烟酸缺乏症的临床及研究现状

烟酸缺乏症是由烟酸缺乏引起的。组临床症候群，与营养不良、酗酒、药物、感染及肿瘤等多种因素有关。町累及皮肤、胃肠道及脑。典型临床表现为皮疹、腹泻和痴呆，但人部分患者只表现其中一种或两种，且临床表现多样。早期症状轻微，可能只出现非特异症状，容易漏诊和误诊。     

A comparison of the nutrient content of uncooked and cooked lean from New Zealand beef and lamb

The composition in terms of proximate analysis, cholesterol, vitamins, minerals, and fatty acids of the lean tissue of 17 beef cuts and 18 lamb cuts was determined on within-cut composite samples (each containing lean tissue from at least 7 animals), following the knife-separation of raw and cooked cuts into lean, fat, and bone. Composite lean samples for 4 beef cuts and 4 lamb cuts were also analysed for amino-acid composition. For analysis, different cuts were the experimental unit as individual animal data were not available. The composition of lean from beef and lamb was shown to be highly desirable with a high nutrient density (mg/kJ) for many nutrients. Although lean from beef and lamb were very similar in many respects, several significant differences were detected. Changes in composition with cooking were largely eliminated when considered on a dry-matter basis, but proportions of the n-3 and n-6 polyunsaturated fatty acids increased with cooking (P < 0.05). The amino acid composition was similar for lean from beef and lamb but showed small deviations from recommended patterns for human nutrition with branched chain amino acids being limiting.     

A case for immediate-release niacin

Niacin is currently a favored drug for increasing high-density lipoprotein, especially in patients with ischemic heart disease or at high risk of developing it. In addition, niacin further decreases low-density lipoprotein in statin-treated patients and has been shown to reduce morbidity and mortality. Among the available niacin preparations, crystalline, immediate-release niacin is the most effective for increasing high-density lipoprotein and is relatively free of hepatic toxicity. We present the case of a patient who had an excellent clinical and laboratory response to 3 g daily of immediate-release niacin, but who later developed clinical hepatitis when he inadvertently switched to the same dose of slow-release niacin. We encourage the use of niacin in general, immediate-release niacin in particular, and caution that niacin is a drug and not a dietary supplement. We also present practical steps for starting niacin, including close patient contact and support, and beginning with a therapeutic dose of 2 g per day right from the start.     

Nicotinic Acid Supplementation in the Context of Alcoholic Liver Injury: Friend or Foe?

Li and colleagues (2014) in this issue report that dietary nicotinic acid (NA) supplementation ameliorates ethanol‐induced hepatic steatosis, but a deficiency does not worsen injury induced by alcohol alone. The authors further present some mechanistic insights into the protective role of NA supplementation. Results of this and other previous studies in the context of alcoholic liver injury raise one important question as to what should be an adequate dose of NA that will provide the maximum benefit to hepatic and extrahepatic tissues and with minimum adverse effects.     

The effects of prednisolone and niacin on chloroquine-induced pruritus in malaria

Summary Chloroquine chemotherapy of malaria fever induces severe generalised pruritus in a large proportion of black Africans. In a double blind, placebo controlled, randomised, parallel group study in 28 historically chloroquine pruritus-reactor (R⁺) patients, with malaria, we evaluated the prophylactic and the palliative antipruritic actions of prednisolone (5 mg) or niacin (50 mg).There was a significant prophylactic effect of both drugs on the pruritogenecity of chloroquine as well as significant reduction in the area under the pruritus intensity-time curve, AUC(0–72 h) by niacin.The salutary effect both of niacin and prednisolone on chloroquine pruritogenecity resulted neither, in the mitigation of malaria parasite clearance, nor in the clinical amelioration following antimalaria therapy.     

Two complex genotypes relevant to the kynurenine pathway and melanotropin function show association with schizophrenia and bipolar disorder

Prior studies of mRNA expression, protein expression, and pathway metabolite levels have implicated dysregulation of the kynurenine pathway in the etiology of schizophrenia and bipolar disorder. Here we investigate whether genes involved in kynurenine pathway regulation might interact with genes that respond to kynurenine metabolites, to enhance risk for these psychiatric phenotypes. Candidate genes were selected from prior studies of genetic association, gene expression profiling and animal models. A single nucleotide polymorphism (SNP) in each of six genes, TDO2, HM74, HM74A, MCHR1, MCHR2 and MC5R, was tested for association with phenotype (475 Caucasians, 88 African Americans with schizophrenia; 97 Caucasians, 3 African Americans with bipolar disorder; 191 Caucasian, 49 African American controls). An A allele in HM74 was significantly associated with schizophrenia and with schizophrenia plus bipolar disorder combined, odds ratios (OR) of 1.48, p = 0.011 and 1.50, p = 0.007, respectively. Augmentation of disease risk was found for the complex genotype HM74[A,any] + MCHR1[T,any] + MCHR2[C,any] which conferred an OR maximal for the combined diagnostic category of schizophrenia plus bipolar disorder (1.70, p = 0.003), carried by 30% of the cases. TDO2[CC] + MC5R[G, any] + MCHR2[GC] conferred an OR maximal for schizophrenia alone (4.84, p = 0.005), carried by 8% of schizophrenia cases. The combined risk posed by these related, complex genotypes is greater than any identified single locus and may derive from co-regulation of the kynurenine pathway by interacting genes, a lack of adequate melanotropin-controlled sequestration of the kynurenine-derived pigments, or the production of melanotropin receptor ligands through kynurenine metabolism.     

The effects of dietary niacin and riboflavin on voluntary intake and metabolism of ethanol in rats.

The effects of dietary deficiency and excess of niacin and riboflavin on voluntary drinking of 10% (v/v) ethanol were studied in male rats. The effectiveness of dietary deficiency and excess of both niacin and riboflavin on tissue levels of these vitamins was demonstrated by measurements of urinary N1-methylnicotinamide and blood glutathione reductase (EC 1.6.4.2) activity. A high-niacin diet containing 75 mg niacin/kg food decreased ethanol intake by about 36% compared to the control diet containing 15 mgniacin/kg. Niacin or riboflavin deficiency and a high-riboflavin diet containing 40 mg rtary levels of niacin or riboflavin did not influence on ethanol elimination rate or levels of blood acetaldehyde during ethanol oxidation. Therefore, blood acetaldehyde was not responsible for the decreased ethanol intake of rats fed with a high-niacin diet. It was concluded that the increased ethanol intake caused by dietary deprivation of B-vitamin complex found in earlier studies is not a result of deficiency of niacin or riboflavin but niacin may be involved in the decrease in ethanol drinking, which follows dietary B-vitamin complex supplementation.