Efecto del ayuno sobre la conducta alimentaria en estudiantes universitarios / Fasting effect on eating behavior in university students

La evidencia científica sobre la caracterización de la conducta alimentaria señala que situaciones de privación de alimento, como el ayuno, aumentan el valor del alimento y modifican el patrón alimentario. En consecuencia se incrementa el consumo de alimentos y por ende el consumo calórico. La situación se agrava cuando los alimentos preferidos después del periodo de privación son poco saludables o se consumen en exceso convirtiéndose en detonadores de problemas de salud (Capaldi, 1993; Gottschalk, Libby & Graff, 2000; Vélez & Garcia, 2003). Con el objetivo de evaluar el efecto del ayuno sobre el consumo calórico y la modificación de las preferencias alimentarias, se diseñó un estudio en el cual participaron nueve jóvenes universitarios que fueron clasificados de acuerdo a su Índice de Masa Corporal (IMC) en tres grupos: Bajo-peso, Normo-peso y Sobre-peso. Fueron expuestos durante la línea base a ocho alimentos diferentes. Durante la fase experimental se expuso a los mismos participantes a un periodo de ayuno y posteriormente a los mismos alimentos registrando su consumo. Los resultados mostraron que el consumo calórico y la preferencia entre alimentos se modificaron. El grupo Bajo-peso aumentó su consumo de alimento mientras que en los grupos Normo-peso y Sobre-peso lo disminuyeron.

Scientific evidence on the characterization of eating behavior indicates that food deprivation situations, such as fasting, the food value increases and alter the feeding pattern. Consequently food consumption increases and therefore caloric intake. The situation worsens when after a deprivation period the preferred foods are unhealthy or consumed in excess becoming tiggers for health problems (Capaldi, 1993; Gottschalk , Libby & Graff , 2000; Velez & Garcia , 2003). The aim of this study was to evaluate the effect of fasting on caloric intake and changing food preferences. This study was conducted with the participation of 9 university students who were classified according to their Body Mass Index (BMI) into three groups: Low-weight, Normo-weight and Over-weight. At the baseline participants were exposed to eight different foods. Same participants during the experimental phase were exposed to a period of fasting, subsequently were exposed to the same foods and record their consumption. Results showed that caloric intake and food preferences were altered after the fasting condition, differential effects among participants were observed. Low-weight group increased their food consumption while Normal-weight and Over-weight groups decreased.

Anti-obesity sodium tungstate treatment triggers axonal and glial plasticity in hypothalamic feeding centers.

OBJECTIVE: This study aims at exploring the effects of sodium tungstate treatment on hypothalamic plasticity, which is known to have an important role in the control of energy metabolism. METHODS: Adult lean and high-fat diet-induced obese mice were orally treated with sodium tungstate. Arcuate and paraventricular nuclei and lateral hypothalamus were separated and subjected to proteomic analysis by DIGE and mass spectrometry. Immunohistochemistry and in vivo magnetic resonance imaging were also performed. RESULTS: Sodium tungstate treatment reduced body weight gain, food intake, and blood glucose and triglyceride levels. These effects were associated with transcriptional and functional changes in the hypothalamus. Proteomic analysis revealed that sodium tungstate modified the expression levels of proteins involved in cell morphology, axonal growth, and tissue remodeling, such as actin, CRMP2 and neurofilaments, and of proteins related to energy metabolism. Moreover, immunohistochemistry studies confirmed results for some targets and further revealed tungstate-dependent regulation of SNAP25 and HPC-1 proteins, suggesting an effect on synaptogenesis as well. Functional test for cell activity based on c-fos-positive cell counting also suggested that sodium tungstate modified hypothalamic basal activity. Finally, in vivo magnetic resonance imaging showed that tungstate treatment can affect neuronal organization in the hypothalamus. CONCLUSIONS: Altogether, these results suggest that sodium tungstate regulates proteins involved in axonal and glial plasticity. The fact that sodium tungstate could modulate hypothalamic plasticity and networks in adulthood makes it a possible and interesting therapeutic strategy not only for obesity management, but also for other neurodegenerative illnesses like Alzheimer's disease.

Involvement of ATP-sensitive potassium (K(ATP)) channels in the loss of beta-cell function induced by human islet amyloid polypeptide.

Islet amyloid polypeptide (IAPP) is a major component of amyloid deposition in pancreatic islets of patients with type 2 diabetes. It is known that IAPP can inhibit glucose-stimulated insulin secretion; however, the mechanisms of action have not yet been established. In the present work, using a rat pancreatic beta-cell line, INS1E, we have created an in vitro model that stably expressed human IAPP gene (hIAPP cells). These cells showed intracellular oligomers and a strong alteration of glucose-stimulated insulin and IAPP secretion. Taking advantage of this model, we investigated the mechanism by which IAPP altered beta-cell secretory response and contributed to the development of type 2 diabetes. We have measured the intracellular Ca(2+) mobilization in response to different secretagogues as well as mitochondrial metabolism. The study of calcium signals in hIAPP cells demonstrated an absence of response to glucose and also to tolbutamide, indicating a defect in ATP-sensitive potassium (K(ATP)) channels. Interestingly, hIAPP showed a greater maximal respiratory capacity than control cells. These data were confirmed by an increased mitochondrial membrane potential in hIAPP cells under glucose stimulation, leading to an elevated reactive oxygen species level as compared with control cells. We concluded that the hIAPP overexpression inhibits insulin and IAPP secretion in response to glucose affecting the activity of K(ATP) channels and that the increased mitochondrial metabolism is a compensatory response to counteract the secretory defect of beta-cells.

Género, Interacción Social y Consumo de Alimento: "El Efecto Eva" / Sex, Social Interaction and Food Consumption: "The Eva Effect"

Diversos elementos proporcionan la información necesaria para el consumo de alimentos, entre ellos: el sabor, la textura y temperatura. Sin embargo, se requiere de su vinculación con la experiencia y las características ambientales para integrar el comportamiento alimentario. La evidencia experimental sugiere que el sexo y la interacción social son factores importantes para el consumo de alimentos. Esta investigación evaluó los efectos del género y de la interacción social sobre el consumo de alimentos. Adicionalmente, para tal objetivo se propone el uso del Catálogo Conductual de Interacción Alimentaria (CCIA). Participaron veinticuatro individuos de ambos sexos, entre 20 y 28 años, desconocidos entre ellos, fueron expuestos a diversos alimentos usuales y novedosos evaluando su interacción alimentaria. Los participantes fueron divididos en tres grupos. El grupo 1 fue integrado por hombres, el grupo 2 por mujeres y el grupo 3 por ambos géneros. Los resultados mostraron que el grupo 1 y 2 consumieron cantidades similares de alimento en comparación con el grupo 3 que presentó un escaso consumo. Se registró una fuerte influencia de las mujeres sobre los hombres para promover su consumo de alimento, fenómeno que fue denominado como "Efecto Eva". Concluimos que el género es un importante factor en el estudio del fenómeno alimentario.

Several elements provide information for food consumption, among them: flavor, texture and temperature. These elements related to environmental characteristics and experience integrate the feeding behavior. Experimental evidence suggests that sex and social interaction are important factors for food consumption. This study evaluated effects of sex and social interaction on food consumption. Additionally, our proposal is to use Behavioral Catalogue of Feeding Interaction (BCFI). Twenty-four human subjects, both sexes, between 20 and 28 years-old, which were not known between them, were exposed to different familiar and novel foods, evaluating the feeding interaction. Subjects were divided in three groups. First group was formed by man, second by woman; and third group by subjects of both sexes. Data suggest that group 1 and 2 registered similar food consumption in comparison with the group 3 that registered a little consumption. A strong influence of women was registered on men to stimulate its food consumption, phenomenon that was denominated "Eva Effect". We conclude that sex is an important factor in the study of feeding phenomenon.

Resistance to diet-induced obesity in mu-opioid receptor-deficient mice: evidence for a "thrifty gene".

Using pharmacological tools, a role for opioid receptors in the regulation of food intake has been documented. However, the involvement of specific receptor subtypes remains questionable, and little information is available regarding a role for opioid receptors in energy metabolism. Using adult male mice lacking the mu-opioid receptor (MOR) gene (MOR-/-), we show that the MOR is not essential for the maintenance of normal levels of ad libitum food intake but does modulate the efficiency of energy storage during high-fat diets through the regulation of energy partitioning. When fed a regular diet, MOR-/- mice displayed only subtle alterations in energy homeostasis, suggesting a relative overuse of fat as a fuel source in the fed state. When fed a high-fat diet, MOR-/- mice were resistant to obesity and impaired glucose tolerance, despite having similar energy intake to wild-type mice. This resistance to obesity was associated with a strong induction of the expression of key mitochondrial enzymes involved in fatty acid oxidation within skeletal muscle. This metabolic role of the MOR, which is consistent with the properties of a "thrifty gene," suggests that the MOR pathway is a potential target for pharmacological intervention in the treatment of obesity associated with the intake of fatty diets.