3 research outputs found

    Identification of anthropometric indices that best correlate with insulin sensitivity and insulin resistance from subjects from central Mexico

    No full text
    "Insulin Sensitivity (IS) and Insulin Resistance (IR) mark the development of Type 2 Diabetes. Many reports have demonstrated that anthropometric indices can detect IS and IR, however ethnic variations can influence the optimal cutoff value. Therefore, the aim of this study was to determine the optimal cutoff value for Waist Circumference (WC), Body-Mass Index (BMI), Waist-To-Hip Ratio (WHR), Waist-To-Height Ratio (WHtR), and percent Body Fat (BF %) to determine IS and IR from subjects from central Mexico. Methods: WC, BMI, WHR, WHtR, BF%, fasting plasma glucose, and insulin were determined in 569 subjects (male=286 & females=283; ages: 18-84). IR and IS were determined by the Homeostatic Model Assessment online calculator and Quantitative Insulin Sensitivity Check Index, respectively. The area under the Receiver Operating Characteristic curve (AUC) and Youden´s index for each anthropometric index was calculated to determine its cutoff value. Cutoff value´s efficiency was measured by determining the test´s accuracy"

    Obese first-degree relatives of patients with type 2 diabetes with elevated triglyceride levels exhibit increased β-cell function

    No full text
    "Type 2 diabetes mellitus (T2DM) is characterized as a disease continuum that is marked by metabolic changes that are present for several years, sometimes well before frank diagnosis of T2DM. Genetic predisposition, ethnicity, geography, alterations in BMI, and lipid profile are considered important markers for the pathogenesis of T2DM through mechanisms that remain unresolved and controversial. The aim of this study was to investigate the relationship between triglycerides (TGs) and β-cell function, insulin resistance (IR), and insulin sensitivity (IS) in obese first-degree relatives of patients with T2DM (FDR-T2DM) among subjects from central Mexico with normal glucose tolerance (NGT). Methods: We studied 372 FDR-T2DM subjects (ages,18-65) and determined body mass index (BMI), fasting plasma glucose (FPG), oral glucose tolerance test (OGTT), insulin, and TGs levels. Subjects were categorized based on glycemic control [NGT, prediabetes (PT2DM), or T2DM]. NGT subjects were further categorized by BMI [normal weight (Ob-) or obese (Ob+)] and TGs levels (TG-, <150 mg/dL, or TG+, ≥150 mg/dL). β-cell function, IR, and IS were determined by the homeostasis model assessment of β-cell function (HOMA2-β), homeostasis model assessment of insulin resistance (HOMA2-IR), and Quantitative Insulin Sensitivity Check Index (QUICKI) indices, respectively"

    Metallothionein-1 and nitric oxide expression are inversely correlated in a murine model of Chagas disease

    No full text
    "Chagas disease, caused by Trypanosoma cruzi, represents an endemic among Latin America countries. The participation of free radicals, especially nitric oxide (NO), has been demonstrated in the pathophysiology of seropositive individuals with T. cruzi. In Chagas disease, increased NO contributes to the development of cardiomyopathy and megacolon. Metallothioneins (MTs) are efficient free radicals scavengers of NO in vitro and in vivo. Here, we developed a murine model of the chronic phase of Chagas disease using endemic T. cruzi RyCH1 in BALB/c mice, which were divided into four groups: infected non-treated (Inf), infected N-monomethyl-L-arginine treated (Inf L-NAME), non-infected L-NAME treated and non-infected vehicle-treated. We determined blood parasitaemia and NO levels, the extent of parasite nests in tissues and liver MT-I expression levels. It was observed that NO levels were increasing in Inf mice in a time-dependent manner. Inf L-NAME mice had fewer T. cruzi nests in cardiac and skeletal muscle with decreased blood NO levels at day 135 post infection. This affect was negatively correlated with an increase of MT-I expression (r = -0.8462, p < 0.0001). In conclusion, we determined that in Chagas disease, an unknown inhibitory mechanism reduces MT-I expression, allowing augmented NO levels"
    corecore