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PubMed1976

Altered insulin and glucagon secretion in treated genetic hyperlipemia: a mechanism of theraphy?

The influence of Halofenate therapy on insulin and glucagon secretion was examined in the Zucker rat with genetic endogenous hyperlipemia. Coincident with the lipid lowering effects of Halofenate, the net change in the basal bihormonal axis favored glucagon, with the I/G molar ratio (Insulin/Glucagon) decreasing from 2.72 +/- 0.53 to 0.96 +/- 0.20 during treatment with this drug. Following arginine stimulation the I/G ratio remained reduced at 0.87 +/- 0.13 in Halofenate treated animals, contrasting with the statistically greater ratio of 2.5 +/- 0.55 in control animals. The Halofenate induced state of reduced insulin:glucagon was associated with hypolipemia, postarginine hyperglycemia, and hyperketonemia,-three metabolic parameters characteristic of glucagon excess relative to insulin. It is suggested that the lipid-lowering action of Halofenate in genetic hyperlipemia may reflect the altered bihormonal axis induced by the drug.

Animals↗
PubMed1975

Efficacy and interactions of oxandrolone, halo-fenate and clofibrate in a factorial study on experimental acute nephrotic hyperlipidemia.

Nephrotic mixed hyperlipidemia may be associated with accelerated coronary artery disease. To investigate the response of experimental nephrotic hyperlipidemia to therapy, a 2(4) factorial study of sodium clofibrate and beta-benzalbutyrate, halofenate and oxandrolone (250, 150, 100 and 10 mg/kg/day, respectively) was carried out. Nephrotic syndrome was induced by a single i.p. injection of puromycin aminonucleoside (90 mg/kg) in 80 female white rats of average weight 160 g. Oxandrolone proved to be significantly hypotriglyceridemic in combined therapy (average fall, 38%; P less than .05), and also lowered serum total cholesterol and phospholipid concentrations (23% and 21% falls, P less than .01) and less than .05), due largely to synergistic interactions with clofibrate-like drugs. Hypocholesteremic effects (23 and 22% average falls) were also significant for halofenate (P less than .01) and clofibrate (P less than .05) . Serum triglyceride levels actually rose significantly (P less than .05) with drug combinations containing beta-benzalbutyrate. Clofibrate and its analogs (halofenate and beta-benzalbutyrate) produced significant hepatomegaly (mean responses of +18, +18 and +10%, respectively) whereas oxandrolone produced significant hepatic shrinkage (-10%)(P less than .05). Secondary effects (drug interactions) were also found; hypotriglyceridemic synergism (effects more than additive) occurred between oxandrolone and clofibrate or its analogs (P less than .05), whereas antagonism (effects less than additive) was observed within the clofibrate-like group (P less than .01 or less .05).

Animals↗
PubMed1977

Determination of various drugs in rodent diet mixtures.

Methods employing solvent extraction, thin-layer chromatography, gas-liquid chromatography, and UV spectrophotometry are described for the quantitative determination of halofenate, cyclobenzaprine and sulindac in rodent diet mixtures. Halofenate was hydrolyzed to its free acid derivative and converted to a methyl ester prior to assay. The drugs were shown to be stable when stored in food mixtures at room temperature for seven days. Diet mixtures containing the three drugs were demonstrated to be uniformly mixed by the procedure employed.

Amitriptyline↗
PubMed1978

Platelet function in hyperbetalipoproteinemia.

Individuals with familial hyperbetalipoproteinemia are at increased risk of premature atherosclerosis and thrombosis. Although there is controversy whether platelet survival is shortened or normal in this disease, several in vitro tests of platelet function are abnormal including a decreased threshold concentration for stimulation of aggregation by ADP, epinephrine and collagen and increased release of nucleotides to the same agents. These functional changes are accompanied by an increase of cholesterol to phospholipid ratio in the platelet membrane and in low density lipoprotein in individuals with type IIa hyperlipoproteinemia. Clofibrate and halofenate reverse some of the abnormalities in vitro and the former drug, when administered for 6 weeks to patients with type IIa hyperlipoproteinemia decreases platelet sensitivity to ADP and epinephrine. The platelet hypersensitivity to aggregating agents can be reproduced in vitro by increasing the cholesterol to phospholipid rather in normal platelets. These artificially hypersensitive platelets can be returned to normal by halofenate in vitro. Incorporation of cholesterol into platelet membranes increases the basal level of the membrane associated enzyme adenylate cyclase. However, the enzyme no longer responds to stimulation by prostaglandin E1, and this is associated with relative resistance of the platelet to inhibition by this pharmacologic agent. These functional alterations produced by cholesterol enrichment of platelet membranes occur is parallel with an increase in platelet membrane microviscosity suggesting that the more rigid membrane can alter the behavior of membrane associated enzymes and receptors. A correlation appears to exist between the ability of certain drugs to induce phase separation in model membranes and the potency in inhibitory platelet aggregation.

Adenosine Diphosphate↗
PubMed1982

Short-term inhibition of fatty acid biosynthesis in isolated hepatocytes by mono-aromatic compounds.

An overview is presented of a selected number of mono-aromatic derivatives and their short-term effects on hepatic fatty acid biosynthesis. The compounds discussed in this paper are ortho-hydroxybenzoate (salicylate), meta-hydroxybenzoate, para-hydroxybenzoate, benzoate, para-t-butylbenzoate, para-aminosalicylate, clofibrate, halofenate, alpha-cyano-4-hydroxycinnamate and benfluorex. All of these drugs inhibit fatty acid biosynthesis by isolated rat liver cells, albeit with different effectiveness. In contrast, the compounds have differential effects on fatty acid esterification and oxidation by isolated hepatocytes. An attempt is made to describe in molecular terms the underlying mechanisms of the acute inhibitory effects of the mono-aromatic derivatives on hepatic lipogenesis. It is proposed that all of the drugs exert an inhibitory action at the level of acetyl-CoA carboxylase, the enzyme generally considered to catalyse the rate-limiting step in hepatic fatty acid synthesis. This inhibitory effect may be either direct, i.e. by an alteration of the enzyme's structure as a result of interaction between drug and enzyme, or indirect, i.e. through a drug-induced change in the cellular levels of allosteric effectors of acetyl-CoA carboxylase.

Acetyl-CoA Carboxylase↗
PubMedDate not supplied

Pharmacokinetic drug interactions with propranolol.

Propranolol is widely used in clinical practice and is frequently administered along with other drugs. The co-administration of propranolol and other drugs may result in either propranolol-induced changes in the disposition of other drugs or in effects of the other drugs on the pharmacokinetics of propranolol. These changes may be due to alteration in absorption, metabolism or to haemodynamic effects such as altered liver blood flow. Understanding the pharmacokinetics of propranolol is important to the rational interpretation of the effects of other drugs on propranolol's disposition. The absorption, protein binding and metabolism of propranolol may all be affected by the co-administration of other drugs. Induction of propranolol's metabolism by halofenate, phenytoin, phenobarbitone, rifampicin and alcohol have all been implicated in altering propranolol clearance, while inhibition of hepatic drug metabolising enzymes by chlorpromazine and cimetidine appear to reduce propranolol clearance. Propranolol may also affect the metabolism of other drugs such as antipyrine, chlorpromazine, theophylline and thyroid hormones. Suggestions that propranolol may alter quinidine's elimination have not been substantiated. By reducing liver blood flow propranolol may reduce the systemic clearance of other high extraction drugs such as lignocaine.

Absorption↗
PubMed1984

Effect of phenoxy acids on rat liver regeneration.

Phenoxy-acids incorporated in a basal region on a weight basis, were fed to male rats from which two-thirds of the liver had been removed and the extent of regeneration or the liver increment was ascertained over a period of 10 days p.o. Stimulatory responses occurred with the hypolipidemic drugs, ethyl clofibrate, at levels of 0.25% higher or by gavage over the 1st 8 days p.o. at an overall dosage of 1275 mg/kg, 2-(p-chlorophenoxy)propionic acid (0.50, 1.0%), the corresponding o-chloro-acids (0.20 and 0.50%, respectively) and several other with branching of the acid side-chain. The latter included phenoxyisobutyric acid (0.50%), 2-phenoxypropionic acid (1.0%), 2-phenoxybutyric acid (1.0%), the phenoxydimethyl-pentanoic acid, gemfibrozil (0.40%), the herbicide, 2-(2,4,5-trichlorophenoxy)propionic acid (0.10%) and as screened on a few males, possibly, halofenate (0.20%). The liver increments were in the control range for compounds containing straight chain acid substituents as 4-(p-chlorophenoxy)-butyric acid (0.35%), 3-phenoxypropionic acid (0.75%), 3-(p-chlorophenoxy)-1,2-propanediol (0.50%) and phenoxyacetic acid derivatives, including p-chloroacetic acid and the herbicides 2,4-dichlorophenoxy-, 2-methyl-4-chlorophenoxy- and 2,4,5-trichlorophenoxyacetic acids at levels of up to about 0.50%. Where effects resulted with the phenoxyacetic acids, these were in the direction of inhibition of the regenerative process. The response of the female rat to clofibrate either by diet or gavage was rather poor or equivocal but was more definite with 2-(2,4,5-trichlorophenoxy)propionic acid (0.10%). However, intact females were more consistent in eliciting wet and dry liver enlargement with clofibrate (0.25%) as noted earlier by others and with gemfibrizol (0.040%) and the trichlorophenoxypropionic acid (0.10%) but not with 2,4,5-trichlorophenoxyacetic acid at 0.10%.

Animals↗
PubMed1976

Drug treatment of hyperlipidemia.

The most frequent indication for treatment of hyperlipidemia is for prevention of arteriosclerosis, a suspected but unproved benefit. The cornerstone of treatment of primary hyperlipidemia is diet; drugs may be added to, but do not replace, diet. When a drug is used with any patient, its potential benefits and hazards must be carefully weighed for the given subject. The subjects should be carefully followed and observed for side effects. Plasma lipids should be monitored during the course of treatment. Five drugs have been approved by the U.S. Food and Drug Administration for the treatment of hyperlipidemia: cholestyramine, clofibrate, nicotinic acid, sodium dextrothyroxine and beta-sitosterol. The use, the actions and the side effects of each and of several nonapproved agents are discussed.

Aminosalicylic Acids↗