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PubMed2006

The nicotinic acid receptor GPR109A (HM74A or PUMA-G) as a new therapeutic target.

Relatively high doses of nicotinic acid induce a profound change in the lipid and lipoprotein profile. In particular, the ability of nicotinic acid to decrease low-density lipoprotein cholesterol levels while increasing high-density lipoprotein cholesterol levels has led to its use as an antidyslipidemic drug. The mechanisms underlying the pharmacological effects of nicotinic acid have been unclear for decades. The recent discovery of a nicotinic acid receptor that is a G-protein-coupled receptor has led to a renewed interest in the pharmacological effects of nicotinic acid. This review summarizes recent progress in understanding the physiological and pharmacological role of the nicotinic acid receptor and discusses its potential use as a new target for the development of antidyslipidemic drugs to prevent and treat cardiovascular diseases.

Animals↗
PubMed1993

The effect of nicotinic acid and acipimox on lipoprotein(a) concentration and turnover.

This study examines the effect of nicotinic acid (1 g t.d.s.) on serum Lp(a) concentration in a group of patients with type II hyperlipidaemia selected on the basis of a plasma Lp(a) concentration greater than 30 mg/dl. Reductions in total cholesterol, triglyceride, LDL-cholesterol and Lp(a) were 16.3%, 25.5%, 23.7% and 36.4%, respectively, with an increase in HDL cholesterol of 37.3%. The reduction in Lp(a) concentration did not correlate with any other lipoprotein changes. In order to establish the mechanism of the fall in Lp(a) concentration, in vivo turnover of autologous Lp(a) was studied in three subjects before and whilst taking nicotinic acid. The fractional catabolic rate in Lp(a) was unaltered in the subjects on therapy, indicating that nicotinic acid did not increase catabolism of Lp(a) but decreased the synthetic rate. Since nicotinic acid was poorly tolerated we examined the effect of acipimox, an analogue of nicotinic acid on lipoproteins using a placebo controlled double-blind crossover design in a group of hyperlipidaemic patients again selected with plasma Lp(a) concentration greater than 30 mg/dl. Acipimox was better tolerated than nicotinic acid but the percentage changes in lipoprotein concentrations were smaller.

Adult↗
PubMed1983

Metabolism of the nicotinic acid moiety of d,l-alpha-tocopheryl nicotinate.

The metabolism of the nicotinic acid (NA) moiety of d,l-alpha-tocopheryl nicotinate (TN) was investigated using radiolabeled TN, with the labeled moiety of the molecule being either NA or tocopherol, and labeled NA. After a single orally administered dose of TN to normal rats, the level of this radiolabeled compound increased gradually in the blood. After the oral administration of NA, the level increased and decreased rapidly initially before coming to a stable level of elevation. Urinary metabolites from rats administered TN were compared with those from rats administered NA. In the case of NA administration, the main metabolites in the urine were nicotinuric acid and NA, while NA was the main metabolite in the urine from rats given TN. These results indicate that the metabolism of the NA moiety of TN differs from that of free NA. The tocopherol moiety of TN was taken up by red blood cell membranes and the NA moiety was distributed among red blood cell contents. The main metabolite in both red blood cell contents and liver after a single orally administered dose of TN was nicotine amide. To determine the metabolism and distribution of TN incorporated into the cellular organelles of the liver, TN was injected intravenously to normal rats and the livers subjected to cell fractionation. TN was distributed in nuclear, mitochondrial, lysosomal, microsomal and supernatant fractions in unchanged form. Several metabolites of TN were detected as minor components in these organelles as well.

Animals↗
PubMed1988

Effect of chronic dietary treatment with nicotinic acid on the development and maintenance of deoxycorticosterone-acetate-salt-induced hypertension.

Chronic dietary administration of either l-tryptophan (5.0%) or nicotinic acid (5.0%) reduced the elevated blood pressure of rats with established, deoxycorticosterone-acetate (DOCA)-salt-induced hypertension without affecting either body weight or cardiac hypertrophy. In a second study, chronic dietary administration of nicotinic acid (2.5 and 5.0%) provided significant protection against the development of an elevated blood pressure in rats treated with DOCA salt. A modest (approximately 10%) reduction in cardiac hypertrophy was also observed in the two nicotinic-acid-treated groups. Treatment with either dose of nicotinic acid did not, however, prevent either the renal hypertrophy characteristic of DOCA-salt-induced hypertension in rats or their reduced renal concentrating ability during a 24-hour dehydration; nor did treatment with nicotinic acid reduce the excessive ingestion of saline characteristic of chronic treatment with DOCA. In contrast, treatment with the higher dose of nicotinic acid prevented the excessive loss of sodium into urine characteristic of DOCA-salt-induced hypertension when the rats were loaded (3% of body weight, i.p.) with a hypotonic (0.075 M) saline solution. These results suggest that increased production of nicotinic acid resulting from dietary administration of tryptophan may play a role in the protective effect of tryptophan against the development of DOCA-salt-induced hypertension. These studies do not, however, provide a mechanism by which nicotinic acid may manifest its beneficial effects.

Animals↗
PubMed1996

Effects of dietary fat with or without nicotinic acid on nutrient flow to the duodenum of dairy cows.

Four Holstein cows, fitted with ruminal and duodenal cannulas, were utilized in a 4 x 4 Latin square design to investigate the effects of supplementing nicotinic acid to diets that contained 35% alfalfa haylage, 15% corn silage, and either 50% of a low fat concentrate or 10% whole raw soybeans and 40% of a high fat concentrate containing tallow. Treatments in a 2 x 2 arrangement were 1) low fat, no supplemental nicotinic acid; 2) low fat, 12 g/d of nicotinic acid; 3) high fat, no supplemental nicotinic acid; and 4) high fat, 12 g/d of nicotinic acid. The DMI and OM apparently and truly digested in the rumen and apparently digested postruminally were not different among treatments. Addition of fat to the diet decreased the concentration of total VFA in ruminal fluid but did not alter the molar proportions of any of the VFA; supplementation of nicotinic acid tended to decrease the molar proportion of acetate. Amounts of NAN, microbial N, nonammonia nonmicrobial N, and AA that flowed to the duodenum were similar among diets. The concentration of urea N in plasma decreased, and concentrations of cholesterol and triglycerides increased, when cows were fed supplemental fat. Milk composition and production of milk, 4% FCM, and milk components were not altered by addition of fat or nicotinic acid to the diet. Supplementation of fat or nicotinic acid to diets of dairy cows was not beneficial in this experiment.

Animal Nutritional Physiological Phenomena↗
PubMed2000

Transcriptional regulation of the Saccharomyces cerevisiae DAL5 gene family and identification of the high affinity nicotinic acid permease TNA1 (YGR260w).

We have studied the transcript levels of YGR260w and YLR004c, two genes encoding members of the yeast Dal5p subfamily of the major facilitator family, and we show that they increase when extracellular nicotinic acid and thiamine, respectively, are absent. The deletion of YGR260w in a bna1 auxotrophic mutant for nicotinic acid prevents growth at low nicotinic acid concentration. This suggests that YGR260w is necessary for nicotinic acid import into the cell. The direct measurement of nicotinic acid uptake on whole cells demonstrates that YGR260w encodes the yeast high affinity nicotinic acid permease. Its apparent K(m) of 1.7 microM is low enough to allow the uptake of the low concentrations of nicotinic acid normally secreted by wild type cells.

Base Sequence↗
PubMed1998

Supplemental fat and nicotinic acid for Holstein cows during an entire lactation.

The objectives of this experiment were to determine long-term responses to supplemental fat (from whole soybeans and liquid animal fat) and to determine whether the supplementation of nicotinic acid would enhance milk protein content or yield. From wk 4 through 43 postpartum, 44 multiparous Holstein cows (10 to 12 per treatment) were assigned to one of four dietary treatments: 1) control, 2) control plus 12 g/d of nicotinic acid, 3) supplemental fat, and 4) supplemental fat plus 12 g/d of nicotinic acid. The dry matter intake of cows did not differ among dietary treatments. Yields of milk, solids-corrected milk, and 3.5% fat-corrected milk were increased by nicotinic acid; the yield of fat-corrected milk during wk 4 to 25 was increased by supplemental fat. Contents of crude protein (CP) and true protein in milk were less for cows fed diets supplemented with fat or nicotinic acid; casein content was decreased by nicotinic acid. Intake of net energy for lactation was greater for cows fed supplemental fat; energy balance was greater during wk 4 to 25 for cows fed diets supplemented with fat. Body condition score and body weight were less when nicotinic acid was added to the control diet than when it was added to the diet supplemented with fat. Supplemental fat increased the concentration of nonesterified fatty acids (NEFA) in plasma; nicotinic acid increased NEFA when it was added to the control diet but decreased NEFA when it was added to the diet supplemented with fat. Nicotinic acid did not prevent the decrease in milk CP content that was induced by dietary fat, but it did increase milk yield and tended to increase the yield of milk CP.

3-Hydroxybutyric Acid↗
PubMed1988

Nicotinic acid: a review of its clinical use in the treatment of lipid disorders.

Nicotinic acid (niacin) is a water-soluble vitamin widely used for the treatment of lipid disorders. In pharmacologic doses (1 g or more/day), alone or in combination with other lipid-lowering drugs, nicotinic acid lowers very low-density (VLDL) and low-density lipoprotein (LDL) levels, while concurrently increasing high-density lipoprotein (HDL) levels. It may reduce long-term mortality in patients with known coronary artery disease and may slow or reverse the progression of atherosclerosis. A major consideration against using nicotinic acid is the occurrence of frequent, bothersome, adverse reactions such as cutaneous flushing, skin rash, and gastric upset. Careful dosing titration may, however, minimize these effects. The beneficial effects, taken together with the low cost of nicotinic acid therapy and the relative freedom from serious side effects, have made nicotinic acid the agent of choice for the treatment of many patients with hyperlipidemia.

Humans↗
PubMed2005

(D)-beta-Hydroxybutyrate inhibits adipocyte lipolysis via the nicotinic acid receptor PUMA-G.

As a treatment for dyslipidemia, oral doses of 1-3 grams of nicotinic acid per day lower serum triglycerides, raise high density lipoprotein cholesterol, and reduce mortality from coronary heart disease (Tavintharan, S., and Kashyap, M. L. (2001) Curr. Atheroscler. Rep. 3, 74-82). These benefits likely result from the ability of nicotinic acid to inhibit lipolysis in adipocytes and thereby reduce serum non-esterified fatty acid levels (Carlson, L. A. (1963) Acta Med. Scand. 173, 719-722). In mice, nicotinic acid inhibits lipolysis via PUMA-G, a Gi/o-coupled seven-transmembrane receptor expressed in adipocytes and activated macrophages (Tunaru, S., Kero, J., Schaub, A., Wufka, C., Blaukat, A., Pfeffer, K., and Offermanns, S. (2003) Nat. Med. 9, 352-355). The human ortholog HM74a is also a nicotinic acid receptor and likely has a similar role in anti-lipolysis. Endogenous levels of nicotinic acid are too low to significantly impact receptor activity, hence the natural ligands(s) of HM74a/PUMA-G remain to be elucidated. Here we show that the fatty acid-derived ketone body (D)-beta-hydroxybutyrate ((D)-beta-OHB) specifically activates PUMA-G/HM74a at concentrations observed in serum during fasting. Like nicotinic acid, (D)-beta-OHB inhibits mouse adipocyte lipolysis in a PUMA-G-dependent manner and is thus the first endogenous ligand described for this orphan receptor. These findings suggests a homeostatic mechanism for surviving starvation in which (D)-beta-OHB negatively regulates its own production, thereby preventing ketoacidosis and promoting efficient use of fat stores.

3-Hydroxybutyric Acid↗
PubMed1979

Dissociation of the effects of nicotinic acid on vasodilatation and lipolysis by a prostaglandin synthesis inhibitor, indomethacin, in man.

The effects of nicotinic acid on plasma free fatty acid (FFA) concentration and forearm blood flow were studied in seven healthy fasting volunteers with and without pretreatment by indomethacin to see if some effects of nicotinic acid are mediated by release of endogenous prostaglandin. 1 g of nicotinic acid per os decreased plasma FFA concentration to a lowest value of 1/4 of initial level and increased forearm blood flow four times. When the same dose of nicotinic acid was given after pretreatment with indomethacin, the blood flow increase was only 1/3 of that without indomethacin. Indomethacin did not alter the rapid initial decrease in plasma FFA, although the period of low FFA concentration was shortened and the rebound to supranormal concentration was abolished. Thus the vasodilatory effect of nicotinic acid seems to be mediated by release of endogenous prostaglandin while the inhibition of lipolysis by the drug is mainly produced by other mechanisms.

Adult↗
PubMed1999

Nicotinic acid and pyridoxine modulate arachidonic acid metabolism in vitro and ex vivo in man.

The in vitro effects of nicotinic acid (10-1000 microM), pyridoxine (0.1-500 microM) and pyridoxal-5'-phosphate (0.1-500 microM) and the ex vivo effects of nicotinic acid (2500 mg orally during 12 h) and pyridoxine (600 mg orally daily for seven days) on arachidonic acid metabolism were investigated in calcium ionophore A23187 (calcimycin)-stimulated human whole blood. In vitro nicotinic acid stimulated prostaglandin E2, thromboxane B2 and leukotriene E4 synthesis. Pyridoxine at all concentrations and pyridoxal-5'-phosphate at the highest concentration stimulated prostaglandin E2 and thromboxane B2 production, but had no effect on leukotriene E4 synthesis. Nicotinic acid treatment increased ex vivo prostaglandin E2, thromboxane B2 and leukotriene E4 synthesis to 185%, 165% and 175% of the initial values, respectively. In the pyridoxine-treated subjects, ex vivo prostaglandin E2, thromboxane B2 and leukotriene E4 synthesis was decreased after seven days to 75%, 65% and 45% of the initial values, respectively. In the present study the effects of nicotinic acid on the 5-lipoxygenase pathway in arachidonic acid metabolism were studied for the first time and the drug was found to stimulate this pathway in vitro and ex vivo. In vitro pyridoxine and pyridoxal-5'-phosphate had no effect on the 5-lipoxygenase pathway. The inhibition of leukotriene synthesis by pyridoxine ex vivo might be of therapeutic importance.

Adult↗
PubMed1995

The prevalence of side effects with regular and sustained-release nicotinic acid.

PURPOSE: To document the prevalence and nature of the side effects that occur with the use of regular and sustained-release nicotinic acid in everyday clinical practice. PATIENTS AND METHODS: One hundred and ten patients seen in a private medical clinic who were given 133 separate trials of nicotinic acid during a 5-year period. The occurrence of side effects, particularly those severe enough to warrant discontinuing the drug, were carefully monitored. RESULTS: Forty-three percent of individuals given regular nicotinic acid and 42% of those given sustained-release nicotinic acid were forced to discontinue the medication because of side effects; some of these side effects necessitating discontinuing nicotinic acid did not occur until the patient had been taking the drug for 1 or 2 years. CONCLUSION: Nicotinic acid in both regular and sustained-release forms is a powerful drug when used in doses needed to treat lipid disorders and causes disturbing side effects a very high percentage of the time. No one should use nicotinic acid in these doses without continued careful supervision of a physician.

Adult↗
PubMed2006

Nicotinic acid and other therapies for raising high-density lipoprotein.

PURPOSE OF REVIEW: The purpose of this review is to describe the high-density-lipoprotein-raising effect of nicotinic acid and the clinical effects of treatment on cardiovascular diseases, particularly in combination with statins. Other treatments for raising high-density lipoprotein, including changes in lifestyle, other drugs and infusions of 'synthetic' (reconstituted) high-density lipoprotein will be summarized. RECENT FINDINGS: Treatment of atherosclerotic cardiovascular disease with nicotinic acid and statin results in a pronounced increase of protective high-density lipoprotein cholesterol and reduces morbidity/mortality. Addition of prolonged-release nicotinic acid to ongoing treatment with statin raises high-density lipoprotein cholesterol and induces regression of atherosclerosis that otherwise would progress during statin treatment. Several new high-density lipoprotein-raising drugs in clinical trials are reported. New proposed mechanisms for the broad-spectrum lipid effects of nicotinic acid are described. SUMMARY: Low plasma concentration of high-density lipoprotein is an important risk factor for atherosclerotic cardiovascular disease. Nicotinic acid has the uncomfortable but harmless side effect of flush. Prolonged-release nicotinic acid gives rise to less flush than immediate-release nicotinic acid. Treatment with nicotinic acid and statin targets the two independent lipid risk factors of low high-density lipoprotein and high low-density lipoprotein and has clinical benefits in secondary prevention of atherosclerotic cardiovascular disease.

Atherosclerosis↗
PubMed1998

Kinetic mechanism of nicotinic acid phosphoribosyltransferase: implications for energy coupling.

Nicotinic acid phosphoribosyltransferase (NAPRTase; EC 2.4.2.11) is a facultative ATPase that uses the energy of ATP hydrolysis to drive the synthesis of nicotinate mononucleotide and pyrophosphate from nicotinic acid (NA) and phosphoribosyl pyrophosphate (PRPP). To learn how NAPRTase uses this hydrolytic energy, we have further delineated the kinetic mechanism using steady-state and pre-steady-state kinetics, equilibrium binding, and isotope trapping. NAPRTase undergoes covalent phosphorylation by bound ATP at a rate of 30 s-1. The phosphoenzyme (E-P) binds PRPP with a KD of 0.6 microM, a value 2000-fold lower than that measured for the nonphosphorylated enzyme. The minimal rate constant for PRPP binding to E-P is 0.72 x 10(5) M-1 s-1. Isotope trapping shows that greater than 90% of bound PRPP partitions toward product upon addition of NA. Binding of NA to E-P.PRPP is rapid, kon >/= 7.0 x 10(6) M-1 s-1, and is followed by rapid formation of NAMN and PPi, k >/= 500 s-1. After product formation, E-P undergoes hydrolytic cleavage, k = 6.3 s-1, and products NAMN, PPi, and Pi are released. Quenching from the steady state under Vmax conditions indicates that slightly less than half the enzyme is in phosphorylated forms. To account for this finding, we propose that one step in the release of products is as slow as 5.2 s-1 and, together with the E-P cleavage step, codetermines the overall kcat of 2.3 s-1 at 22 degrees C. Energy coupling by NAPRTase involves two strategies frequently proposed for ATPases of macromolecular recognition and processing. First, E-P has a 10(3)-fold higher affinity for substrates than does nonphosphorylated enzyme, allowing the E-P to bind substrate from low concentration and nonphosphorylated enzyme to expel products against a high concentration. Second, the kinetic pathway follows "rules" [Jencks, W. P. (1989) J. Biol. Chem. 264, 18855-18858] that minimize unproductive alternative reaction pathways. However, an analysis of reaction schemes based on these strategies suggests that such nonvectorial reactions are intrinsically inefficient in ATP use.

Adenosine Triphosphatases↗
PubMedDate not supplied

[Modification of pathologic fatty acid patterns in old age by combined clofibrinic and nicotinic acid treatment].

71 patients (42 men and 29 women, aged between 45 and 76) with primary hyperlipoproteinaemia (HLP) types IIa, IIb and IV, were treated with clofibric acid (Regadrin) and nicotinic acid derivatives (Radecol, Jupol) over a three-year period. Every four months, they underwent gas chromatographic analyses of the fatty acid spectrum (fa) in the fractions of cholesterol ester (Chol.E) and triglyceride (TGL) of the serum. The therapy resulted in an increase in the linoleic, linolenic, arachidonic, and eicosapentaenoic acids, and a fall in the palmitic, palmitoleic, stearic, oleic and eicosatrienic acid levels in the Chol.E fraction in the case of HLP types IIa and IIb, and in the TGL fraction in the case of HLP types IIb and IV. Selective competitive inhibition by unesterified fatty acids, blocked lipolysis, an impaired hepatogenic fatty-acid metabolism, an affected LCAT and an increased esterification of polyunsaturated fatty acids are discussed as possible mechanisms. The increase in polyunsaturated fatty acids and the decrease of saturated and monounsaturated fatty acids must be considered, as they are interrelated with the prostaglandin metabolism, to be a positive and vasoprotective effect which assumes special importance in middle and older age.

Aged↗
PubMed1979

Antagonistic effects of prostaglandin E1 and nicotinic acid on the human fat cell adenylate cyclase.

Both prostaglandin E1 and nicotinic acid markedly reduce 3',5'-cyclic AMP-accumulation and lipolysis in adipose tissue. These effects were assumed to be mediated via inhibition of the fat cell adenylate cyclase. Therefore, the effects of prostaglandin E1 and nicotinic acid on the human fat cell adenylate cyclase were compared. Prostaglandin E1 caused a dose-dependent stimulation of the enzyme, whereas nicotinic acid was found to act as an unspecific inhibitor depressing all expressions of enzyme activity including prostaglandin E1-stimulated rates of 3',5'-cyclic AMP formation. It is concluded that the common metabolic effects of nicotinic acid and prostaglandin E1 are unlikely to be mediated via the membrane-bound adenylate cyclase in human adipose tissue.

Adenylyl Cyclase Inhibitors↗
PubMedDate not supplied

The effect of nicotinic acid on the metabolism of the plasma lipoproteins of rhesus monkeys.

The effect of nicotinic acid was investigated in Rhesus monkeys. Subcutaneous injections of nicotinic acid lower the plasma very low density lipoprotein (VVLDL) and low density lipoprotein (HDL) concentration. The fall in LDL concentration is not accompained by any change in the lipid or protein composition of either lipoprotein. Analysis by Sephadex gel chromatography and polyacrylamide-gel electrophoresis showed that the proteins of monkey VLDL and LDL are qualitatively similar to those of human VLDL and LDL, although there are differences in the proportions of the various proteins present in the two species. Subcutaneous injections of nicotinic acid diminish the maximum incorporation of 14C from [14C]threonine into VLDL and LDL apoproteins, but have no effect on incorporation into albumin or HDL apoprotein. Peak incorporations into the apo-B and apo-C of VLDL are diminished to about equal extents by nicotinic acid. Comparison of the amount of 14C lost from apo-B of VLDL after the peak of incorporation, with that gained by apo-B of LDL during the same period, suggests that some of the circulating apo-B of LDL IS DERIVED FROM SOURCES OTHER THAN CIRCULATING VLDL.

Animals↗
PubMed1996

Effectiveness of low-dose crystalline nicotinic acid in men with low high-density lipoprotein cholesterol levels.

BACKGROUND: Hypoalphalipoproteinemia (low serum concentration of high-density lipoprotein cholesterol [HDL-C]) is a common pattern of dyslipidemia associated with coronary heart disease. High doses of nicotinic acid effectively raise HDL-C levels in this condition, but they are commonly accompanied by side effects. The efficacy of low doses of nicotinic acid that may produce fewer side effects has not been adequately studied. OBJECTIVE: To determine the effects of low-dose nicotinic acid on HDL-C levels in patients with hypoalphalipoproteinemia. METHODS: Forty-four men with low HDL-C levels (< 1.03 mmol/L [< 40 mg/dL]) entered the study. Twenty-four patients otherwise had normal lipid levels, and 20 were moderately hypertriglyceridemic (range of plasma triglyceride levels, 2.82 to 5.64 mmol/L 250 to 500 mg/dL). The trial consisted of 3 phases; each phase lasted 8 weeks. The first phase was diet only (30% fat diet); in the second phase, crystalline nicotinic acid was added at 1.5 g/d; and in the third phase, the dose was increased to 3 g/d. RESULTS: Of the 44 patients who entered the study, 37 completed the low-dose phase (1.5 g/d); the remaining patients were withdrawn because of side effects to nicotinic acid. Four other patients who completed the low-dose phase were excluded from the higher dose phase because of side effects that developed when they were receiving the low dose. Ten other patients withdrew during the high-dose phase because of side effects. In both groups, responses to nicotinic acid therapy tended to be dose-dependent. For both groups, the higher dose generally produced a greater reduction in apolipoprotein B-containing lipoproteins and a greater rise in HDL-C levels. However, for both groups, the low dose of nicotinic acid gave an average 20% increase in HDL-C levels. CONCLUSIONS: A low dose (1.5 g/d) of crystalline nicotinic acid causes an average 20% increase in HDL-C levels and significantly lowers triglyceride levels in both normolipidemic and hyperlipidemic patients with low HDL-C levels. Although the changes induced by this dose are less than those that can be achieved by a higher dose, the lower dose is better tolerated. Nicotinic acid may be useful in combined drug therapy for secondary prevention of coronary heart disease, and if higher doses cannot be tolerated, use of a lower dose should still be useful for producing a moderate rise in HDL-C levels in patients with hypoalphalipoproteinemia.

Crystallization↗