Disease relevance of nicotinic acid

• We concluded that 1) basal plasma FFAs exerted physiologically important, long-lasting effects supporting 25-33% of basal insulin secretion in nondiabetic and diabetic subjects; 2) basal plasma FFAs were responsible for some of the hyperinsulinemia in normoglycemic obese subjects; and 3) NA had no direct effect on insulin secretion [1].
• 14C-Nicotinic acid (NA) incorporation into nicotinamide adenine dinucleotide (NAD) was studied in cultures from 7 normal human pituitaries and 13 chromophobe adenomas [2].

High impact information on nicotinic acid

• In summary, our data suggest that (a) acute changes in plasma FFA produce acute changes in GNG and reciprocal changes in GL; (b) the decrease in EGP between 16 and 24 hours of fasting is due to a fall in GL; and (c) NA has no direct effect on GNG [3].
• CONCLUSIONS: Short-term beta-cell compensation to NA-induced insulin resistance was incomplete and did not differ by genetic predisposition [4].
• Phosphorylation of p38 MAPK was increased (P<0.05) by NA treatment at rest, and this correlated (r2=0.84, P<0.01) with increased PGC1alpha [5].
• Hence, despite the fact that NA ingestion decreased FFA availability, it promoted the induction of PPARalpha/delta and PGC1alpha gene expression to a similar degree as prolonged exercise [5].
• The HDL/LDL ratio was higher on NA than clofibrate (0.47 +/- 0.19 vs. 0.38 +/- 0.09, P less than 0.05) [6].

Biological context of nicotinic acid

• These studies suggest that the induction of insulin resistance with NA is associated with changes in the fatty acid composition of PC in man [7].
• Data on other pharmacological properties of beta-PC and/or NA that might contribute to antihyperlipidemic efficacy (e.g., fibrinolysis, inhibition of platelet aggregation, erythrocyte membrane changes) were also included where available [8].
• NA causes vasodilation via the activation of phospholipase A2 (PLA2) leading to the release of free fatty acids from membrane phospholipids and the subsequent production of prostaglandins [9].

Anatomical context of nicotinic acid

• Results Vastus lateralis IMCL was significantly elevated in LC (13.3 +/- 1.1 x 10(-3)) and LC + NA (13.5 +/- 1.1 x 10(-3)) (P < 0.01 for both), but was not different between conditions (P > 0.05) [10].
• To evaluate the hypothesis that NA, LVP and adrenaline release PA from the endothelial cells of the vessel wall through their common effect on vascular motility, PA has been characterized by means of a histochemical technique on vein biopsies obtained from human volunteers after infusion of the compounds [11].
• In vitro control studies revealed that NA did not have a direct effect on skeletal muscle LPL activity [12].
• The excretion of 14C after SN in the urine is about half of that after NA whereas excretion in the feces is several times greater [13].

Associations of nicotinic acid with other chemical compounds

• ABBOTT-81988 (A-81988), 2-(N-propyl-N[(2'-[1H-tetrazol-5-yl]biphenyl- 4yl)methyl] amino) pyridine-3-carboxylic acid, a nonpeptide angiotensin II (AII) antagonist was studied in the conscious spontaneously hypertensive rate (SHR) (male, 18 to 21 weeks) for cardiovascular effects of oral administration [14].
• Adsorption of aromatic organic acids: benzoic acid (BA), salicylic acid (SA), p-aminobenzoic acid (pABA) and nicotinic acid (NA), onto high area activated carbon cloth from solutions in 0.4 M H(2)SO(4), in water at natural pH, in 0.1 M NaOH and also from solutions having pH 7.0 were studied by in situ UV-spectroscopic technique [15].

Gene context of nicotinic acid

• To assess the effect of lipolytic suppression on the exercise-induced IL-6 response, seven active, but not specifically trained, men performed two experimental exercise trials with (NA) or without [control (Con)] NA ingestion 60 min before (10 mg/kg body mass) and throughout (5 mg/kg body mass every 30 min) exercise [16].
• However, even in these subjects, HSL activity was not further increased during the NA trial [17].

Analytical, diagnostic and therapeutic context of nicotinic acid

• The extent of the hyperbilirubinemic response to NA load, and of the NA half-life, together with physical examination over a one-year period were in good agreement with the diagnosis of Gilbert's syndrome in the patient's father and siblings [18].

References