Association of the melanocortin 4 receptor gene rs17782313 polymorphism with rewarding value of food and eating behavior in Chilean children

Studies conducted in monozygotic and dizygotic twins have established a strong genetic component in eating behavior. Rare mutations and common variants of the melanocortin 4 receptor (MC4R) gene have been linked to obesity and eating behavior scores. However, few studies have assessed common variants in MC4R gene with the rewarding value of food in children. The objective of the study was to evaluate the association between the MC4R rs17782313 polymorphism with homeostatic and non-homeostatic eating behavior patterns in Chileans children. This is a cross-sectional study in 258 Chilean children (44 % female, 8-14 years old) showing a wide variation in BMI. Anthropometric measurements (weight, height, Z-score of BMI and waist circumference) were performed by standard procedures. Eating behavior was assessed using the Eating in Absence of Hunger Questionnaire (EAHQ), the Child Eating Behavior Questionnaire (CEBQ), the Three-Factor Eating Questionnaire (TFEQ), and the Food Reinforcement Value Questionnaire (FRVQ). Genotype of the rs17782313 nearby MC4R was determined by a Taqman assay. Association of the rs17782313 C allele with eating behavior was assessed using non-parametric tests. We found that children carrying the CC genotype have higher scores of food responsiveness (p value = 0.02). In obese girls, carriers of the C allele showed lower scores of satiety responsiveness (p value = 0.02) and higher scores of uncontrolled eating (p value = 0.01). Obese boys carrying the C allele showed lower rewarding value of food in relation to non-carriers. The rs17782313 C allele is associated with eating behavior traits that may predispose obese children to increased energy intake and obesity (AU)

No disponible

Molecular mechanisms of steatosis in non alcoholic fatty liver disease / Mecanismos moleculares de la esteatosis en la patología de hígado graso no alcohólico

Non alcoholic fatty liver disease (NAFLD) is the most important cause of chronic liver disease and is considered the hepatic manifestation of the metabolic syndrome associated with diabetes mellitus type 2. The prevalence of NAFLD in the general population reaches 15-20%. It is also estimated that non alcoholic steatohepatitis (NASH)affects 3% of the population. NAFLD refers to a wide spectrum of liver damage, which ranges from simple steatosis or intracellular triglyceride accumulation, to inflammation (NASH), fibrosis and cirrhosis. The mechanisms involved in the accumulation of triglycerides in the liver and subsequent hepatocellular damage are multifactorial and are not completely understood. However, metabolic changes such as insulin resistance (IR) are developed, being a common factor in the retention of fatty acids (FA) within the hepatocytes with oxidation and production of free radicals at the mitochondrial level, which are capable of causing lipid peroxidation, cytokine production, and necrosis. In addition, there are alterations in the hepatic bioavailability of long chain n-3 polyunsaturated fatty acids, conditions that alter the expression of a series of transcriptional factors involved in lipolytic and lipogenic processes in the liver. A greater knowledge of the etiopathogenic mechanisms of NAFLD is fundamental for the development of future effective therapeutic strategies. The pathophysiological fundamentals of liver steatosis are analyzed in this study (AU)

La enfermedad de Hígado graso no alcohólico (HGNA)es la causa más importante de enfermedad hepática crónica y es considerado la manifestación hepática del síndrome metabólico asociado a obesidad y diabetes mellitus tipo 2. La prevalencia de la enfermedad de HGNA en la población general alcanza el 15-20%, estimándose además que la esteatohepatitis no-alcohólica (EHNA) afecta al 3%. El HGNA se refiere a un amplio espectro de daño hepático, que va desde esteatosis simple o acumulación intracelular de triacilglicéridos (TAGs), a inflamación(EHNA), fibrosis y cirrosis. Los mecanismos implicados en la acumulación de TAGs a nivel hepático y subsecuente daño hepatocelular son de carácter multifactorial y no se conocen completamente. Sin embargo, es reconocido que existen alteraciones metabólicas, siendo la resistencia a la insulina (RI) un factor común que genera retención de ácidos grasos y TAGs dentro de los hepatocitos, con la producción de radicales libres a nivel mitocondrial capaces de inducir lipoperoxidación, producción decitoquinas y necrosis. Además, existen alteraciones en labio disponibilidad hepática de ácidos grasos poli-insaturados de cadena larga de la serie n-3, condiciones que alterarían la expresión de una serie de factores de transcripción involucrados en el proceso de lipólisis y lipogénesisa nivel hepático. Un mayor conocimiento de los mecanismos etiopatogénicos de la enfermedad de HGNA es fundamental para el desarrollo de estrategias terapéuticas eficaces a futuro. Los fundamentos fisiopatológicos de la esteatosis son analizados a continuación (AU)