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Results for “NICOTINIC ACID”

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At least 721 records · Page 40Linked to original sources
PubMed1981

Familial type II hyperlipoproteinemia with coronary heart disease: effect of diet-colestipol-nicotinic acid treatment.

Heterozygous familial type II hyperlipoproteinemia (F type II) is primarily manifested in hypercholesterolemia (due to low density lipoprotein-cholesterol [LDL-C] elevation) and premature coronary heart disease (CHD). We studied sequentially the effects of low cholesterol-low saturated fat-low simple carbohydrate diet; diet and colestipol, 30 g/day; and diet, colestipol, plus nicotinic acid (NA) 3 to 7 g/day on plasma cholesterol (Ch), LDL-C, triglyceride (TG), high density lipoprotein-cholesterol (HDL-C) and angiographically documented coronary arterial lesions of 32 F type II patients. Effective control of F type II resulted in arresting the progression of angiographically demonstrated coronary arterial lesions.

Adult↗
PubMedDate not supplied

Safety and feasibility of cardiac FDG SPECT following oral administration of Acipimox, a nicotinic acid derivative: Comparison of image quality with hyperinsulinemic euglycemic clamping in nondiabetic patients.

BACKGROUND: Image quality of cardiac fluorine-18-deoxyglucose (FDG) studies is highly dependent on the metabolic conditions during the study; hyperinsulinemic euglycemic clamping ensures adequate image quality. However, the approach is time-consuming. Data in a small number of patients suggest that oral administration of a nicotinic acid derivative (Acipimox, 250 mg; Byk, The Netherlands) results in good image quality. METHODS AND RESULTS: The safety and image quality of cardiac FDG single photon emission computed tomography studies after Acipimox administration were evaluated (21 patients, group 2); the results were compared with studies performed during hyperinsulinemic euglycemic clamping (69 patients, group 1). Image quality was assessed visually and quantitatively with use of heart-to-lung, heart-to-liver, and myocardium-to-background ratios. Blood samples were drawn at baseline and at the time of FDG injection to determine levels of glucose, free fatty acids, and insulin. Baseline characteristics of group 1 and 2 patients were comparable. No side effects occurred in group 1. Four patients in group 2 (19%) had paroxysmal flushing. Image quality, assessed visually, was good in 100% of group 1 patients and in 86% of group 2 patients. Images were uninterpretable in only 1 patient in group 2 (5%). All quantitative parameters of image quality (heart-to-lung, heart-to-liver, and myocardium-to-background ratios) were comparable between group 1 and 2 patients. Baseline plasma levels of all substrates were comparable between groups. At the time of FDG injection, plasma levels of glucose and free fatty acids were comparable between groups; insulin was higher in group 1 patients. CONCLUSIONS: Cardiac FDG single photon emission computed tomography after Acipimox is a simple and safe approach that renders comparable image quality to that obtained during hyperinsulinemic euglycemic clamping.

Administration, Oral↗
PubMed1978

A review of nicotinic acid, N-methylated indoleamines and schizophrenia.

The hypothesis that endogenously formed, N-methylated metabolites of indoleamines may play a role in the pathogenesis of schizophrenia was reviewed. Although N-methylated indoleamines can be produced in vivo and have significant psychotomimetic effects, there is little evidence for a specific increase in the methylation of indoleamines in schizophrenic patients. It was noted that even if the relationship between schizophrenia and N-methylated indoleamines had existed, nicotinic acid would not be an appropriate therapeutic agent.

Bufotenin↗
PubMed1977

Reduction of myocardial reinfarction by the combined treatment with clofibrate and nicotinic acid.

In an ongoing study 558 consecutive survivors of myocardial infarction below 70 years, mean age 59 years, were randomly allocated 4 months after the acute episode into a control group or a chemotherapy group from December 1972 to April 1976. Both groups were given moderate advice about diet and the chemotherapy group was prescribed clofibrate, 1 g twice daily, and nicotinic acid 1 g three times daily. Serum cholesterol and triglycerides were lowered around 15-20% and 30% respectively in the chemotherapy group while only insignificant reductions were observed in the control group. Until December 1976 total mortality and mortality from IHD has been the same in the two groups. The number of non-fatal myocardial infarctions has been 38 in the control and 19 in the chemotherapy group, a statistically significant reduction (P less than 0.01).

Cholesterol↗
PubMed1989

[The use of mixed feed with reduced content of vitamin A, E and nicotinic acid in the fattening of cairinas].

In three fattening experiments with 1344 male cairinas (Cairina moschata domestica L.) from hatching to the 77th day vitamin A supplement was reduced to 2500 IU/kg feed from hatching to the 21st day and to 1250 IU/kg feed from the 22nd to the 77th day. There was no supplementation of the feed with vitamin E or nicotinic acid. The reduction and elimination of the vitamin supplements on average did not have significant effects on fattening performance, feed intake, body weight, feed conversion and losses of animals in the starter and fattening periods. In the fattening period there was a tendency towards a higher intake and expenditure of feed in two experiments. Presumably the supplementation of 1250 IU/kg mixed feed is not always sufficient for an optimal fattening performance. In three production experiments with 33,850 cairinas no disadvantageous influence on fattening performance could be ascertained after a supplementation of 4,000 IU in the starter feed and 2,000 IU vitamin A in the fattening feed.

Animal Feed↗
PubMed1995

Comparison of lovastatin (20 mg) and nicotinic acid (1.2 g) with either drug alone for type II hyperlipoproteinemia.

Our study indicates that the combination of nicotinic acid (1.2 g/day) and lovastatin (20 mg/day) is more effective than either drug alone in reducing total and LDL cholesterol. Although HDL cholesterol was not significantly improved by these doses of agents over the duration of this study, LDL/HDL and HDL/total cholesterol ratios were improved due to the beneficial actions on total and LDL cholesterol. No serious side effects or changes in serum chemistries were observed, and the combination was well tolerated.

Aged↗
PubMed2004

Lysosome-sarcoplasmic reticulum junctions. A trigger zone for calcium signaling by nicotinic acid adenine dinucleotide phosphate and endothelin-1.

Previous studies on pulmonary arterial smooth muscle cells have shown that nicotinic acid adenine dinucleotide phosphate (NAADP) evokes highly localized intracellular Ca(2+) signals by mobilizing thapsigargin-insensitive stores. Such localized Ca(2+) signals may initiate global Ca(2+) waves and contraction of the myocytes through the recruitment of ryanodine receptors on the sarcoplasmic reticulum via Ca(2+)-induced Ca(2+) release. Here we show that NAADP evokes localized Ca(2+) signals by mobilizing a bafilomycin A1-sensitive, lysosome-related Ca(2+) store. These lysosomal stores facilitate this process by co-localizing with a portion of the sarcoplasmic reticulum expressing ryanodine receptors to comprise a highly specialized trigger zone for NAADP-dependent Ca(2+) signaling by the vasoconstrictor hormone, endothelin-1. These findings further advance our understanding of how the spatial organization of discrete, organellar Ca(2+) stores may underpin the generation of differential Ca(2+) signaling patterns by different Ca(2+)-mobilizing messengers.

Animals↗
PubMed2000

The nicotinic acid analogue acipimox increases plasma leptin and decreases free fatty acids in type 2 diabetic patients.

The effect of 3 days of intensive treatment with acipimox, an antilipolytic nicotinic acid derivative, on plasma leptin levels was studied in eight patients with Type 2 diabetes mellitus in a double-blind, placebo-controlled, cross-over study. Acipimox reduced plasma free fatty acids (FFA) markedly and lowered plasma triglycerides, glucose and insulin. Plasma leptin levels were elevated in all eight patients during 3 days of acipimox treatment (mean increase+/-s.e.: 2.38+/-0.57ng/ml, P<0.005) and the 24h mean effect of acipimox on leptin levels increased during the experimental period (P<0.03). The effect on plasma insulin and glucose resembled a mirror image of the effect on plasma leptin during 3 days of treatment. The suggestion that leptin mediates insulin resistance and may be involved in the development of the diabetic syndrome cannot be supported by the present results. It has been reported that FFA stimulates leptin secretion. Surprisingly, despite a markedly reduced FFA level, leptin concentration increased in the present study. We suggest that a primary acipimox effect is to increase leptin secretion, and that this prevails over the reduced FFA stimulus.

Area Under Curve↗
PubMed1979

Nicotinic acid metabolism. 2,3-Dimethylmalate lyase.

1) A new enzyme, 2,3-dimethylmalate lyase, was purified from Clostridium barkeri to about 80% homogeneity. Some of the properties of the enzyme are described. 2) It is shown that the 2,3-dimethylmalic acid (m.p. 143 degrees C) described in the literature represents only one racemic pair. This pair is not attacked by 2,3-dimethylmalate lyase. 3) The isolation of both racemic pairs of 2,3-dimethylmalic acid is described. Half of one pair, m.p. 104-106 degrees C, was converted to propionate and pyruvate by 2,3-dimethylmalate lyase. 4) In combination with earlier work performed by E.R. Stadtman and coworkers the results given under points 1--3 establish 2,3-dimethylmalate as an intermediate in the degradation of nicotinic acid by C. barkeri. 5) Experimental evidence indicates the 2,3-dimethylmalate lyase is no acyl-S-enzyme and that it is different in this respect as well as in quaternary structure from the apparently related enzymes citrate lyase and citramalate lyase.

Clostridium↗
PubMedDate not supplied

Differential effect of nicotinic acid derivatives on smooth muscle and endothelial cell proliferation.

The pathogenesis of atherosclerosis is a multifactorial process. A possible anti-atherosclerotic drug should therefore interfere with different targets that are important during the development of an atherosclerotic lesion. Two of the early events are the activated migration and proliferation of arterial smooth muscle cells. Here we investigated in several in vivo and in vitro experiments the effect of two nicotinic acid derivatives L44 and L44-0, on smooth muscle cell migration and proliferation. Balloon catheter de-endothelialization was used as an animal model for intimal lesion formation. Migration was subsequently quantified in vitro using the explant outgrowth technique. Subcultured smooth muscle and endothelial cells were used to test the effect of the drugs on proliferation. Time-lapse video microscopy was applied to differentiate between smooth muscle cell migration and proliferation on the level of individual cells. We showed that L44 and L44-0 are very effective in decreasing smooth muscle cell proliferation and migration. Endothelial cell proliferation, important to re-establish endothelial integrity was, however, not affected.

Animals↗