Disease relevance of Miscleron

• Increase in lipoprotein lipase during clofibrate treatment of hypertriglyceridemia in patients on hemodialysis [1].
• Clofibrate effect on alkaline phosphatase in renal failure [2].
• Clofibrate-induced muscle damage with myoglobinuria and cardiomyopathy [3].
• The highest TNF levels (500 and 250 pg/mL) were observed in 2 patients with Enterobacter cloacae bacteremia who had received the placebo and antilipid A antibody, respectively [4].
• Plasma tumor necrosis factor levels in patients with presumed sepsis. Results in those treated with antilipid A antibody vs placebo [4].

Psychiatry related information on Miscleron

• Enhancement of voluntary alcohol consumption in rats by clofibrate feeding [5].
• Those with persistently elevated levels of blood pressure and/or serum LDL-C require nonpharmacologic intervention initially, but may require antihypertensive or antilipid medication if unresponsive to behavioral modification for diet, physical activity, and cigarette smoking [6].
• Water deprivation tests before and during treatment showed significantly higher basal, final, and peak urinary osmolalities (Uosm) and lower free water clearance (CH20) on chlorpropamide, singly and in combination: clofibrate raised Uosm less but significantly decreased CH2O [7].
• Effect of clofibrate, cholestyramine, cholesterol and feeding pattern on the diurnal variation of cholesterol 7 alpha-hydroxylation in swine [8].

High impact information on Miscleron

• We studied the effect of th bite acid sequestrant colestipol, alone and in combination with clofibrate or niacin, in patients with heterozygous familial hypercholesterolemia who were given a diet low in cholesterol and saturated fat [9].
• Low pretreatment lipoprotein-lipase activity in adipose-tissue specimens and postheparin plasma increased to normal with clofibrate, whereas low hepatic triglyceride lipase activity did not change [1].
• Synaptic transmission is partially impaired in syd-2 mutants. syd-2 encodes a member of the liprin (for LAR-interacting protein) family of proteins which interact with LAR-type (for leukocyte common antigen related) receptor proteins with tyrosine phosphatase activity (RPTPs) [10].
• Unique, spindle-shaped particles (phi bodies) and rods with peroxidatic activity are found in certain epithelial cells of normal mice, clofibrate-fed rats, and in leukemic leukocytes [11].
• These two hypolipidemic peroxisome proliferators are structurally different from ethyl a-p-chlorophenozyisobutyrate (clofibrate) and other hypolipidemic, arylocyisobutyrate derivatives which cause hepatic peroxisome proliferation [12].

Chemical compound and disease context of Miscleron

• Reduced lipoprotein-lipase activity may cause hypertriglyceridemia and decreased high-density-lipoprotein cholesterol in patients on hemodialysis; clofibrate may correct these abnormalities by increasing lipoprotein-lipase activity to normal [1].
• (3) Toxicity was attenuated by pretreatment with butylated hydroxyanisole or clofibrate (two inducers of microsomal epoxide hydrolase) and markedly increased by phorone-induced glutathione depletion [13].
• Among the patients treated with clofibrate, no change from baseline was found in mean ALT, aspartate transaminase (AST), GGT, bilirubin, triglycerides, and cholesterol, or in histological grade of steatosis, inflammation, or fibrosis after 12 months of treatment as compared with entry [14].
• In severe hypertriglyceridemia, clofibrate, gemfibrozil, or fenofibrate may reduce the very low-density lipoprotein and chylomicron levels adequately [15].
• Patients with angina only were shown to benefit from treatment with clofibrate, but prospective trials with dipyridamole or aspirin in the primary or secondary prevention of myocardial infarction did not reveal a significant reduction in morbidity or mortality in the experimental group [16].

Biological context of Miscleron

• Inhibition of hormone-stimulated lipolysis by clofibrate. A possible mechanism for its hypolipidemic action [17].
• In contrast, in adult clofibrate-treated rats and rats on the day of birth whose mothers received clofibrate during the gestation period, the hepatocytes showed microbodies that were greater in both number and size, and the catalase activity in the liver was definitely elevated [18].
• 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) [19].
• RESULTS: We show that peroxisome proliferator-activated receptor-alpha agonists (WY-14643, bezafibrate, clofibrate, and phthalate) induce human cytochrome P450 1A1 gene expression, whereas 2,4-thiazolidinedione, a specific peroxisome proliferator-activated receptor-gamma agonist, represses it [20].
• Clofibrate may act as an enzyme inducer and the hypothesis is that enzyme induction is responsible for this pattern [21].

Anatomical context of Miscleron

• Hepatic peroxisome proliferation: induction by two novel compounds structurally unrelated to clofibrate [12].
• A hyperplastic state of hepatocytes induced by hepatocarcinogens might be related to the formation of these inclusions in response to clofibrate [22].
• In contrast, activators of the PPARalpha, oleic acid, linoleic acid, and clofibrate, accelerated epidermal development, resulting in mature lamellar membranes, a multilayered SC, and a competent barrier after 2 d of incubation [23].
• Response of microbodies in Morris hepatoma 9618A to clofibrate [18].
• Regulation of the formation of microbodies in Morris hepatoma 9618A was studied by examination of the response of the organelles to clofibrate [18].

Associations of Miscleron with other chemical compounds

• In the presence of procaine-HC1, which blocks hormone-stimulated lipolysis without inhibiting cyclic AMP accumulation, addition of clofibrate prevented the hormone-stimulated rise in cyclic AMP [17].
• Abnormal inclusions in microbodies were induced by clofibrate in hepatocytes of hyperplastic liver nodules in rats fed 2-acetylaminofluorene [22].
• SCD1 mRNA was analyzed from the livers of BALB/c mice that had been fed diets supplemented with clofibrate or gemfibrozil [24].
• X-ray analysis showed that three pairs of molecules of clofibric acid, the active metabolite of clofibrate, bound to the walls of the internal cavity of deoxyhemoglobin A; only one pair bound to a quite different site, between helices A, E, and H of the alpha chains of carbon monoxide hemoglobin A [25].
• The structurally diverse peroxisome proliferators ciprofibrate, clofibrate, and bis(2-ethylhexyl) phthalate [(EtHx)2 greater than Pht] increase the activities of hepatic catalase and peroxisomal fatty acid beta-oxidation enzymes in conjunction with profound proliferation of peroxisomes in hepatocytes [26].

Gene context of Miscleron

• Clofibrate was found to induce liver SCD1 mRNA levels 3-fold within 6 hr to a maximum of 22-fold in 30 hr [24].
• In white adipose tissue of KKAy obese mice, thiazolidinedione PPARgamma activators (pioglitazone and troglitazone) induced FAT and FATP more efficiently than the PPARalpha activator, clofibrate [27].
• KIF1A colocalizes with liprin-alpha in various subcellular regions of neurons [28].
• KIF1A cofractionates and coimmunopreciptates with liprin-alpha and various liprin-alpha-associated membrane, signaling, and scaffolding proteins including alpha-amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid receptors, GRIP/ABP, RIM, GIT1, and beta PIX [28].
• The PPs Wy-14643, mono-ethylhexyl phthalate, clofibrate, ciprofibrate ethyl ester, and eicosatetraynoic acid each caused large increases in COX-2 mRNA and protein, with maximal expression seen approximately 10 h after treatment of quiescent cells [29].

Analytical, diagnostic and therapeutic context of Miscleron

• Using an enzyme-linked immunosorbent assay, we measured plasma levels of tumor necrosis factor (TNF) in 38 patients who were treated with either antilipid A antibody or a placebo for presumed gram-negative bacteremia [4].
• A patient with primary biliary cirrhosis is reported in whom the administration of clofibrate in a dose of 1 g per day for 2 months resulted in a marked increase in hypercholesterolemia, and endoscopic retrograde cholangiography showed multiple intrahepatic gallstones [30].
• Rapid purification of cytosolic epoxide hydrolase from normal and clofibrate-treated animals by affinity chromatography [31].
• Western blot analysis indicated that a similar sex dependence characterizes both the basal expression and the clofibrate inducibility of the corresponding P450 4A proteins [32].
• Peroxisomes were purified by differential and equilibrium density centrifugation from the livers of rats treated with clofibrate to enhance their peroxisomal system of fatty acid oxidation [33].

References