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At least 973 records · Page 54Linked to original sources
PubMed2002

Cyclic ADP-ribose (cADPR) and nicotinic acid adenine dinucleotide phosphate (NAADP): novel regulators of Ca2+-signaling and cell function.

Ca2+ ions are involved in the regulation of many diverse functions in animal and plant cells, e.g. muscle contraction, secretion of neurotransmitters, hormones and enzymes, fertilization of oocytes, and lymphocyte activation and proliferation. The intracellular Ca2+ concentration can be increased by different molecular mechanisms, such as Ca2+ influx from the extracellular space or Ca2+ release from intracellular Ca2+ stores. Release from intracellular Ca2+ stores is accomplished by the small molecular compounds D-myo-inositol 1,4,5-trisphosphate (InsP3), cyclic ADP-ribose (cADPR) and nicotinic acid adenine dinucleotide phosphate (NAADP). This review concentrates on (i) receptor-mediated formation of cADPR by ADP-ribosyl cyclases, (ii) intracellular and extracellular effects of cADPR in a variety of cell types, and (iii) cADPR in the nucleus. Though our understanding of the role of NAADP is still unclear in many aspects, important recent findings are reviewed, e.g. Ca2+ release activity and binding studies in mammalian cell types.

Animals↗
PubMed1988

Integrated metabolic control of food intake after 2-deoxy-D-glucose and nicotinic acid injection.

We measured the minute-to-minute respiratory quotient (RQ), total metabolic rate, and the intensity and energy cost of locomotor activity in unrestrained rats with a recently developed open-circuit metabolic device. These measures permitted calculation of the resting metabolic rate (designated métabolisme de fond or MF). Simultaneous monitoring of the meal patterns of the animals allowed correlations between MF and feeding behavior. The major hypotheses proposed to account for the onset of feeding were challenged by pharmacological inhibition of the utilization of glucose and/or lipids. When injected together, 2-deoxy-D-glucose, which blocks glucose utilization, and nicotinic acid, which blocks lipid utilization, had a synergistic effect on MF and on the feeding response. The RQ, which reflects the relative rate of glucose-to-lipid utilization, showed that neither the inhibition of utilization of glucose nor the inhibition of utilization of lipids could account for the magnitude of the feeding response. The signal that best accounted for these examples of experimentally induced feeding is ischymetric (power or rate of energy) in nature rather than solely glucostatic or solely lipostatic.

Animals↗
PubMed1986

Inhibition of esophageal carcinogenesis in corn-fed rats by riboflavin, nicotinic acid, selenium, molybdenum, zinc, and magnesium.

The effect of individual vitamins and minerals on esophageal carcinogenesis was assessed by supplementing a diet (based on corn) that was marginally deficient in many micronutrients. The test diets were fed to weanling inbred BD IX rats for 45 days; they were then given five subcutaneous doses (3 mg/kg body wt) N-nitrosomethylbenzylamine (MBN) over two and one-half weeks. The diets were continued until termination: 150 days later; at that time all rats were still clinically normal. Marked reductions in the number of tumors and tumor-bearing rats were recorded in groups of rats given supplements of riboflavin, nicotinic acid, zinc, magnesium, selenium, and molybdenum. Various combinations of nutrients did not distinctly reduce the tumor yield further; however, tissue analyses suggest that individual supplements could enhance the status of other marginally deficient nutrients. When the experiment was repeated, but was varied by commencing the supplements only well after the cessation of MBN exposure, inhibitory effects on tumorigenesis were still exerted by most nutrients. We emphasized that these nutritional effects along with the epidemiological evidence in humans are relevant to early prevention; also, the treatment of premalignant esophageal changes by high doses of these nutrients may be unwise. The merits of food supplementation schemes are discussed.

Animals↗
PubMed1987

Unconjugated hyperbilirubinaemia in HBV carriers. Discriminant value of nicotinic acid (NA) test.

Recently an unconjugated hyperbilirubinaemia, without any other abnormalities in liver function test, in 14.3% of HBV Japanese carriers has been noticed. Therefore, it would be possible to argue that the persistent infection of HBV in hepatocytes might play a role in an hypothetical metabolic derangement of bilirubin clearance. Twenty-five subjects in a group of 468 HBsAg+ patients (equal to 5.33%) presented an hyperbilirubinaemia. This percentage was not different from the 5.83% found in 3083 HBsAg- controls coming from the same institution. Therefore we could exclude that in our population the presence of HBV surface antigen itself would determine a statistically higher level of total bilirubin (TB) than in controls. The nicotinic acid (NA) loading test may reveal some bilirubin metabolic defects (i.e. Gilbert syndrome), even in subjects with normal basal values of TB. According to this background, we performed in 11 HBsAg+ males with basal TB higher than 17.1 mumol/l (1 mg%) (group A/1), 13 HBsAg+ males with basal TB lower or equal to 17.1 mumol/l (group A/2) and 14 HBsAg- normal controls matched for sex and age (group B) the NA test according to Röllinghoff et al. All the parameters calculated by the NA test resulted significantly different in the A/1 group compared with the B group, but not different from those found by several authors in the Gilbert's syndrome. On the contrary, no significant differences have been noticed between the latter group and the A/2 group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1982

[Positive diagnosis of Gilbert syndrome. Retrospective analysis of 59 cases with special reference to the nicotinic acid test].

The results of a retrospective analysis of 59 patients with Gilbert's syndrome are presented. All the patients were selected on the basis of repeatedly documented, predominantly unconjugated hyperbilirubinemia in the absence of liver or hemolytic disease. The peak incidence of Gilbert's syndrome was in the 15-30 years age group with males predominating almost fivefold. Scleral icterus or a laboratory finding of hyperbilirubinemia represented the major reasons for workup. Presenting symptoms such as fatigue, upper abdominal pain and fat intolerance were largely nonspecific. Whereas minimal values for total serum bilirubin concentrations were, at l.57 +/- 0.56 mg/dl (mean +/- S.D.), often within the normal range (less than 1.2), maximal values were always clearly elevated (2.05 +/- 0.65). The sex difference in bilirubin levels was also maintained in the Gilbert's syndrome, since mean values in women were lower than in men. As expected, neither liver scan nor histology yielded evidence of structural abnormalities. The results of liver function studies such as galactose elimination capacity, aminopyrine breath test, or fasting and postprandial serum bile acids, were all within normal limits. In contrast, the initial plasma disappearance of bromsulphthalein (BSP-k1) was reduced in 6 patients to a mean of 8.7% per min (normal value 12.6 +/- 1.6), which suggests that these subjects belong to the Gilbert type with diminished hepatic clearance of anionic dyes. The hematological investigations, including hemoglobin electrophoresis, Coombs tests and erythrocyte enzymes, yielded normal results. However, osmotic fragility was increased in 5 cases and erythrocyte survival reduced to less than 24 days in 9 cases (of 17 investigated). In 35 patients, a nicotinic acid test was performed in which total serum bilirubin rose within 3 hours from a mean of 1.66 +/- 0.7 to 3.51 +/- 0.75 mg/dl. Between the third and fifth hour bilirubin levels plateaued, yielding retention values of 98%, 92% and 92% respectively. These retention values may be considered in indirect estimate of bilirubin clearance. Retentions exceeding 70% after 5 hours correspond to bilirubin clearances of less than 20 ml/min, representing evidence in favour of the diagnosis of Gilbert's syndrome.

Acetylation↗