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Results for “NICOTINIC ACID”

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At least 685 records · Page 38Linked to original sources
PubMed1977

Transmethylation hypothesis of schizophrenia: methionine and nicotinic acid.

The transmethylation hypothesis of schizophrenia was reviewed with considerations that large doses of methionine when combined with a monoamine oxidase inhibitor lead to exacerbation of psychotic symptoms in a significant percentage of chronic schizophrenic patients. It was noted that nicotinic acid in the dosage of 3,000 mg/day can neither prevent nor counteract the psychopathology thus induced.

Catechol O-Methyltransferase↗
PubMed1980

Prevention of the teratogenic effect of 6-aminonicotinamide in chick embryos by nicotinic acid and L-methionine.

Administration of 6-aminonicotinamide into eggs may interfere with the development of the chick embryo. The prevention of this effect by nicotinamide has been shown before. In the present study, it could be demonstrated that a combination of nicotinic and L-methionine may also produce this effect. If applied alone nicotinic acid exhibited low effectiveness and L-methionine none at all.

6-Aminonicotinamide↗
PubMed1993

[The use of Enduracin--a prolonged-action form of nicotinic acid--in correcting atherogenic dyslipidemias].

The hypolipidemic effects of induracin, a new long-acting nicotinic acid dosage form based on the waxy matrix, and its tolerance were studied in 31 patients with Types IIa and IIb hyperlipoproteinemias in a 6-month blind crossover study. There were decreases in the levels of total cholesterol by 9-13% and low density lipoprotein cholesterol by 12-22%, an increase in high density lipoprotein cholesterol by 12-15%, and a good dynamics in the ratio of blood lipid-transport proteins--a 12-16% increase to the levels of apoprotein AI to a 29% decrease in those of apoprotein B. The drug is well tolerated by patients and may be recommended for correction of atherogenic dyslipidemias.

Adult↗
PubMed1975

Nicotinic acid and the endogenous production of carbon monoxide.

The endogenous production of carbon monoxide (VCO) has been followed with the aid of a rebreathing system for 3 hours in four healthy volunteers after i.v. injection of 50 mg nicotinic acid (NA). After an initial slight decrease for 15-30 min in the CO hemoglobin per cent saturation (COHb), a rapid increase was registered for 120 min, whereafter the VCO returned to the normal preinjection level. The amount of "extra" CO produced varied between 4.1 and 2.2 ml, corresponding to 2.9 and 1.6 g Hb or 182 and 98 mumol heme,respectively. These figures are 3-5 times higher than those reported in the literature, calculated from increases in serum iron, bilirubin and COHb (without the use of a rebreathing system). When related to the total body heme (TBH) estimated with the CO dilution technique, the amount of "extra" heme metabolized after NA corresponded to 0.30% (range 0.26-0.32) of the TBH (a fourth of the total daily heme turnover or a third of the daily HB heme catabolism.

Adult↗
PubMed1976

[Effect of nicotinic acid derivatives on the cholesterol metabolism with special regard to biosynthesis, absorption and excretion of cholesterol in the salivary gland (author's transl)].

The cholesterol metabolism of the salivary gland of mice fed on a diet containing 0.5% nicotinic acid derivative, 2, 2, 6, 6, tetrakis--(nicotinoyl-oxymethyl)--cyclohexanol (K-31) was as follows. 1. Total cholesterol level of sublingual and submaxially glands decreased in mice fed on normal diet as well as cholesterol-added diet. 2. The in vivo cholesterol biosynthesis from the acetate-1-14C increased in the sublingual gland, while it was not affected in the submaxillary gland. However, in vitro cholesterol synthesis decreased in both sublingual and submaxillary glands. 3. The disappearance of cholesterol-4-14C injected into the mice was more rapid in the K-31 treated mice than in the control after 30 days. 4. The incorporation of cholesterol-7-3h with a constant specific radioactivity administered orally for 37 days was reduced in the sublingual and submaxillary glands of K-31 treated mice. 5. When the mice were maintained on cholesterol-added diet for 21 days after cholesterol-4-14C injection, the excretion of sterol-14C in the feces was increased in K-31 treated mice. Thus, it was considered that the decrease of the cholesterol level of salivary glands by oral administration of K-31 is due to the increase of the excretion of cholesterol, the decrease of the uptake of the external cholesterol and the increase of excretion of sterol in the feces. These alterations of the cholesterol metabolism appear to induce cholesterol biosynthesis.

Animals↗
PubMed1978

Relative increase in apolipoprotein CII content of VLDL and chylomicrons in a case with massive type V hyperlipoproteinaemia by nicotinic acid treatment.

VLDL of fasting serum was fractionated into 4 fractions of decreasing particle size by preparative ultracentrifugation in a density gradient from a patient with massive type V hyperlipoproteinaemia before and after treatment with 12 g daily of nicotinic acid. Serum triglycerides fell from 58 to 9 mmol/1 in response to treatment due particularly to reduction of larger VLDL particles. Total, insoluble (apoprotein B) and soluble protein of all VLDL fractions also fell but the ratio of these 3 protein fractions to triglyceride rose particularly in the smaller VLDL fractions. The relative amount of apolipoprotein CII increased in all fractions and the ratio apo CII to triglycerides increased by 60--90% in all VLDL fractions. The relative amounts of apo CI, apo CII-2 and apo E appeared also to increase. The results are consistent with the hypothesis that low amounts of apo CII may play a role for the development of hypertriglyceridaemia.

Apolipoproteins↗
PubMed1985

Impaired plasma clearance of nicotinic acid and rifamycin-SV in Gilbert's syndrome: evidence of a functional heterogeneity.

Patients with Gilbert's syndrome (GS) have impaired clearance by the liver of some organic anions. We looked for possible differences in hepatic clearance of nicotinic acid (NA) and rifamycin-SV (R-SV) among GS patients, and examined the effect produced by these anions on the plasma levels of unconjugated bilirubin (UCB). Two subgroups of GS patients, GS1 and GS2, were differentiated according to their ability to handle R-SV and NA. Compared with a control group, the alteration of the half-life both of NA and R-SV was less marked in GS1 than in GS2. UCB plasma concentration after NA and R-SV loading was more greatly increased in GS2 than in GS1 patients. In addition, a striking correlation was found in all subjects studied between UCB and the half-life of NA and R-SV. These related alterations of plasma UCB and plasma half-life or organic anions suggests a common defect of hepatic uptake. It is hypothesized that this defect is located at the level of a hepatic plasma membrane carrier.

Adolescent↗
PubMed1988

Effects of nicotinic acid on concentrations of serum apolipoproteins B, C-I, C-II, C-III and E in hyperlipidemic patients.

Twenty-four patients with Type IIa, IIb, III and IV hyperlipoproteinemia (HLP) were treated with 4 g of nicotinic acid daily with the purpose to study its effect on serum apolipoprotein B, C-I, C-II, C-III and E concentrations. Triglyceride and total cholesterol concentrations of whole serum and of different serum lipoprotein fractions were also determined. Analyses were performed prior to and after a drug treatment period of 6 weeks, during which all the patients were weight stable. Treatment caused a decrease in serum concentrations of apolipoproteins C-I, C-II, C-III and E. These highly significant reductions were all positively correlated to a reduction of very low density lipoprotein triglyceride levels of serum (r-values greater than 0.76, p less than 0.001). There were highly significant decreases in serum levels of apolipoprotein B and low density lipoprotein total cholesterol. These reductions were positively intercorrelated (r = 0.55; p less than 0.01). Similar effects were observed in the different HLP types and in both sexes. Treatment resulted in normolipidemia in 12 patients, who were hypercholesterolemic (7 type IIa, 3 type IIb, 2 type III hyperlipoproteinemia) prior to treatment. The serum apolipoprotein B concentrations of these 12 patients fell after therapy to values which, however, remained abnormally high. We suggest that serum lipid adjusting treatment should aim at a normalization not only of serum lipid concentrations but also of the serum apolipoprotein B concentration in order to achieve a maximal antiatherogenic effect.

Adult↗
PubMed1988

Reduction of mortality in the Stockholm Ischaemic Heart Disease Secondary Prevention Study by combined treatment with clofibrate and nicotinic acid.

Consecutive survivors of a myocardial infarction from the Southern Hospital, below 70 years of age, were randomized into a Control group (n = 276) and a Treatment group (n = 279). The latter was openly prescribed the combination of clofibrate and nicotinic acid for serum lipid lowering. Each patient should remain in the study for 5 years and be seen regularly every 4 months at a special IHD outpatient clinic within the hospital. The concentration of serum cholesterol and triglyceride was lowered by 13% and 19%, respectively, in the Treatment group compared to the Control group. Total mortality was 82 cases in the Control group and 61 in the Treatment group, a 26% reduction (p less than 0.05). For patients above 60 years of age in the Treatment group the reduction in mortality was 28% (p less than 0.05). IHD mortality was reduced by 36% (p less than 0.01) in the Treatment group compared to the Control group. The beneficial effect of the serum lipid lowering treatment was related to the serum triglyceride concentration in two ways. First, it only occurred in patients with a triglyceride level greater than 1.5 mmol/l (n = 216). Secondly, it was most pronounced in the 44% of the treated patients who had a lowering of the serum triglyceride by 30% or more, and in this subgroup the reduction of IHD mortality was 60% (p less than 0.01). For serum cholesterol there were no such relations. The difference between serum triglycerides and cholesterol concerning these relations to the treatment outcome may be due to the fact that hypertriglyceridaemia was the most common hyperlipidaemia among our patients, occurring in 50%, while hypercholesterolaemia only occurred in 13%. Caution should be exercised in the interpretation of the results as the trial was not blind. However, the fact that the decrease in IHD deaths was directly related to the degree of serum triglyceride lowering indicates that it was the drug effect on serum lipids that was responsible for the beneficial effect of the treatment.

Aged↗