Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “NICOTINIC ACID”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 865 records · Page 48Linked to original sources
PubMedDate not supplied

[Effect of acetylsalicyclic and nicotinic acids and complamin on the formation of a prostacyclin-like substance by the aortic wall].

Experiments on Wistar rats have shown that single oral administration of acetylsalicylic (300 mg/kg), nicotinic (3 mg/kg) acids and complamin (2 mg/kg) inhibits platelet aggregation. It has been established that acetylsalicylic acid inhibits, as an antiaggregation agent, platelet aggregation and synthesis of a prostacycline-like substance by the aortal wall, and decreases its antiaggregation activity. Nicotinic acid and complamin inhibit platelet aggregation but do not lower antiaggregation activity of the aortal wall. Therefore, these latter drugs compare very favorably with acetylsalicylic acid as antiaggregation agents.

Animals↗
PubMedDate not supplied

Extracranial carotid arterial disease in patients with familial hypercholesterolemia and coronary artery disease treated with colestipol and nicotinic acid.

Carotid bifurcation atherosclerosis was demonstrated in 34 of 108 patients with familial hypercholesterolemia and coronary artery disease by B-scan, continuous-wave Doppler sonography, and intravenous digital subtraction angiography. An intensive combined therapy of diet, colestipol, and nicotinic acid was mounted to control the hypercholesterolemia of these patients. Their serial sonographies and digital subtraction angiography were evaluated independently by technical specialists who served as coinvestigators. The data obtained suggest that extracranial arterial disease can develop concurrently with coronary artery disease in a significant proportion of patients with familial hypercholesterolemia, and amaurosis fugax, transient ischemic attack, cerebral infarction, and myocardial infarction did not recur during 58-72 months of control of familial hypercholesterolemia in this series of patients.

Adult↗
PubMed1991

Effect of the antilipolytic nicotinic acid analogue acipimox on whole-body and skeletal muscle glucose metabolism in patients with non-insulin-dependent diabetes mellitus.

Increased nonesterified fatty acid (NEFA) levels may be important in causing insulin resistance in skeletal muscles in patients with non-insulin-dependent diabetes mellitus (NIDDM). The acute effect of the antilipolytic nicotinic acid analogue Acipimox (2 X 250 mg) on basal and insulin-stimulated (3 h, 40 mU/m2 per min) glucose metabolism was therefore studied in 12 patients with NIDDM. Whole-body glucose metabolism was assessed using [3-3H]glucose and indirect calorimetry. Biopsies were taken from the vastus lateralis muscle during basal and insulin-stimulated steady-state periods. Acipimox reduced NEFA in the basal state and during insulin stimulation. Lipid oxidation was inhibited by Acipimox in all patients in the basal state (20 +/- 2 vs. 33 +/- 3 mg/m2 per min, P less than 0.01) and during insulin infusion (8 +/- 2 vs. 17 +/- 2 mg/m2 per min, P less than 0.01). Acipimox increased the insulin-stimulated glucose disposal rate (369 +/- 49 vs. 262 +/- 31 mg/m2 per min, P less than 0.01), whereas the glucose disposal rate was unaffected by Acipimox in the basal state. Acipimox increased glucose oxidation in the basal state (76 +/- 4 vs. 50 +/- 4 mg/m2 per min, P less than 0.01). During insulin infusion Acipimox increased both glucose oxidation (121 +/- 7 vs. 95 +/- 4 mg/m2 per min, P less than 0.01) and nonoxidative glucose disposal (248 +/- 47 vs. 167 +/- 29 mg/m2 per min, P less than 0.01). Acipimox enhanced basal and insulin-stimulated muscle fractional glycogen synthase activities (32 +/- 2 vs. 25 +/- 3%, P less than 0.05, and 50 +/- 5 vs. 41 +/- 4%, P less than 0.05). Activities of muscle pyruvate dehydrogenase and phosphofructokinase were unaffected by Acipimox. In conclusion, Acipimox acutely improved insulin action in patients with NIDDM by increasing both glucose oxidation and nonoxidative glucose disposal. This supports the hypothesis that elevated NEFA concentrations may be important for the insulin resistance in NIDDM. The mechanism responsible for the increased insulin-stimulated nonoxidative glucose disposal may be a stimulatory effect of Acipimox on glycogen synthase activity in skeletal muscles.

Biological Transport↗
PubMed1990

Normalisation of the composition of very low density lipoprotein in hypertriglyceridemia by nicotinic acid.

Large (Sf greater than 100) and small (Sf 100-20) very low density lipoprotein (VLDL) particles were isolated by density gradient ultracentrifugation and characterized chemically in 8 patients with primary hypertriglyceridemia before and after 6 weeks treatment with 4 grammes daily of nicotinic acid (NA). Concomitant changes in high density lipoprotein (HDL) subclass distribution were determined by gradient gel electrophoresis. Small VLDL was subjected to lipolysis in vitro by incubation with bovine lipoprotein lipase before and after NA, and the change in the lipolytic end-product isolated in the low density lipoprotein (LDL) fraction was investigated. Reductions were achieved in the plasma levels of triglycerides, free and esterified cholesterol, phospholipids and proteins in the two VLDL subfractions. In all, the composition of both large and small VLDL particles changed towards potentially less atherogenic particles that were poorer in cholesteryl esters. The HDL cholesterol concentration increased and the HDL protein distribution on gradient gel electrophoresis changed towards larger particles. The mechanism behind the change in cholesterol distribution between VLDL and HDL after NA treatment is unclear, but it could possibly relate to decreased lipid transfer activity. NA reduced the content of apolipoprotein B in both VLDL subclasses and did not decrease the calculated particle size or the number of triglyceride molecules per particle, indicating a reduction of VLDL particle number rather than of particle size. The LDL density fraction isolated after lipolysis in vitro of small VLDL contained less total cholesterol and phospholipids and had a density profile more similar to native LDL after the patients had been treated with NA.

Adult↗
PubMedDate not supplied

Acute encephalopathy due to coexistent nicotinic acid and thiamine deficiency.

We report the case of an alcoholic woman with confusion, catatonia and extrapyramidal signs, who developed features of the Wernicke-Korsakoff syndrome after treatment with intravenous high potency vitamins. We emphasise that this should arouse the suspicion of nicotinic acid deficiency even in the absence of gastrointestinal symptoms or skin lesions.

Adult↗