El sistema de regulación celular de envejecimiento / No disponible

Los animales longevos tienen niveles bajos de producción mitocondrial de ROS y de insaturación de los ácidos grasos de las membranas celulares. La restricción de calorías, de proteínas, o de metionina, y la rapamicina, que son las cuatro manipulaciones experimentales conocidas que aumentan la longevidad de los mamíferos, también disminuyen la producción mitocondrial de ROS en el complejo I y el daño oxidativo al ADNmt. Esto parece contribuir a aumentar la longevidad porque disminuye la acumulación de fragmentos del ADNmt insertados dentro del ADN nuclear. La señalización pre-nuclear de la longevidad, el programa nuclear del envejecimiento, y los efectores de envejecimiento, son los tres constituyentes principales del sistema de regulación del envejecimiento celular (CARS). Los tres efectores del envejecimiento mejor conocidos de los tejidos aerobios son la producción mitocondrial de ROS, la insaturación de los ácidos grasos de las membranas, y la autofagia. El programa de envejecimiento nuclear reacciona a las proteínas citoplásmicas de señalización influenciadas a su vez por nutrientes, fármacos y hormonas, variando al menos dos efectores, la producción mitocondrial de ROS y la autofagia. Un programa análogo, aunque con clusters génicos adicionales implicados, y con mayor nivel de expresión génica, puede determinar la longevidad de las distintas especies animales (AU)

The mitochondrial rate of reactive oxygen species (ROS) production and the degree of fatty acid unsaturation of cellular membranes are low in longlived animals. Dietary restriction, protein and methionine restriction, and rapamycin, the four known experimental manipulations which increase mammalian longevity, also decrease mitROSp at complex I and oxidative damage to mtDNA. This could increase longevity by decreasing mtDNA fragments accumulation inside nuclear DNA. Pre-nuclear signaling of longevity, the nuclear aging program, and the aging effectors are the three main constituents of the cellular aging regulation system (CARS). The three best known aging effectors of the genetic aging program of aerobic tissues are mitochondrial ROS production, membrane fatty acid unsaturation, and autophagy. This program reacts to cytoplasmic signaling proteins, influenced by nutrients, drugs and hormones, varying the activity of the mitROSp and autophagy aging effectors. An analogous program, although with additional gene clusters of aging involved and wider output activity, can determine longevity in different animal species (AU)

Déficit de 3-hidroxiacil-CoA-deshidrogenasa de cadena larga: a propósito de un caso / Long-chain 3-hydroxyacyl-CoA dehydrogenase deficiency: A case report

CASO CLÍNICO: Paciente de 5 años de edad remitido para valoración oftalmológica con el diagnóstico de déficit de 3-hidroxiacil-CoA deshidrogenasa de cadena larga. Presentaba como antecedente la aparición de crisis metabólicas agudas precipitadas por infecciones banales y rabdomiólisis. El examen oftalmoscópico reveló una atrofia coriorretiniana peripapilar y una maculopatía granular difusa. La agudeza visual era de 6/6 en ambos ojos y las pruebas electrofisiológicas normales. DISCUSIÓN: Se realiza una revisión de la bibliografía y los conocimientos recientes de esta enfermedad mediante la descripción de un caso clínico documentando los hallazgos obtenidos mediante autofluorescencia y tomografía de coherencia óptica para mejorar el conocimiento existente sobre ella

CLINICAL CASE: A five-year-old patient, with a diagnosis of long-chain 3-hydroxyacyl-CoA dehydrogenase deficiency, was referred for an ophthalmological examination. He had a history of acute metabolic crises precipitated by intercurrent infections,as well as rhabdomyolysis. The fundoscopic examination revealed a peripapillary chorioretinal atrophy and a diffuse granular appearance of the macular retinal pigment epithelium. Best corrected visual acuity was 6/6 in both eyes, and he had a normal electroretinography test. DISCUSSION: We perform a review of the literature and recent findings in relation to this disease through the description of a clinical case in order to improve the knowledge of this uncommon disorder

SREBP-1c, ChREBP y LXR: Su influencia en el desarrollo del hígado graso no alcohólico / SREBP-1c, ChREBP and LXR: Their role in the pathogenesis of the non-alcoholic fatty liver

El hígado graso no alcohólico (HGNA) es una enfermedad que se define como un espectro continuo que oscila entre una esteatosis macrovesicular, de curso clínico favorable, hasta un cuadro de esteatohepatitis no alcohólica (EHNA), que da lugar a daños irreversibles y que se ha convertido en los últimos años en un problema sanitario de primera magnitud. El HGNA se caracteriza por una infiltración grasa de los hepatocitos que se asocia con un estado de resistencia a la insulina y por ello ligado, como factor de riesgo, al síndrome metabólico. Los factores de transcripción SREBP-1c (proteína de unión al elemento regulador del esterol), ChREBP (proteína de unión al elemento de respuesta a carbohidratos) y LXR (receptor X hepático) son reguladores fundamentales de la homeostasis lipídica y glucídica y de la inflamación, cuya activación regula al alza genes implicados en la síntesis de novo de los ácidos grasos en respuesta a insulina, glucosa y oxiesteroles, tanto en condiciones fisiológicas como patológicas. En esta revisión se describen datos recientes sobre la biología, la regulación y la coordinación funcional entre SREBP-1c, ChREBP y LXR y su relación con el HGNA. El desarrollo de agonistas selectivos de estos factores les hacen ser prometedoras dianas en el tratamiento del HGNA y de la EHNA

Nonalcoholic fatty liver disease (NAFLD) has become a major public health issue that comprises a disease spectrum which ranges from benign hepatic steatosis to non-alcoholic steatohepatitis (NASH), leading to irreversible liver damages. Deposition of excess triglycerides within liver cells is the hallmark of NAFLD, which is associated with a loss of insulin sensitivity. A growing body of evidence implicates the lipogenic transcription factors SREBP-1c (sterol regulatory element-binding protein), ChREBP (carbohydrate responsive element-binding protein) and LXR (liver X receptor) in the pathogenesis of NAFLD. These factors have emerged as central regulators of the de novo fatty acid synthesis, the glucose homeostasis and the inflammation in response to insulin, glucose and oxysterols, under both physiological and physiopathological conditions. In this review we describe recent findings in the biology, the function and the cross-regulation between SREBP-1c, ChREBP and LXR on the control of lipid and glucose metabolism and their link to NAFLD. Specific pharmacologic ligands are available, making them attractive therapeutic targets for NAFLD and NASH

El papel de la inmunidad innata en la obesidad / The role of innate immunity in obesity

La obesidad en México es un problema de salud preocupante por el incremento en la prevalencia en adultos y niños, y se considera un factor de riesgo para el desarrollo de resistencia a la insulina, así como de otras alteraciones metabólicas. En esta patología se ha observado un incremento en la expresión de los receptores tipo Toll (TLRs) en el adipocito, receptores con participación crucial en la respuesta inmune innata. Se propone que los TLRs están implicados en la inflamación sistémica y en el desarrollo de la resistencia a la insulina. La activación de los TLRs es mediada por ácidos grasos y su expresión está regulada por leptina, adiponectina y PPAR. El conocimiento de la función de los TLRs, tanto en la inflamación como en la diferenciación del adipocito es importante en la búsqueda de nuevos blancos terapéuticos antiinflamatorios que coadyuven en el tratamiento de la obesidad.

Obesity in Mexico is alarmingly increasing in prevalence in adults and children, and it is a risk factor for the development of insulin resistance, as well as, of other metabolic alterations. The discovery of the expression of the Toll-like receptors (TLRs) in adipocytes, suggests an important role in innate immunity. In different models of obesity, there has been observed an increase of TLRs expression in the fat tissue, therefore TLRs could be involved in systemic inflammation in this disease, and in the development of insulin resistance. TLR activation is mediated by fatty acids and their expression is regulated by leptin, adiponectin and PPARs. Knowledge of the role of TLRs in inflammation and adipocyte differentiation and their regulation, then it is important to try to develop new therapeutic anti-inflammatory targets that contribute in the treatment of obesity.

Motilidad intestinal y microflora / Intestinal motility and microflora

La microflora es el conjunto de colonias microbacterianas que cubren la superficie del tubo digestivo. Cada sujeto humano alberga unos 100 billones de colonias de unas 400 especies distintas, biodiversidad que facilita la vida y el desarrollo del conjunto. La concentración de bacterias va aumentando a lo largo del tubo digestivo, alcanzando concentraciones de 1012 UFC/ml. en el colon. La motilidad del intestino delgado es propulsiva con una fase de barrido que no permite el crecimiento de bacterias. Por el contrario, la motilidad del colon es muy lenta y no propulsiva durante el ayuno y el sueño. Sólo en vigilia y en período postprandial existen ondas de contracción de alta amplitud y rápidamente progresivas en dirección oral-anal. La interacción entre las bacterias presentes en el lumen y las ondas de contracción motora es muy difícil de evaluar. Este efecto se ha estudiado en base a los fármacos que alteran la motilidad y que al aumentar ésta, barren con la flora bacteriana presente. En ese sentido se sabe que el uso de cisaprida acelera el tránsito, reduciendo la densidad de bacterias metanogénicas con un aumento de la excreción de hidrógeno. En cambio, loperamida disminuye el tránsito, aumentando la flora metanogénica (hecho que representa lo que sucede a pacientes constipadas, que tienen flora mayoritariamente productora de metano). Conclusión: La interacción entre motilidad y flora bacteriana es compleja y está poco estudiada fundamentalmente debido a dificultades técnicas.

Microflora is the set of microbacterium colonies covering the digestive tract surface. Each human subject hosts ca. 100 billions of colonies of 400 different species, b23wiodiversity that facilitates life and development of the whole. Bacteria concentration increases throughout the digestive tract, reaching concentrations of 1012 CFU/ml in the colon. Motility of the small intestine is propulsive with a sweeping phase, allowing for the growth of bacteria. On the contrary, motility of the colon is very slow and non-propulsive during fasting and sleeping. Only during wakefulness and postprandial period there are wide-ranging and quickly progressive contraction waves in oral-anal direction. Interaction between bacteria present in lumen and the contraction waves is very hard to assess. This effect has been studied based on drugs that alter motility, and when it increases, they sweep the existing gut flora. In this sense, it is known that the use of cisapride accelerates the transit, reducing the density of methanogenic bacteria with an increase in the hydrogen excretion. On the other hand, loperamide slows down transit, causing an increase of the methanogenic flora (which represents what happens to constipated patients with flora that produces mainly methane). Conclusion: Interaction between motility and gut flora is complex and has not been enough studied mainly due to technical difficulties.

Nuestra experiencia diagnóstica en enfermedades peroxisomales con alteración del perfil de ácidos grasos / Our experience in the diagnosis of peroxisomal diseases with an abnormal fatty acid profile

Introducción. Las enfermedades peroxisomales tienen una gran heterogeneidad etiológica y clínica. Un perfil alterado de ácidos grasos de cadena muy larga (AGCML) es común a muchas de ellas, lo que facilita su orientación diagnóstica.Pacientes y métodos. Se revisa nuestra experiencia diagnóstica en los casos de enfermedad peroxisomal con patrón alterado de AGCML, que se determinaban en suero sólo ante fuerte sospecha clínica hasta finales de 1998, fecha en que se introdujo en nuestro laboratorio su cuantificación por cromatografía. Resultados. En la base de datos de neuropediatría de mayo de 1990 a 1 de octubre de 2007 figuran 10.239 casos. Se han identificado 10 casos de enfermedad peroxisomal con patrón alterado de AGCML, todos varones: dos casos de espectro de síndrome de Zellweger, un defecto de la beta-oxidación peroxisomal sin tipificar y siete adrenoleucodistrofias ligadas a X (cuatro con afectación neurológica y tres sin daño neurológico; dosidentificados por ser hermanos de enfermos y el otro por presentar un síndrome de Addison). Conclusiones. En nuestros 10 casos, el diagnóstico se orientó por el cuadro clínico o familiar que llevó a la determinación de AGCML. La disponibilidad de la determinación de AGCML permite el diagnóstico siste-mático de pacientes de forma precoz. Actualmente, la realizamos ante sospecha clínica del espectro Zellweger, sospecha de adrenoleucodistrofia/adrenomieloneuropatía ligada a X, leucoencefalopatías de causa no aclarada, enfermedad de Addison, tanto en varones como mujeres, y ante toda encefalopatía crónica de causa no aclarada de inicio prenatal o no

Introduction. The aetiology and clinical features of peroxisomal diseases vary widely. An altered very-long-chain fatty acid (VLCFA) profile is commonly found in many of these diseases, and this makes it easier to point the diagnosis in the right direction. Patients and methods. We review our experience in the diagnosis of cases of peroxisomal diseases with analtered VLCFA pattern; these were determined in serum only when there was a strong clinical suspicion up to the end of 1998, when their quantification by chromatography was introduced into our laboratory. Results. The neuropaediatric database included 10,239 cases between May 1990 and 1st October 2007. Ten cases of peroxisomal disease with an altered VLCFApattern were identified, all of them males. There were two cases of Zellweger syndrome spectrum, one unclassified peroxisomal oxidation defect and seven X-linked adrenoleukodystrophies (four with neurological compromise and three with no neurological damage; two were identified in siblings of patients and the other due to the presence of Addison’s syndrome).Conclusions. In our 10 cases, the diagnosis was guided by the clinical or familial features that led to the determination of VLCFA. Being able to determine VLCFA makes early systematic diagnosis of patients possible. At present, VLCFA determination is performed when there is a clinical suspicion of Zellweger spectrum, suspected X-linked adrenoleuko - dystrophy/adrenomyeloneuropathy of unclear causation, Addison’s disease, both in males and females, and above all in cases of chronic encephalopathy of unknown causation, with or without prenatal onset

Implicaciones de los ácidos grasos en la salud ocular / Implications of fatty acids in ocular health

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Modulação da ativação dos receptores ativados por proliferadores de peroxissoma (PPAR) e dos receptores X hepáticos (LXR) por LN´O IND. 2´ / Modulation of activity of peroxissome prolifetor-activated (PPAR) and liver X receptors(LXR) by LN´O IND. 2´

A atividade dos receptores ativados por proliferadores de peroxissoma (PPAR) e receptor X hepático (LXR) são regulados por ácidos graxos. Entretanto, o papel do LNO2, um produto endógeno da nitração do ácido linoléico por espécies reativas derivadas de óxido nítrico (•NO), na via de sinalização que regula a ativação destes receptores ainda não está elucidada. Assim, considerando a propriedade do LNO2 como doador de NO, nós investigamos a participação da via de sinalização p21Ras/Raf/ERK na ativação de PPAR e LXR por LNO2. Os resultados obtidos demonstraram que LNO2, na concentração de 0.01µM, foi um potente ativador de PPAR quando comparado ao ligante natural ácido linoléico, o qual apresentou ativação equivalente do PPAR na concentração de 0.01µM. O LN02, contudo não teve efeito na ativação de LXR. LNO2 foi um potente ativador de p21Ras quando comparado ao ácido linoléico. A ativação de Ras ocorreu após 5 minutos de incubação com LNO2 em células parentais. Entretanto, em células transfectadas com p21RasC118S, o LNO2 não foi capaz de ativar Ras. A ativação de Ras e PP AR foi dependente da liberação de NO a partir de LN02, o que foi evidenciado na presença de C-PTIO, um seqüestrador de NO. LNO2 ativou ERK, mas não demonstrou efeito relevante na ativação de p38 MAP kinase...

Regulation of lypolysis in white adipose tissues of lean and obese Zucker rats

Obese Zucker rat is often used as a model of genetic obesity to understand themechanism of the development of obesity. In the present work, in order to betterunderstand the regulation of lipolysis in the Zucker rat, the lipolytic activities ofadipocytes isolated from different adipose depots of lean and obese Zucker rats, inthe basal state or after catecholamine stimulation have been measured. The obeseZucker rat presents hyperinsulinemia without hyperglycemia and with elevated plasmafree fatty acids, suggesting a dyslipidemia. Morphological studies of three adiposedeposits show a marked hypertrophic and hyperplastic type of obesity, much pronouncedin the subcutaneous depot. In the current study we show that the basallipolytic rate is higher in adipocytes from each deposit of obese rats (when results arecorrected for cell surface area). This finding, associated with the increase of alldeposits, could contribute to the elevated plasma FFA observed. Investigation of theresponsiveness of dibutyril cAMP (DBcAMP) points out that the defect in the NEresponsiveness is essentially located at post-receptor level. Nevertheless, a receptordefect could not be excluded as suggested by a decrease of the Beta-ARs observed in alldeposits. Our study points out that the lipolytic resistance to catecholamines in adiposetissue of obese Zucker rats appears to counteract the increase in the lipolyticrate, in order to moderate the increase in plasma FFA levels that may contribute tothe hyperinsulinemia observed, characteristic of an insulino-resistant state (AU)

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PPAR-gamma, hipertensión arterial y riñón / PPAR-Gamma, arterial hypertesnion and the kidney

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Cambios en los acidos grasos de membranas de Microbacterium esteraromaticum GNP-5 con diferentes temperaturas y osmolaridades / Changes in Membrane Fatty Acids of Microbacterium esteraromaticum GNP5 with Changes of Temperature and Osmolarity

Microbacterium esteraromaticum es un microorganismo que se aísla con frecuencia de landfarming o procesos de biorremediación de hidrocarburos en la meseta de la Patagonia central (Argentina) y se halla sometido a variaciones de temperatura y a cambios de salinidad que se producen naturalmente. Su adaptabilidad a esos cambios climáticos indujo al estudio de las modificaciones que se producen en su membrana celular para resistirlos. En este trabajo se estudió el efecto conjunto de la temperatura y la concentración de cloruro de sodio sobre la composición de los ácidos grasos de membrana en la cepa de Microbacterium esteraromaticum GNP5b. M. esteraromaticum utiliza, frente al incremento de la temperatura, la estrategia es aumentar la longitud de sus ácidos grasos de cadenas ramificada impar (17 átomos de carbono) con disminución de 15:0 anteiso, así como el porcentaje de ácidos grasos 15:0 iso (de mayor punto de fusión) a partir del respectivo anteiso. El aumento de la salinidad modifica la composición de ácidos grasos siguiendo patrones diferentes según sea la temperatura de incubación. A 14 y 28 °C incrementa los 15:0 iso y 17:0 iso en detrimento de sus homólogos anteiso. A 37 °C este grupo de ácidos grasos no sigue los mismos patrones anteriores. La longitud de cadena, expresada como el índice C15/C17, es errática con el aumento de la salinidad.

Citocinas, disfunção endotelial e resistência à insulina / Cytokines, endothelial dysfunction, and insulin resistance

A disfunção endotelial está associada a diversas alterações vasculares, como a aterosclerose, hipertensão arterial, hiperlipidemia e diabetes mellitus, que têm em comum a resistência à insulina (RI). Citocinas são proteínas de baixo peso molecular, com diversas funções metabólicas e endócrinas, que participam da inflamação e resposta do sistema imune. Várias dessas citocinas são consideradas como fatores de risco independentes para doenças da artéria coronária e cerebrovascular. As principais fontes de citocinas (adipocinas) são os tecidos adiposos subcutâneo e visceral. Assim, aumento da massa de tecido adiposo está associado com alterações da produção de adipocina com aumento da expressão de fator de necrose tumoral alfa (TNF-alfa), interleucina 6 (IL-6), inibidor do fator ativador de plasminogênio 1 (PAI-1), e diminuição da expressão de adiponectina no tecido adiposo. A condição pró-inflamatória associada a essas alterações sugere ligação entre RI e disfunção endotelial no estágio inicial do processo de aterosclerose, em indivíduos obesos e em pacientes diabéticos tipo 2. A redução da massa de tecido adiposo, por redução de peso associada a exercício físico, reduz TNF-alfa, IL-6 e PAI-1, aumenta adiponectina, e melhora tanto a sensibilidade à insulina quanto a função endotelial. A interação entre adipocinas e insulina no controle da função endotelial será discutida, bem como o conceito de que a alteração da secreção de adiponectinas na RI e/ou obesidade piora a função endotelial, além de diminuir ainda mais a sensibilidade à insulina.

Endothelial dysfunction is associated with several vascular conditions as atherosclerosis, hypertension, hyperlipidemia and diabetes mellitus. In all these conditions insulin resistance (IR) is present. Cytokines are low molecular weight proteins with several endocrine and metabolic functions that participate of inflammation and immune response. Several of these cytokines are independent risk factors for cerebrovascular and coronary artery disease. The major sources of cytokines (adipokines) are the visceral and subcutaneous adipose tissues. Thus, increased adipose tissue mass is associated with alteration in adipokine production as over expression of tumor necrosis factor alpha, interleukin 6, plasminogen activator inhibitor 1, and under expression of adiponectin in adipocite tissue. The pro-inflammatory status associated with these changes provides a potential link between IR and endothelial dysfunction, the early stage in the atherosclerotic process, in obese individuals, and type 2 diabetic patients. Reduction of adipose tissue mass through weight reduction in association with exercise reduces TNF-alpha, IL-6, and PAI-1, increases adiponectin, and is associated with improved insulin sensitivity and endothelial function. This review will focus on the evidence for regulation of endothelial function by insulin and the adypokines such as adyponectin, leptin, resistin, IL-6 and TNF-alpha. Interaction between insulin signaling and adypokines will be discussed, as well as the concept that aberrant adypokine secretion in IR and/or obesity impairs endothelial function and contributes further to reduce insulin sensitivity.

Ácidos grasos: importancia en el cáncer colorrectal / Fatty acids: importance in colorectal cancer

Fundamento: existen evidencias que sugieren que las grasas de la dieta están asociadas con el riesgo de cáncer colorrectal. Los efectos de las grasas no sólo dependen de la cantidad sino de su contenido específico de ácidos grasos. Métodos: revisión bibliográfica de los estudios publicados que relacionan los tipos de ácidos grasos y el riesgo de cáncer colorrectal. Resultados: elevadas concentraciones de ácidos grasos de cadena corta, así como el ácido eicosapentanoico parecen tener un efecto protector frente al cáncer colorrectal. Elevadas concentraciones de ácidos grasos de cadena media y el ácido araquidónico podrían estar asociadas a un aumento del riesgo de cáncer colorrectal. Por último, indicar que los ácidos grasos de cadena larga, ácidos grasos monoinsaturados, ácidos grasos trans, ácidos grasos poliinsaturados tales como el ácido linoleico, alfa-linoleico, ácido docosahexaenoico, muestran unos resultados inciertos en la génesis del cáncer colorrectal. Conclusiones: la sustitución de los ácidos grasos monoinsaturados de cadena corta y del ácido araquidónico por ácidos grasos de cadena corta y el ácido eicosapentanoico puede contribuir a la reducción del riesgo de cáncer colorrectal (AU)

Effect of fatty acids on leukocyte function

Fatty acids have various effects on immune and inflammatory responses, acting as intracellular and intercellular mediators. Polyunsaturated fatty acids (PUFAs) of the omega-3 family have overall suppressive effects, inhibiting lymphocyte proliferation, antibody and cytokine production, adhesion molecule expression, natural killer cell activity and triggering cell death. The omega-6 PUFAs have both inhibitory and stimulatory effects. The most studied of these is arachidonic acid that can be oxidized to eicosanoids, such as prostaglandins, leukotrienes and thromboxanes, all of which are potent mediators of inflammation. Nevertheless, it has been found that many of the effects of PUFA on immune and inflammatory responses are not dependent on eicosanoid generation. Fatty acids have also been found to modulate phagocytosis, reactive oxygen species production, cytokine production and leukocyte migration, also interfering with antigen presentation by macrophages. The importance of fatty acids in immune function has been corroborated by many clinical trials in which patients show improvement when submitted to fatty acid supplementation. Several mechanisms have been proposed to explain fatty acid modulation of immune response, such as changes in membrane fluidity and signal transduction pathways, regulation of gene transcription, protein acylation, and calcium release. In this review, evidence is presented to support the proposition that changes in cell metabolism also play an important role in the effect of fatty acids on leukocyte functioning, as fatty acids regulate glucose and glutamine metabolism and mitochondrial depolarization

Efecto inhibitorio del nonanoato de potasio y el fluoruro de sodio en la acidogenicidad de la placa dental humana in vitro / In vitro inhibitory effect of potassium nonanoate and sodium fluoride on acidogenity of human dental plaque

El ácido nonanoico es un ácido graso saturado de 9 carbonos el cual se ha demostrado reduce la aparición de caries de fisura en ratas cuando es incluido en la dieta (Hayes y Berkovitz, 1979). En 1979 Griffiths demostró que el nonanoato de potasio agregado en enjuagues con sacarosa inhibe la producción de ácidos por parte de la bacaterias de la placa dental en humanos. El objetivo de esta invesstigación fue estudiar el efecto de ácidos grasos y fluoruros en la producción de ácidos en placa dental de humanos in vitro. Para ello se recolectó placa dental en ayunas de 3 horas, en niños con caries activa y con edades comprendidas entre los 5 y 12 años. La producción de ácidos fue determinada por el método de titulación reportado por Hayes y Roberts (1980), luego de la adición de la glucosa exógena. Los resultados demostraron que a pH 7,4 el NK (3mM) y el NaF (13mM) produjeron una inhibición en la producción de ácidos en un 45 por ciento y 54,5 por ciento respectivamente, mientras que con la mezcla se observó un reducción de un 39 por ciento. A pH 5,5 el NK y el NaF a una concentración de 0,26mM produjeron una inhibición de 21,2 por ciento y 29,3 por ciento respectivamente y cuando se mezclaron esta inhibición se incrementó a 49,3 por ciento. Estos resultados sugieren que a pHs cercanos a la neutralidad (7,4) no hay efecto adhitivo del NK y el NaF, mientras que a pH ácido (5,5) la combinación de estos compuestos incrementó significativamente (p<0,01) su efectividad

Trans fatty acid isomers in human health and in the food industry

Trans fatty acids are unsaturated fatty acids with at least one double bond in the trans configuration. These fatty acids occur naturally in dairy and other natural fats and in some plants. However, industrial hydrogenation of vegetable or marine oils is largely the main source of trans fatty acids in our diet. The metabolic effect of trans isomers are today a matter of controversy generating diverse extreme positions in light of biochemical, nutritional, and epidemiological studies. Trans fatty acids also have been implicated in the etiology of various metabolic and functional disorders, but the main concern about its health effects arose because the structural similarity of these isomers to saturated fatty acids, the lack of specific metabolic functions, and its competition with essential fatty acids. The ingestion of trans fatty acids increases low density lipoprotein (LDL) to a degree similar to that of saturated fats, but it also reduces high density lipoproteins (HDL), therefore trans isomers are considered more atherogenic than saturated fatty acids. Trans isomers increase lipoprotein(a), a non-dietary-related risk of atherogenesis, to levels higher than the corresponding chain-length saturated fatty acid. There is little evidence that trans fatty acids are related to cancer risk at any of the major cancer sites. Considerable improvement has been obtained with respect to the metabolic effect of trans fatty acids due the development of analytical procedures to evaluate the different isomers in both biological and food samples. The oleochemical food industries have developed several strategies to reduce the trans content of hydrogenated oils, and now margarine and other hydrogenated-derived products containing low trans or virtually zero trans are available and can be obtained in the retail market. The present review provides an outline of the present status of trans fatty acids including origin, analytical procedures, estimated ingestion, metabolic effects, efforts to reduce trans isomers in our diet, and considerations for future prospects on trans isomers

Hyperlipidaemia and insulin resistance

There is reason to believe that increased plasma fatty acid (FFA) levels may be a cause for the strong association between fat ingestion and obesity. It has been recently shown in offspring of parents with non-insulin dependent diabetes mellitus (NIDDM), known to be at high risk to develop the disease, that elevated FFA levels were associated with insulin resistance. Moreover, 80-85 percent of patients with NIDDM are obese, are insulin-resistant, and many have elevated FFA levels which correlate with glucose tolerance. In support of the notion that plasma FFA are responsible for the insulin resistance observed in obesity, it was demonstrated more than 30 years ago that increased availability of FFA decreased CHO oxidation and glucose uptake in perfused rat heart and to a lesser extent in rat diaphragm. Based on these findings, the researchers proposeda glucose-fatty acid cycle presumed to be of fundamental importance for the control of blood glucose and insulin sensitivity both in normal and in diabetic subjects. This intriguing concept has remained controversial mainly because many investigators were unable to reproduce the fatty acid-mediated inhibition of glucose uptake in striated muscle that had been observed in perfused rat hearts. We have recently reinvestigated that onset and duration of the inhibitory effect of intravascular lipolysis, produced by intravenous infusion of triglycerides and heparin, on total body CHO oxidation and glucose disappearance in normal men during euglycaemic-hyperinsulinaemia. These studies demonstrated that the fatty acid-mediated inhibition of insulin-stimulated CHO oxidation occurred early, i.e., within the first 20 minutes while the inhibition of glucose uptake developed after only 3-4 hours of fat infusion. Thus, insufficient time of fat infusion (2 hours in most studies) was the most likely reason why the inhibitory effect of FFA on glucose uptake was not found in many studies. In subsequent studies, we have examined the dose dependency of the fatty acid effect on insulin-stimulated glucose uptake. The results showed that FFA inhibited glucose uptake in a dose-dependent fashion throughout the physiological range of plasma FFA concentration (AU)