19 research outputs found
Comparison of Risk Factors for Developing Liver Fibrosis in Subjects With and Without Metabolic Syndrome: A Cohort Study.
Background:
Metabolic syndrome (MS), a combination of diabetes, high blood pressure and obesity, is a well-known risk factor for developing non-alcoholic fatty liver disease, condition that can lead to serious liver damage such as liver fibrosis (LF), which is characterized by excessive deposition of connective tissue, progressing to cirrhosis and hepatocellular carcinoma. Nevertheless, subjects without MS may also develop LF. Non-invasive LF predictors based upon anthropometric and biochemical data have been reported.
Aim:
To compare anthropometric, genetic, and biochemical parameters in subjects with or without MS, and at risk for developing liver fibrosis.
Methods:
A randomized sample of 200 individuals was taken from the 2015 Nuevo León State Health Survey. Inclusion criteria were age ≥18 and a previously stored blood sample. According to the parameters obtained, subjects were classified as either with or without MS and their NAFLD fibrosis score was calculated considering variables such as age, BMI, glycemia, albumin, platelets, and AST/ALT ratio, to establish a high or low risk of LF. Comparisons of weight, age, BMI, blood glucose, total cholesterol, triglycerides, platelets, albumin, AST/ALT ratio, and HDL were made between groups. DNA was extracted from stored blood samples and genotyped, using q-PCR, according to variants in four genes related to: fatty acid (FA) metabolism (PNPLA3, rs738409), adipocyte differentiation (PLIN2, rs35568725), glucose metabolism (GCKR, rs1260326 and rs780094), and BMI (UCP2, rs659366). Statistical analysis was performed with SPSS v.22. A p value <0.05 was taken as level of significance.
Results:
A total of 134 subjects were included and divided into four groups (n): With MS+ high risk (35), With MS+ low risk (34), Without MS+ high risk (32), Without MS+ low risk (33). Table 1 shows the main significative findings. Higher age, low platelet count, and increased AST/ALT ratio, were significantly different in high risk subjects, independently of the presence of MS. No association between the polymorphisms and risk for fibrosis was found. In subjects at high risk for LF, statistical significance was found for high cholesterol blood levels (OR= 20.0 (95%CI 2.87;139.38) in carriers of the T allele of GCKR rs780094 polymorphism.
Conclusion:
Aging, thrombocytopenia, and increased transaminases, the last two indicators of liver disfunction, were found as important risk factors for LF in subjects without metabolic syndrome. None of the genetic variants analyzed resulted associated to risk of LF, although sample size could be a factor. GCKR rs780094 variant was found related with risk for hypercholesterolemia, even though dyslipidemia was not found associated with risk of LF in the present study.  
Genetic variants in KCNJ11, TCF7L2 and HNF4A are associated with type 2 diabetes, BMI and dyslipidemia in families of Northeastern Mexico: A pilot study
Abstract. The aim of the present study was to investigate whether genetic markers considered risk factors for metabolic syndromes, including dyslipidemia, obesity and type 2 diabetes mellitus (T2DM), can be applied to a Northeastern Mexican population. A total of 37 families were analyzed for 63 single nucleotide polymorphisms (SNPs), and the age, body mass index (BMI), glucose tolerance values and blood lipid levels, including those of cholesterol, low-density lipoprotein (LDL), very LDL (VLDL), high-density lipoprotein (HDL) and triglycerides were evaluated. Three genetic markers previously associated with metabolic syndromes were identified in the sample population, including KCNJ11, TCF7L2 and HNF4A. The KCNJ11 SNP rs5210 was associated with T2DM, the TCF7L2 SNP rs11196175 was associated with BMI and cholesterol and LDL
levels, the TCF7L2 SNP rs12255372 was associated with BMI and HDL, VLDL and triglyceride levels, and the HNF4A SNP rs1885088 was associated with LDL levels (P<0.05)
Molecular cloning of the myo-inositol oxygenase gene from the kidney of baboons
Abstract. The enzyme myo-Inositol oxygenase (MIOX) is also termed ALDRL6. It is a kidney‑specific member of the aldo‑keto reductase family. MIOX catalyzes the first reaction involved in the myo‑inositol metabolism signaling pathway and is fully expressed in mammalian tissues. MIOX catalyzes the oxidative cleavage of myo‑Inositol and its epimer, D-chiro-Inositol to D-glucuronate. The dioxygen-dependent cleavage of the C6 and C1 bond in myo‑Inositol is achieved by utilizing the Fe2+/Fe3+ binuclear iron center of MIOX. This enzyme has also been implicated in the complications of diabetes, including diabetic nephropathy. The MIOX gene was amplified with reverse transcription‑polymerase chain reaction from baboon tissue samples, and the product
was cloned and sequenced. MIOX expression in the baboon kidney is described in the present study. The percentages of nucleotide and amino acid similarities between baboons and humans were 95 and 96%, respectively. The MIOX protein of the baboon may be structurally identical to that of humans. Furthermore, the evolutionary changes, which have affected these sequences, have resulted from purifying forces.
Key words: animal models, gene expression, kidney, myo-inositol oxygenase, Old World monke
Relatório de estágio em farmácia comunitária
Relatório de estágio realizado no âmbito do Mestrado Integrado em Ciências Farmacêuticas, apresentado à Faculdade de Farmácia da Universidade de Coimbr
Análisis de los valores sanguíneos de carnitina y aminoácidos en embarazos complicados con preeclampsia y síndrome de HELLP
Tesis doctoral inédita leída en la Universidad Autónoma de Madrid, Facultad de Medicina. Departamento de Medicina. Fecha de lectura: 3 de Julio de 200
Actividad antituberculosa de dos colectas del alga marina Sargassum horridum
Trabajo presentado en la 9a Reunión Internacional de Investigadores en Productos Naturales, celebrada en Pachuca (México) del 29 al 31 Mayo de 2013Peer Reviewe
Deficiencia de vitamina D en madres y neonatos mexicanos
El objetivo es establecer la prevalecencia de la deficiencia de vitamina D en madres y sus neonatos, y analizar factores de riesgo asociado
Molecular evolution and expression profile of the chemerine encoding gene RARRES2 in baboon and chimpanzee
BACKGROUND: Chemerin, encoded by the retinoic acid receptor responder 2 (RARRES2) gene is an adipocytesecreted protein with autocrine/paracrine functions in adipose tissue, metabolism and inflammation with a recently described function in vascular tone regulation, liver, steatosis, etc. This molecule is believed to represent a critical endocrine signal linking obesity to diabetes. There are no data available regarding evolution of RARRES2 in non-human primates and great apes. Expression profile and orthology in RARRES2 genes are unknown aspects in the biology of this multigene family in primates. Thus; we attempt to describe expression profile and phylogenetic relationship as complementary knowledge in the function of this gene in primates. To do that, we performed A RT-PCR from different tissues obtained during necropsies. Also we tested the hypotheses of positive evolution, purifying selection, and neutrality. And finally a phylogenetic analysis was made between primates RARRES2 protein. RESULTS: RARRES2 transcripts were present in liver, lung, adipose tissue, ovary, pancreas, heart, hypothalamus and pituitary tissues. Expression in kidney and leukocytes were not detectable in either species. It was determined that the studied genes are orthologous. CONCLUSIONS: RARRES2 evolution fits the hypothesis of purifying selection. Expression profiles of the RARRES2 gene are similar in baboons and chimpanzees and are also phylogenetically related