RESUMO
Chromium is an indispensable nutrient for the carbohydrates and lipids metabolism. In this study the chromium content in the twenty main foods of the diet from Northwestern Mexico was determined, as well as the daily mean intake which was estimated based on the food intake basket of this region. Chromium content was analyzed by atomic absorption spectrophotometry using the graphite furnace technique and previous digestion of foods in microwave oven. The chromium mean intake was estimated considering the chromium daily mean intake for person per day and the chromium content of the foods analyzed in this study. The range chromium content in the foods analyzed was between 0.0004 and 0.1641 microgram/g dry weight. White cheese showed the highest chromium content followed by pasta soup, wheat tortilla, bread and meat. The main foods chromium contributors in the diet were: wheat tortilla (20%), white cheese (11%), corn tortilla (11%), pasta soup (10%), milk (10%), meat (9%) and white bread (8%). The daily chromium intake was 30.43 +/- 1.6 micrograms/d. Chromium values obtained in the food analyzed are considered low. Moreover, chromium intake obtained from the diet is not enough to meet the safety and adequate daily chromium intake. Therefore, the population from the Northwestern Mexico has a suboptimal dietary chromium intake.
Assuntos
Cromo/análise , Dieta/normas , Análise de Alimentos , Cromo/administração & dosagem , Comportamento Alimentar , Humanos , México , Espectrofotometria AtômicaRESUMO
Vogt-Koyanagi-Harada's syndrome (VKH) is an autoimmune disease prevalent in Mongoloids with evident participation of HLA. The aim of this study was to identify the class II DNA sequences involved in the etiopathogenesis of VKH in Mexican Mestizos. This study included 46 VKH patients and 170 controls. 75% were females (mean age at onset of 33.5 years). The disease evolved to chronicity (68%) and 25% of the patients were unresponsive to corticotherapy. DNA typing of HLA-DRB1, DQA1 and DQB1 was done following the 12th International Histocompatibility protocols. VKH was strongly dependent of DRB1 gene; DRB1*04 was found in 78.2% of the patients vs. 50.6% of the controls (p = 0.001). No particular DRB*04 subtype was significantly increased, suggesting that residues E-9 V-11; H-13; H-33 and Y-37 shared by all DR4s are implicated in susceptibility to VKH. However DRB1*0101 (p = 0.009, OR = 4.2) was clearly associated. This allele shares the motif LLEQRRAAG located at position 67-74 and 86 of DRB1 with *0405 associated in Japanese. Two HLA associated mechanisms may be triggering the autoimmune phenomena. One involving critical polymorphic residues expressed in different alleles. Secondly, some peptides may anchor to the conserved residues leaving other sequences to bind to the T cell receptor.
Assuntos
Antígenos HLA-DQ/genética , Antígenos HLA-DR/genética , Síndrome Uveomeningoencefálica/genética , Adulto , Alelos , Feminino , Frequência do Gene , Cadeias alfa de HLA-DQ , Cadeias beta de HLA-DQ , Cadeias HLA-DRB1 , Humanos , Masculino , México , Síndrome Uveomeningoencefálica/etnologia , Síndrome Uveomeningoencefálica/imunologiaRESUMO
Type I diabetes is an autoimmune and a polygenic disease, in which MHC-class II genes contribute to 48% of the disease. The aim of the present study, is to provide a guideline to understanding the molecular association of these genes, through the immunogenetic analysis of 3 Latin american mestizo populations. We included 606 individuals, 349 patients with DMDI and 257 healthy controls coming from 3 geographical areas: Mexico City, Mexico; Caracas, Venezuela and Medellin, Colombia. The results clearly indicate that in mestizo groups, the diabetogenic haplotypes are from mediterranean ancestry, while protection is due to Amerindian genes. It was demonstrated that the relevant sequences for IDDM expression are located to DRB1 and DQB1 loci with a minimal contribution of DQA1 residues. The sequences determining peptide recognition and the induction of TH1 cells mediating the cellular autoimmune response are in positions DRB1-57 and 74 (an aspartic acid and a glutamic acid respectively, confer protection), modulated by D-57 in the DQ, 8 chain. These data show that DRB1-DQB1 haplotypes are central for IDDM expression and open new pathways for the disease management.
Assuntos
Doenças Autoimunes/epidemiologia , Diabetes Mellitus Tipo 1/epidemiologia , Genes MHC da Classe II , Adolescente , Adulto , Idade de Início , Ásia/etnologia , Doenças Autoimunes/etnologia , Doenças Autoimunes/genética , Criança , Pré-Escolar , Colômbia/epidemiologia , Diabetes Mellitus Tipo 1/etnologia , Diabetes Mellitus Tipo 1/genética , Suscetibilidade a Doenças , Etnicidade/genética , Europa (Continente)/etnologia , Feminino , Genótipo , Antígenos HLA-DQ/genética , Cadeias alfa de HLA-DQ , Cadeias beta de HLA-DQ , Antígenos HLA-DR/genética , Cadeias HLA-DRB1 , Haplótipos , Humanos , Indígenas Norte-Americanos , Indígenas Sul-Americanos , Lactente , América Latina/epidemiologia , Masculino , México/epidemiologia , Fatores de Risco , Venezuela/epidemiologia , População BrancaRESUMO
La diabetes tipo I es una enfermedad autoinmune, poligénica con una contribución del 48 por ciento de los genes MHC Case II. El objeto de este trabajo es proveer una explicación para las asociaciones moleculares de dichos genes, mediante el análisis de la inmunogenética de 3 poblaciones mestizas de Latinoamérica. Se estudiaron un total de 606 individuos, 349 pacientes con DMDI y 257 sujetos sanos de tres localidades México DF, Caracas, Venezuela, Medellín, Colombia. Los resultados indican que en los grupos mestizos, los haplotipos diabetogénicos son de contribución mediterránea y que la mayoría de los hoplatipos de protección son de origen indígena. Se demostró que las secuencias relevantes en la expresión de la enfermedad están en los loci DRB1 y DQB1, con un aporte mínimo de DQA1 y que las secuencias relevantes en el reconocimiento del péptido y en la inducción de las células Th1 mediadoras de la activación de la respuesta celular, están localizadas en DRB1-57 y 74 (la presencia de ac. aspártico y ac. glutámico confieren resistencia), moduladas por la presencia de D-57 en DQp del antígeno DQ. Estos datos demuestran la participación de DRB1-DQB1 en la enfermedad y abren caminos para un nuevo manejo de la DMDI