Central GIP signaling stimulates peripheral GIP release and promotes insulin and pancreatic polypeptide secretion in nonhuman primates

Glucose-dependent insulinotropic polypeptide (GIP) has important actions on whole body metabolic function. GIP and its receptor are also present in the central nervous system and have been linked to neurotrophic actions. Metabolic effects of central nervous system GIP signaling have not been reported. We investigated whether centrally administered GIP could increase peripheral plasma GIP concentrations and influence the metabolic response to a mixed macronutrient meal in nonhuman primates. An infusion and sampling system was developed to enable continuous intracerebroventricular (ICV) infusions with serial venous sampling in conscious nonhuman primates. Male baboons (Papio sp.) that were healthy and had normal body weights (28.9 ± 2.1 kg) were studied (n = 3). Animals were randomized to receive continuous ICV infusions of GIP (20 pmol·kg−1·h−1) or vehicle before and over the course of a 300-min mixed meal test (15 kcal/kg, 1.5g glucose/kg) on two occasions. A significant increase in plasma GIP concentration was observed under ICV GIP infusion (66.5 ± 8.0 vs. 680.6 ± 412.8 pg/ml, P = 0.04) before administration of the mixed meal. Increases in postprandial, but not fasted, insulin (P = 0.01) and pancreatic polypeptide (P = 0.04) were also observed under ICV GIP. Effects of ICV GIP on fasted or postprandial glucagon, glucose, triglyceride, and free fatty acids were not observed. Our data demonstrate that central GIP signaling can promote increased plasma GIP concentrations independent of nutrient stimulation and increase insulin and pancreatic polypeptide responses to a mixed meal

Regional-level estimation of expected years of life lost attributable to overweight and obesity among Mexican adults

Background: Excess body weight has become a major public health problem worldwide, and the burden of overweight and obesity was calculated in this work from a health economics perspective. Objective: To estimate the burden of disease attributable to overweight and obesity among males and females aged 20 years and older using years of life lost (YLL) and age-standardized YLL rates (ASYLL), and to rank the leading causes of premature death. Design: A cross-sectional study took place (2010–2014) and 6,054 deaths were analyzed. Thirteen basic causes of death associated with overweight or obesity were included. The population attributable fraction (PAF), YLL, and ASYLL were calculated. Results: The overall burden attributable to overweight and obesity was 36,087 YLL, and the estimated ASYLL per 10,000 persons was 1,098 and 1,029 in males and females, respectively. Type 2 diabetes mellitus was the main cause of premature death (males, 968 ASYLL; females, 772 ASYLL). Conclusions: Overweight and obesity are major risk factors of chronic diseases that are main causes of premature death in the study population. Strategies for preventing overweight and obesity may decrease the incidence and mortality associated with these non-communicable diseases. ASYLL seems to be an indicator that is particularly well adapted to decision-making in public health

Association of the polymorphism 12109g>A from the gene as a risk factor for preterm birth

Introduction: Preterm birth is the most important cause of neonatal mortality and morbidity. It is a multifactorial disease with different etiologies, including genetic factors. Genetic variability is represented by single nucleotide polymorphisms (SNPs) in genes of proteins involved in the contractile activity. We determine the association between SNP 12109G> A in REN associated with preterm birth and premature rupture of membrane. Materials and methods: A study of cases ( N =112, 22–36 weeks of gestation; mean: 31, 95% confidence interval 30.7–32.2) and controls ( N =66; 38–40 weeks of gestation from the last menstrual period; mean: 39.8, 95% confidence interval 38.9–39.4) was performed. Genomic DNA was isolated in all patients from peripheral blood. The SNP 12109G> A ( Mbo I) in REN was typified by PCR-restriction fragment length polymorphism. Results: A significant difference in the case group for the SNP 12109G>A was observed. The A allele was increased in women with preterm birth (81% cases vs . 15% control, p A has odds ratio 6.62 (95% confidence interval 3.14–14.15), which means a high risk of preterm birth/premature rupture of membrane in presence of allele A, both in homozygotes and in heterozygotes. Conclusion: Allelic frequency of A of SNP 12109G>A was higher in women with preterm birth than in women with normal vaginal delivery and could be considered a risk factor

Reference values for amino acids and acylcarnitines in peripheral blood in Quarter horses and American Miniature horses

Abstract Background Free amino acids and acylcarnitines circulating in the blood can be used for diagnosis for metabolic illness and imbalances. To date, the normal reference ranges of amino acids and acylcarnitines in horse peripheral blood have not been established. In this study, the concentrations of 12 amino acids and 26 acylcarnitines were determined by tandem mass spectrometry in complete blood from 100 healthy horses (50 Quarter horses (QH) [23 males and 27 females] and 50 American Miniature horses (AMH) [15 males and 35 females]) with no signs of metabolic disease. The means and standard deviations were determined and data statistically analyzed. Findings Concentrations of short, medium, and long chain acylcarnitines were significantly higher in male AMH than in male QH. The concentrations of the amino acids alanine, arginine, glycine, proline (glycogenic), and leucine (ketogenic) were higher in the QH than in the AMH. Female AMH had higher concentrations of propionylcarnitine, leucine, proline, arginine, and ornithine than female QH. Conclusions Normal reference ranges of amino acids and acylcarnitines were established for AMH and QH. Significant differences were found in concentration of these compounds between breeds and gender