Exogenous niacin treatment increases NADPH oxidase in kiwifruit / O tratamento com niacina exógena NADPH oxidase em kiwis

Abstract Kiwifruit are a popular fruit worldwide; however, plant growth is threatened by abiotic stresses such as drought and high temperatures. Niacin treatment in plants has been shown to increase NADPH levels, thus enhancing abiotic stresses tolerance. Here, we evaluate the effect of niacin solution spray treatment on NADPH levels in the kiwifruit cultivars Hayward and Xuxiang. We found that spray treatment with niacin solution promoted NADPH and NADP+ levels and decreased both O2·- production and H2O2 contents in leaves during a short period. In fruit, NADPH contents increased during early development, but decreased later. However, no effect on NADP+ levels has been observed throughout fruit development. In summary, this report suggests that niacin may be used to increase NADPH oxidases, thus increasing stress-tolerance in kiwifruit during encounter of short-term stressful conditions.

Resumo Kiwis são uma fruta popular em todo o mundo; No entanto, o crescimento das plantas é ameaçado por estresses abióticos como a seca e as altas temperaturas. O tratamento com niacina em plantas mostrou aumentar os níveis de NADPH, aumentando assim a tolerância a stress abiótico. Aqui, avaliamos o efeito do tratamento com spray de solução de niacina sobre os níveis de NADPH nos cultivares de kiwis Hayward e Xuxiang. Descobrimos que o tratamento por spray com solução de niacina promoveu níveis de NADPH e NADP + e diminuiu a produção de O2·- e os teores de H2O2 nas folhas durante um curto período. Nos frutos, os teores de NADPH aumentaram durante o desenvolvimento precoce, mas diminuíram mais tarde. No entanto, não se observou qualquer efeito nos níveis de NADP + ao longo do desenvolvimento do fruto. Em resumo, este relatório sugere que a niacina pode ser utilizada para aumentar NADPH oxidases, aumentando assim a tolerância ao estresse em kiwis durante o encontro de condições estressantes de curto prazo.

El ácido nicotínico aumenta el transporte celular de colesterol de las lipoproteínas de alta densidad en pacientes con hipoalfalipoproteinemia / Nicotinic acid increases cellular transport of high density lipoprotein cholesterol in patients with hypoalphalipoproteinemia

Background: Plasma high density lipoproteins (HDL) are involved in reverse cholesterol transport mediated by the scavenger receptor class B type I (SR-BI). Nicotinic acid increases HDL cholesterol levels, even though its specific impact on SR-BI dependent-cellular cholesterol transport remains unknown. Aim: To determine the effect of nicotinic acid on HDL particle functionality in cholesterol efflux and uptake mediated by SR-BI in cultured cells in hypoalphalipoproteinemic patients. Material and Methods: In a pilot study, eight patients with low HDL (≤ 40 mg/dL) were treated with extended release nicotinic acid. HDL cholesterol and phospholipid levels, HDL2 and HDL3 fractions and HDL particle sizes were measured at baseline and post-therapy. Before and after nicotinic acid treatment, HDL particles were used for cholesterol transport studies in cells transfected with SR-BI. Results: Nicotinic acid treatment raised total HDL cholesterol and phospholipids, HDL2 levels as well as HDL particle size. Nicotinic acid significantly increased HDL cholesterol efflux and uptake capacity mediated by SR-BI in cultured cells. Conclusions: Nicotinic acid therapy increases SR-BI-dependent HDL cholesterol transport in cultured cells, establishing a new cellular mechanism by which this lipid-lowering drug appears to modulate HDL metabolism in patients with hypoalphalipoproteinemia.

Dislipidemias: ¿qué hay de nuevo? / Dyslipidemia: what's new?

En los últimos años han surgido algunas investigaciones y guías de práctica clínica relacionadas con el diagnóstico y tratamiento de las dislipidemias, que aportaron nuevos conocimientos (y controversias) sobre dicha problemática. En este resumen se describen, en primer lugar, las características de las "nuevas guías" norteamericanas para el manejo del colesterol publicadas a fines de 2013 y se comparan con las recomendaciones tradicionales. En segundo lugar, se analizan los últimos estudios que evaluaron el impacto cardiovascular de otros fármacos hipolipemiantes (ezetimibe y ácido nicotínico) en pacientes en prevención secundaria tratados con estatinas. Finalmente, se mencionan las nuevas drogas hipolipemiantes desarrolladas en los últimos años, como el lomitapide, el mipomersen y los inhibidores de la PCSK9, y se comentan el mecanismo de acción, su eficacia, sus efectos colaterales y los escenarios clínicos en donde podrían utilizarse. (AU)

In recent years, some research and clinical practice guidelines related to the diagnosis and treatment of dyslipidemia, which provided new knowledge (and controversy) about this problem have emerged. In this review, the characteristics of the American "new guidelines" for cholesterol management published by the end of 2013 are described, and they are compared with the traditional recommendations. In addition, recent studies assessing the cardiovascular impact of other lipid-lowering drugs (ezetimibe and nicotinic acid) in patients in secondary prevention treated with statins are analyzed. Finally, new hypolipidemic drugs developed in recent years are mentioned (lomitapide, mipomersen and PCSK9 inhibitors), discussing the mechanism of action, efficacy, side effects and clinical settings where they could be used. (AU)

Onychomatricoma: a tumor unknown to dermatologists

A sixty-one year old white female was referred to the Dermatology Department to treat an ingrown nail in the inner corner of the left hallux. Examination of the entire nail unit showed the presence of xanthonychia in the outer corner besides thickening and increase in the transverse curvature of the nail plate. Dermoscopy and nuclear magnetic resonance of the free edge of the nail plate detected characteristic signs of onychomatricoma, a diagnosis that was later confirmed by anatomopathological exam.

Compositional studies and biological activities of some mash bean (Vigna mungo (L) Hepper) cultivars commonly consumed in Pakistan

BACKGROUND: In recent years, the desire to adopt a healthy diet has drawn attention to legume seeds and food products derived from them. Mash bean is an important legume crop used in Pakistan however a systematic mapping of the chemical composition of mash bean seeds is lacking. Therefore seeds of four mash bean (Vigna mungo (L.) Hepper, family Leguminoseae) cultivars (NARC-Mash-1, NARC-Mash-2, NARC-Mash-3, NARC-Mash-97) commonly consumed in Pakistan have been analyzed for their chemical composition, antioxidant potential and biological activities like inhibition of formation of advanced glycation end products (AGE) activity and tyrosinase inhibition activity. RESULTS: The investigated cultivars varied in terms of biochemical composition to various extents. Mineral composition indicated potassium and zinc in highest and lowest amounts respectively, in all cultivars. The amino acid profile in protein of these cultivars suggested cysteine is present in lowest quantity in all cultivars while fatty acid distribution pattern indicated unsaturated fatty acids as major fatty acids in all cultivars. All cultivars were found to be rich source of tocopherols and sterols. Fourier transform infrared spectroscopy (FTIR) fingerprints of seed flour and extracts indicated major functional groups such as polysaccharides, lipids, amides, amines and amino acids. Results indicated that all investigated cultivars possessed appreciable antioxidant potential. CONCLUSIONS: All cultivars are rich source of protein and possess sufficient content of dietary fiber, a balanced amino acid profile, low saturated fatty acids and antioxidant capacity that rationalizes many traditional uses of seeds of this crop besides its nutritional importance. The collected data will be useful for academic and corporate researchers, nutritionists and clinical dieticians as well as consumers. If proper attention is paid, it may become an important export commodity and may fetch considerable foreign exchange for Pakistan.

Valores de referencia de niacina para la población venezolana / Reference values of niacin for the Venezuelan population

La niacina es una vitamina hidrosoluble, conocida también como ácido nicotínico o vitamina B3. La nicotinamida es un derivado de la niacina (amida del ácido nicotínico), y es utilizada por el cuerpo para producir las coenzimas nicotinamida adenina dinucleótido (NAD) y nicotinamida adenina dinucleótido fosfato (NADP). En esta revisión de los requerimientos de niacina para Venezuela, encontramos que los datos nacionales no son suficientes para establecer las recomendaciones de consumo de este nutriente, por lo tanto, al igual que en la revisión del año 2000, las recomendaciones actuales se basan en las definidas para la población de Estados Unidos. Las Ingestas Dietéticas Recomendadas (RDAs) para Venezuela son: menores de 1 año (2-4 mg/día), niños entre 1 y 8 años (6-8 mg/día), niños entre 9 y 13 años (12 mg/día), adolescentes y adultos del sexo femenino (14 mg/día), adolescentes y adultos del sexo masculino (16 mg/día), embarazadas (18 mg/día) y lactancia (17 mg/ día). En cuanto al Requerimiento Promedio Estimado (EAR): 5-9 mg/día para niños, 11 mg/día para adolescentes y adultos del sexo femenino y 12 mg/día para adolescentes y adultos del sexo masculino, aumentado a 14 mg/día para embarazadas y a 13 mg/ día durante la lactancia. Los Niveles de Ingesta Máximos Tolerables (UL) son: niños entre 1 y 3 años (10 mg/día), niños entre 4 y 8 años (15 mg/día), niños entre 9 y 13 años (20 mg/día), adolescentes (30 mg/día) y adultos (35 mg/día). Es necesario realizar estudios donde se evalúe el estado nutricional de esta vitamina en diferentes grupos de la población, que incluya no solo la estimación del consumo, sino la utilización de indicadores bioquímicos, como la medición de los niveles de las coenzimas NAD y NADP en eritrocitos o sangre completa y la determinación de los principales metabolitos urinarios de la vitamina.

Niacin is a water soluble vitamin, also known as nicotinic acid or Vitamin B3. Nicotinamide is a derivative of niacin (amide of nicotinic acid), and is used by the body to produce the coenzyme nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP). In preparing this review about the niacin requirements for Venezuela, it was found that there is not enough national data to establish recommendations, therefore, as in the 2000 review of the Venezuelan Recommended Dietary Allowances (RDAs), the actual recommendations for intake of niacin, are based on those reported for the United States population. The RDAs for Venezuela are: 2-4 mg/day for infants less than 1 year old, 6-8 mg/ day for children between 1 and 8 years, 12 mg/day for children between 9 and 13 years, 14 mg/day for adolescents and female adults, 16 mg/day for adolescents and adult males, 18 mg/day during pregnancy and 17 mg/day during lactation. The estimated average requirement (EAR) is: 6-9 mg/day for children, 11 mg/ day for adolescents and female adults and 12 mg/day for adolescents and adult males, increasing to 14 mg/day during pregnancy and to 13 mg/day during lactation. The niacin Tolerable Upper Intake Levels (UL) are: 10 mg/day for children between 1 and 3 years, 15 mg/day for children between 4 and 8 years, 20 mg/day for children between 9 and 13 years, 30 mg/day for adolescents and 35 mg/day for adults. It is necessary to perform studies where the nutritional status of this vitamin is evaluated for different population groups, including not only the estimation of consumption, but the use of biochemical indicators, such as measuring the levels of the coenzymes NAD and NADP in erythrocytes or whole blood and determination of the major urinary metabolites of the vitamin.

Lipid profiles of rats fed with diets supplemented with vitamins niacin and pyridoxine

Hypercholesterolemia is a major risk factor for cardiovascular disease. Supplements containing the vitamins niacin (B3) and pyridoxine (B6) can promote the reduction of total cholesterol and an increase in HDL cholesterol. In this study, the effects of diets supplemented with niacin (B3) and pyridoxine (B6) on the hepatic and serum lipid profiles of Wistar rats were assessed. The diets were prepared with combinations of three concentrations of niacin (3, 4 and 5 g/kg) and pyridoxine (6, 12 and 18 mg/kg) and one with neither vitamin. The animals were divided into eleven experimental groups of six animals per group, and nine groups were fed on a standard diet with 7.5% fat and vitamin supplementation. Another group was fed with 7.5% fat without vitamin supplements. A control group received the standard diet (AIN-93M) without modifications (4% fat). The weight gain, food intake, serum and hepatic total cholesterol, serum cholesterol fractions (HDL, LDL, and VLDL), serum and hepatic triacylglycerols and hepatic and fecal lipid contents were measured after 30 days. The diet with the highest concentration of niacin and lowest concentration of pyridoxine had the lowest level of total hepatic cholesterol. Hepatic triacylglycerols were reduced by the highest concentration of niacin (5 g/kg), and this reduction was enhanced by increasing the pyridoxine concentration. The diets supplemented with niacin and pyridoxine reduced the levels of serum total cholesterol, LDL, VLDL, triacylglycerols and hepatic lipids. These effects on the lipid profile varied with the concentrations of the two vitamins and the interactions between them.

Caso 6 Mulher, 54 anos, procurou atenção básica em município de Minas Gerais com queixa de lesões descamativas e pruriginosas em área de exposição solar, há cerca de 2 meses / Case 6

Mulher, 54 anos, procurou atenção básica em município de Minas Gerais com queixa de lesões descamativas e pruriginosas em área de exposição solar, há cerca de 2 meses. Essa é a segunda vez que manifesta estes sinais e não sabe precisar há quanto tempo ocorreu o primeiro episódio. Relata que no intervalo entre eles não apresentou qualquer tipo de lesão cutânea. A paciente é alcoolista, tabagista, hipertensa e não faz uso de medicamentos.

Dislipidemias y riesgo cardiovascular: ¿Tiempo para un nuevo enfoque en lípidos? / Dyslipidemias and cardiovascular risk: time for a new appoach to lipid disorders?

La enfermedad coronaria es una entidad con causas múltiples, la primera causa de mortalidad en el mundo actual y, para el año 2025, la primera causa de morbilidad mundial. Dado su origen multicausal, el enfoque debe ser también múltiple; con revisión a todos los factores. Uno de los factores de riesgo, la dislipidemia, tiene varios aspectos que necesitan atención y control, aunque ésta se haya centrado tradicionalmente en el c-LDL, sin prestar mayor cuidado a las otras subfracciones. Los estudios clásicos en lípidos, principalmente con estatinas, han dirigido su atención, al c-LDL y se encuentran estudios en los que hay reducción en c-LDL sin cambios (o con muy pocos) en c-HDL. Aunque hay disminución en el riesgo de eventos y mortalidad, pueden apreciarse riesgos residuales significativos. Un estudio con fibratos tuvo los resultados opuestos, un aumento significativo en el c-HDL sin cambio en el c-LDL, y se observó una reducción interesante en el riesgo, pero con un riesgo similar al observado en los estudios con estatinas. Los estudios con intervenciones múltiples que impactan todas las subfracciones lipídicas, han mostrado cambios significativamente mejores en riesgo. La adición de niacina de liberación extendida al armamentario terapéutico ha permitido, en combinación con estatinas, obtener un mejor control de todas las subfracciones lipídicas, así como reducciones significativas en riesgo y en crecimiento de placa. Los efectos de la niacida de liberación extendida son reducción de c-LDL y triglicéridos, aumento en c-HDL y también reducción en LP(a), así como cambios benéficos en apoA y apoB. Las reacciones adversas, como el enrojecimiento, pueden controlarse y en muchos casos evitarse, y han mostrado ser pasajeras y disminuir hasta desaparecer con el tiempo.

Coronary artery disease is an entity with multiple causes. It is the first cause of mortality in the world, and for the year 2025, will be the first cause of morbidity. Given its multi-causal origin, the approach must also be multiple and all factors should be controlled. Dyslipidemia, one of the main risk factors, has several aspects that need attention and control, although the attention has traditionally been focused on LDL-c, disregarding other lipidic subfractions. Classical lipid studies mainly those with statins, have directed their attention to LDL-c, and there are studies in which there is a LDL-c reduction without little or no change in HDL-C. Even though events and mortality risks decrease, significant residual risks can be appreciated. A study with fibrates had the opposite results, showing significant increase in HDL-c without any change in LDL-c, and an interesting decrease in risk but also with a similar risk to that found in previous studies with statins was observed. Studies with multiple interventions that impact all lipidic sub-fractions have shown better significant changes in risk. Addition of niacin extended release to the pool of drugs in combination witn statins, has allowed to achieve a better control of all the lipidic subfractions as well as significant reductions in risk and plaque growth. The effects of the niacin extended release are reduction of LDL-c and triglycerides, increase in HDL-c and also LP(a) reduction, as well as beneficial changes in ApoA and ApoB. Adverse reactions, such as flushing, can be controlled and in many cases avoided, and have shown to be transient and to decrease and even disappear with time.

Vitamins B1, B2, B6 and PP contents in royal jelly

Hydrosoluble vitamins B1, B2, B6 and PP are essential organic substances for human organism, functioning as coenzymes on several metabolic cycles. In the present investigation four vitamins of B complex and its vitamers contents were determined in royal jelly samples marketed in São Paulo, Brazil. A single extraction process was employed, and each vitamin was determined by HPLC using C18 column and detected by fluorescence. Four samples from different suppliers were analyzed, and the results varied from 0.08 to 0.41 mg/100g (vitamin B1 orthiamine); from 0.01 to 0.05 mg/100g (vitamin B2 or ribofl avin); from 0.13 to 0.38 mg/100g (piridoxal - vitamin B6); from 0.26 to 1.38 mg/100g (piridoxamine - vitamin B6); from 0.21 to 0.57 mg/100g (niacin - vitamin PP);and from 1.56 to 2.00 mg/100g (niacinamide - vitamin PP). These data show that royal jelly is not an important source of the analyzed vitamins, though the results indicate that the employed technique is suitable for determining these four vitamins and its vitamers.

Elevando el colesterol HDL: ¿Cuál es la mejor estrategia?: [revisão] / Raising HDL cholesterol: which is the best strategy?: [review]

Após atingir as metas para os níveis de LDL-colesterol, é imperativo alcançar a meta do HDL-colesterol, por suas conhecidas propriedades antiaterogênicas confirmadas amplamente em muitos estudos epidemiológicos. Esta revisão analisa de maneira objetiva e concisa as diversas alternativas disponíveis na prática clínica diária para aumentar os níveis de HDL-colesterol em nosoos pacientes, com o objetivo de alcançar melhores prognósticos em termos de morbimortalidade cardiovascular.

After having reached the objective for the LDL cholesterol levels, it becomes imperative to reach the objective for HDL cholesterol, known for its anti-atherogenic properties, generally confirmed in many epidemiological studies. This review deals, in a clear and concise manner, with the different alternatives available in daily clinical practice to raise the HDL cholesterol levels of patients, to achieve better outcomes in terms of morbidity and mortality in cardiovascular disease.

Lipoproteína A, "el colesterol malísimo" / A lipoprotein

La hiperlipidemia por lipoproteína a -LDL más apo a- es un factor de riesgo vascular aterotrombótico, familiar, independiente y poderoso, llamativamente desconsiderado. Este trabajo tiene como objetivo su mejor diagnóstico y tratamiento.

Tratamento das dislipidemias: como e quando indicar a combinação de medicamentos hipolipemiantes / Treatment of dyslipidemia: how and when to combine lipid lowering drugs

Hiperlipidemia combinada familiar (HCF) é a forma mais comum de hiperlipidemia familial e se caracteriza por resistência à insulina, níveis baixos de HDL-C, níveis altos de triglicérides (TGC) e colesterol total associados a vários fenótipos dentro da mesma família. HCF associa-se, também, a um alto risco cardiovascular (RCV), e os níveis-alvo de tratamento das anormalidades lipídicas têm se modificado recentemente. Reduzir os níveis de LDL-C e não HDL-C devem ser os alvos da terapia. Níveis de LDL-C abaixo de 70 mg/dl têm se mostrado benéficos na RCV em pacientes de alto risco. Várias estatinas com diferentes potências e interações medicamentosas estão disponíveis no mercado. A terapia combinada de estatinas com seqüestradores de ácidos biliares ou ezetimiba pode ser necessária para se alcançar os valores-alvo de LDL-C estabelecidos pelas diretrizes. Níveis altos de TGC e baixos de HDL-C devem ser também considerados no tratamento, e freqüentemente somente o uso das estatinas se mostra insuficiente para normalizá-los. A combinação de estatinas com fibratos pode auxiliar para reduzir os níveis de colesterol e aumentar os de HDL-C, mas está associada à maior freqüência de miopatia e toxicidade hepática. Assim, a avaliação cuidadosa dos riscos e benefícios da terapia é recomendável. A associação de estatina e niacina parece ser útil para pacientes com HCF, particularmente por aumentar os níveis de HDL-C, uma vez que tem sido menos relacionada à alta freqüência de miopatia. A niacina pode ser causa de flushings que podem ser reduzidos com o uso de aspirina. O efeito pode também ser minimizado com o uso de formas de liberação lenta (Niaspan). A niacina pode também elevar os níveis de glicemia e ácido úrico. Assim, os riscos e benefícios da associação devem ser avaliados.

Familial combined hyperlipidemia (FCH) is a frequent familial lipid disorder associated with insulin resistance, low HDL cholesterol, high triglycerides and cholesterol levels with variable phenotypes within the same family. FCH is linked to a high risk for cardiovascular diseases. Treatment goals for lipid abnormalities are changing in recent years. Lowering elevated levels of LDL e Non HDL-cholesterol levels are primary targets of therapy. Lower LDL-C than 70 mg/dL seems to be useful to lower cardiovascular risk in patients with very high risk. Many statins are available, with different potencies and drug interactions. Combination therapy of statins and bile acid sequestrants or ezitimibe may be necessary to further decrease LDL cholesterol levels in order to meet guideline goals. High triglycerides and low HDL cholesterol are also important goals in the treatment of these patients, and frequently statins alone are insufficient to normalize the lipid profile. Combination therapy with fibrates will further lower triglycerides and increase HDL cholesterol levels; this combination is also associated with higher incidence of myopathy and liver toxicity; appropriate evaluation of patients' risk and benefits is necessary. Association of statin/niacin seems be very useful in patients with FCH, especially as niacin is the best drug to increase HDL cholesterol; this association is not linked to a higher frequency of myopathy. Niacin causes flushing, that can in part be managed with use of aspirin and extended release forms (Niaspan); niacin also may increase plasma glucose and uric acid levels. Evaluation of risks and benefits for each patient is needed.

Mecanismos de hepatotoxicidade / Mechanisms of hepatotoxicity

Hepatopatia relacionada ao uso de drogas hipolipemiantes tem sido definida como um dano celular (aumento das enzimas AST e ALT) sem alterações colestáticas (aumento de bilirrubinas e/ou fosfatase alcalina). Seis mecanismos são propostos para a hepatopatia: 1. Reações de alta energia no citocromo P450 comprometendo a homeostase do cálcio com a ruptura de fibrilas intracelulares e lise de hepatócitos. 2. Disfunção de proteínas transportadoras relacionadas com o fluxo de ácidos biliares (mecanismo proposto para a toxicidade hepática dos fibratos). 3. Reações imunes geradas pela formação de metabólitos das drogas hipolipemiantes formados no fígado. 4. Hepatoxicidade promovida por células T com inflamação adicional mediada por neutrófilos. 5. Apoptose mediada por TNF e Fas (imune-mediada). 6. Estresse oxidativo gerado por dano a organelas intracelulares. Ainda, idade avançada, consumo excessivo de álcool, altas doses de drogas hipolipemiantes, interação com outros fármacos, e doença hepática ativa prévia podem aumentar a hepatotoxidade.

Combinação de fármacos na abordagem das dislipidemias: associação entre estatinas e niacina / Combination of drugs: statins and niacin

A combinação de estatinas com niacina se apresenta como uma atraente associação, na presença de dislipidemia mista com níveis de HDL baixo, quando monoterapia é insuficiente para o alcance das metas lipídicas. Benefícios clínicos foram observados com a combinação de estatinas com niacina nos estudos FATS, HATS e ARBITER 2, mostrando atenuação no desenvolvimento da aterosclerose e/ou redução de eventos coronários, acompanhados de alterações lipídicas favoráveis. Em geral, esta combinação é bem tolerada. Recomenda-se monitoração adequada das enzimas hepáticas e muscular e, ainda, titulação cuidadosa de cada uma das drogas combinadas.

Farmacologia da niacina ou ácido nicotínico / Pharmacology of niacin or nicotinic acid

Niacina ou ácido nicotínico é uma vitamina solúvel com propriedades hipolipemiantes. Niacina reduz triglicérides (20 por cento - 50 por cento), LDL (5 por cento - 25 por cento), e aumenta HDL (15 por cento - 35 por cento). O estudo Coronary Drug Project mostrou que o uso de niacina foi associado com redução de eventos coronários e mortalidade total, e mais recentemente, foi demonstrado que niacina combinada com outras drogas hipolipemiantes pode atenuar a progressão da aterosclerose coronária. A niacina parece reduzir a mobilização de ácidos graxos livres dos adipócitos, agindo em receptores específicos, diminuindo a formação de lipoproteínas ricas em triglicérides pelo fígado. Existem duas formas de niacina, uma de absorção rápida (cristalina), mais comumente associada com flushing, e outra de liberação extendida, recentemente referida como de melhor tolerabilidade. O uso de niacina pode associar-se com dispepsia, aumento dos níveis plasmáticos de enzimas hepáticas e também com modestas elevações na glicose e ácido úrico, ao menos na utilização de doses até 2g / dia da forma de liberação prolongada.

Ação da frutose-1, 6-biofosfato sobre a toxicidade aguda do ácido nicotínico / Fructose-1, 6-bisphosphate action in nicotinic acid acute toxicity-induced

O ácido nicotínico (niacina) se mostra como um agente que reduz o nível de colesterol total, lipídios de baixa densidade (LDL) e triglicerídeos, sendo efetivo na terapia para regulação lipoprotéica e redução de risco cardiovascular. A toxicidade hepática é um efeito potencialmente sério da terapia com niacina. Já são bem descritos os efeitos da frutose-1,6-biofosafato na injúria de diferentes órgãos, além de apresentar-se protetora em lesões tóxicas. A toxicidade aguda sobre os perfis lípidico e hepático do ácido nicotínico, bem como a ação da frutose-1,6-biofosfato, como proteção na ação letal do ácido, são os alvos deste estudo. A dose de 800mg/kg intraperitoneal de ácido nicotínico é capaz de levar a óbito 25% dos ratos analisados. Mostra-se que o ácido exerce ação sobre os lípídios, diminuindo os valores de colesterol, mas não os de triglicérides. A lesão hepática decorrente do uso crônico do ácido nicotínico não é reproduzido na análise aguda, sendo que a causa da mortandade dos animais não é conhecida. Elucida-se também que a frutose-1,6-bisfosfato 500mg/kg, via subcutânea, não é competente no alento dos ,ales causados pelo ácido, ao contrário, potencializa a ação da niacina ao provocar aumento dos níveis de lactato desidrogenase.