascular disease, tubo-eruptive xanthomas, and type III hyperlipoproteinemia (HLP) associated with familial apolipoprotein (apo) E deficiency was examined. Homozygotes (n = 4) had marked increases in cholesterol-rich very low density lipoproteins (VLDL) and intermediate density lipoproteins (IDL), which could be effectively lowered with diet and medication (niacin, clofibrate). Homozygotes had only trace amounts of plasma apoE, and accumulations of apoB-48 and apoA-IV in VLDL, IDL, and low density lipoproteins. Radioiodinated VLDL apoB and apoE kinetic studies revealed that the homozygous proband had markedly retarded fractional catabolism of VLDL apoB-100, apoB-48 and plasma apoE, as well as an extremely low apoE synthesis rate as compared to normals. Obligate heterozygotes (n = 10) generally had normal plasma lipids and mean plasma apoE concentrations that were 42% of normal. The data indicate that homozygous familial apoE deficiency is a cause of type III HLP, is associated with markedly decreased apoE production, and that apoE is essential for the normal catabolism of triglyceride-rich lipoprotein constituents.
319 citations
Journal Article•
319 citations
Related Topics (5)
Performance Metrics
| Year | Papers |
|---|---|
| 2025 | 2 |
| 2024 | 4 |
| 2023 | 10 |
| 2022 | 17 |
| 2021 | 3 |
| 2020 | 6 |