Clofibrate hormonal

Rifampin is known to induce the hepatic microsomal enzymes that metabolize various drugs such as acetaminophen, oral anticoagulants, barbiturates, benzodiazepines, beta blockers, chloramphenicol, clofibrate, oral contraceptives, corticosteroids, cyclosporine, disopyramide, estrogens, hydantoins, mexiletine, quinidine, sulfones, sulfonylureas, theophyllines, tocainide, verapamil, digoxin, enalapril, morphine, nifedipine, ondansetron, progestins, protease inhibitors, buspirone, delavirdine, doxycycline, fluoroquinolones, losartan, macrolides, sulfonylureas, tacrolimus, thyroid hormones, TCAs, zolpidem, zidovudine, and ketoconazole. The therapeutic effects of these drugs may be decreased. 

The barbiturate type, the clofibrate type, the polycyclic hydrocarbon type, the steroid hormone type, and alcohol/acetone/isoniazid type. For example, the polycyclic hydrocarbon type act through a receptor. The barbiturate type increase liver blood flow. 

Albumin is the most abundant protein in human and other animal plasma. It is estimated that up to 40% of the total albumin in humans is in circulation transporting essential nutrients, especially those that are sparingly soluble in aqueous-based plasma. For example, the fatty acids, which are important fuel molecules for the peripheral tissue, are distributed by albumin. In addition, albumin is the plasma transport protein for other substances including bilirubin, thyroxine, and steroid hormones. Also, many drugs including aspirin, sulfanilamides, clofibrate, and digitalis bind to albumin and are most likely carried to their sites of action by the protein. 

Clofibrate has a mild antidiuretic effect (13), and animal studies suggest that this is due to release of antidiuretic hormone (ADH) (14). This effect has been used in the treatment of cranial diabetes insipidus (15). 

Epigenetic Promotors (phenobarbital) Cytotoxic/mitogenic agents (d-limonene, saccharin) Hormone-modifiers (estrogen) Immunosuppressors (cyclophoshamide) Peroxisome proliferators (clofibrate) Receptor-mediated (dioxins) Miscellaneous mechanisms (sodium nitrilotriacetic acid) Mostly in one species, strain or sex At high dose levels (MTD) Long latency period Threshold considerable for extrapolation to humans... 

Currently, over 100 compounds have been identified as PPs. The literature indicates that induction of peroxisome proliferation is not limited to exogenous chemicals. A number of endogenous substances, such as the steroid hormones, thyroid hormones, mor-phogenes, and fatty acids, are also involved in peroxisome proliferation. Peroxisome proliferation in hepatic parenchymal cells of rats and mice following the administration of clofibrate has been reported by numerous investigators. Compounds that are structurally unrelated to clofibrate, such as acetaminophen and Wy-14,643, can also cause peroxisome proliferation (Table 1). The industrial solvent trichloroethylene, the industrial plasticizers dill-ethyl hexyl) phthalate (DEHP) and di(2-ethyl hexyl) adipate (DEHA), have also been found to be hepatic peroxisome proliferators. 

Csaba, G., A. Inczefi-Gonda, C. Karabelyos and E. Pap. Hormonal imprinting neonatal treatment of rats with the peroxysome proliferator clofibrate irreversibly affects sexual behaviour. Physiol. Behav. 58 1203-1207, 1995. 

The barbiturate type the clofibrate type the polycyclic hydrocarbon type the steroid hormone type alcohol/acetone/isoniazid type. 

Among the numerous discoveries that we owe to botanists and pharmacognosts are the development of tryptophan metabolites, and especially indolylacetic acid. This compound acts as growth hormone in plants. Para-chlorinated phenoxyacetic acids (MCPA or methoxone 2,4-D or chloroxone) are mimics of indolylacetic acid (bioisostery) and show similar phytohormonal properties at high doses they serve as weeders. Ring-chlorinated phenoxyacetic acids were later introduced in molecules as varied as meclofenoxate (cerebral metabohsm), clofibrate (Upid metabolism) and ethacrynic acid (diuretic). 

Of the hyperlipidemic drugs, clofibrate appears to decrease fecal elimination of bile acids (278-280). However, this decrease is less than the increase of the neutral steroid output, so the net elimination of cholesterol is increased (280). Thyroid hormones may occasionally, especially if associated with diarrhea, cause a marked increase in bile acid elimination (see Section VIIB), while nicotinic acid only occasionally augments fecal bile salt output (221, 281). Of the more recently developed absorbable hypolipidemic drugs, DH-581 appears to stimulate bile acid excretion at least transiently, probably by inhibiting intestinal bile acid reabsorption (282). 

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