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Titolo:
The metabolism of nicotinamide in human liver cirrhosis: A study on N-methylnicotinamide and 2-pyridone-5-carboxamide production
Autore:
Pumpo, R; Sarnelli, G; Spinella, A; Budillon, G; Cuomo, R;
Indirizzi:
Univ Naples Federico II, Dipartimento Med Clin & Sperimentale, I-80131 Naples, Italy Univ Naples Federico II Naples Italy I-80131 tale, I-80131 Naples, Italy Univ Salerno, Fac Sci, Dipartimento Chim, I-84100 Salerno, Italy Univ Salerno Salerno Italy I-84100 rtimento Chim, I-84100 Salerno, Italy
Titolo Testata:
AMERICAN JOURNAL OF GASTROENTEROLOGY
fascicolo: 4, volume: 96, anno: 2001,
pagine: 1183 - 1187
SICI:
0002-9270(200104)96:4<1183:TMONIH>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
RAT-LIVER; METHYLATION; N1-METHYLNICOTINAMIDE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
23
Recensione:
Indirizzi per estratti:
Indirizzo: Cuomo, R Univ Naples Federico II, Dipartimento Med Clin & Sperimentale, Via Sergio Pansini 5, I-80131 Naples, Italy Univ Naples Federico II Via Sergio Pansini 5 Naples Italy I-80131
Citazione:
R. Pumpo et al., "The metabolism of nicotinamide in human liver cirrhosis: A study on N-methylnicotinamide and 2-pyridone-5-carboxamide production", AM J GASTRO, 96(4), 2001, pp. 1183-1187

Abstract

OBJECTIVES: Nicotinamide methylation followed by urinary excretion of N-methylnicotinamide increases in cirrhotic patients, despite the derangement of the overall methylation processes in liver disease. The rise in N-methylnicotinamide could depend, at least in part, on a reduced transformation of this molecule into 2-pyridone-5-carboxamide. The aim of this study was to investigate this hypothesis. METHODS: Serum and urinary levels (mean +/- SEM) of N-methylnicotinamide and urinary excretion of 2-pyridone-5-carboxamide were measured in 10 healthy controls and 10 patients with liver cirrhosis in basal conditions and after a nicotinamide oral load (1.5 mg/kg body weight). RESULTS: N-methylnicotinamide serum levels increased significantly (p < 0.01) in cirrhotic patients compared to controls, both as basal values (0.43 /- 0.07 nmol/ml; 0.15 +/- 0.01) and as area under the curve 5 h after a nicotinamide load (cirrhotics: 562.4 +/- 50.5 nmol/ml . min; controls: 314.4 /- 23.8). Twenty-four-hour urinary excretion of N-methylnicotinamide and 2-pyridone-5-carboxamide was also significantly (p < 0.05) increased in cirrhotic patients versus controls, both in basal conditions (N-methylnicotinamide: 82.0 +/- 8.4 mu mol, 48.8 +/- 4.8; 2-pyridone-5-carboxamide: 129.3 +/-23.0, 64.6 +/- 9.8) and after a nicotinamide oral load (N-methylnicotinamide: 290.1 +/- 23.1, 180.8 +/- 7.4, 2-pyridone-5-carboxamide : 694.7 +/- 32.5, 391.0 +/- 21.9). Moreover, 24 h N-methylnicotinamide/2-pyridone-5-carboxamide ratio was similar in patients and controls (basal: 0.78 +/- 0.39, 0.90 +/- 0.51; load: 0.42 +/- 0.11, 0.48 +/- 0.16). CONCLUSIONS: In cirrhotic patients nicotinamide methylation is increased, as shown by the rise in urinary N-methylnicotinamide and 2-pyridone-5-carboxamide that is concurrent and proportional (constant 24-h metabolite ratio). The hyperfunction of this methylating pathway might play a protective role against the toxic effect of intracellular accumulation of nicotinamide deriving from the catabolic state of cirrhosis. (Am J Gastroenterol 2001;96:1183-1187. (C) 2001 by Am. Coll. of Gastroenterology).

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Documento generato il 14/07/20 alle ore 10:18:52