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      Obesity is associated with the Arg389Gly ADRB1 but not with the Trp64Arg ADRB3 polymorphism in children from San Luis Potosí and León, México

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          Abstract

          This research was designed to analyze the possible associations of Arg389Gly ADRB1 and Trp64Arg ADRB3 polymorphisms in children with obesity. A cross-sectional study included 1,046 school-age Mexican participants (6-12 years old) from the cities of San Luis Potosí and León. Children were classified as non-obese or obese according to their body mass index (BMI) percentile; obese children had a BMI≥95th percentile for sex and age. Biochemical data were collected. Polymorphisms were detected using TaqMan qPCR assay. A logistic regression analysis was used to calculate the risk of obesity based on genotypes. Differences were found between groups where obese children had a significant increase in systolic and diastolic blood pressure, fasting plasma glucose, insulin, HOMA-IR, LDL-cholesterol, triglycerides, and lower HDL-cholesterol compared with the normal weight group ( P < 0.05). The distribution of allele frequency in the population was Arg = 87.4 and Gly = 12.6 (Hardy Weinberg equilibrium χ 2 = 3.16, P = 0.07 ); Trp = 81.5 and Arg = 18.5 (Hardy Weinberg equilibrium χ 2 = 2.2, P = 0.14 ) for ADRB1 and ADRB3, respectively. Even though no different frequencies of Arg389Gly polymorphism between groups were found ( P = 0.08), children carriers of one Gly389 ADRB1 allele had a risk for obesity of OR = 1.40 (95%CI, 1.03–1.90, P = 0.03) after adjustment for age and gender. No other association was found for Trp64Arg ADRB3 polymorphism. Only the Arg389Gly ADRB1 polymorphism was associated with risk for obesity in Mexican children.

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          Centers for Disease Control and Prevention 2000 growth charts for the United States: improvements to the 1977 National Center for Health Statistics version.

          To present a clinical version of the 2000 Centers for Disease Control and Prevention (CDC) growth charts and to compare them with the previous version, the 1977 National Center for Health Statistics (NCHS) growth charts. The 2000 CDC percentile curves were developed in 2 stages. In the first stage, the empirical percentiles were smoothed by a variety of parametric and nonparametric procedures. To obtain corresponding percentiles and z scores, we approximated the smoothed percentiles using a modified LMS estimation procedure in the second stage. The charts include of a set of curves for infants, birth to 36 months of age, and a set for children and adolescents, 2 to 20 years of age. The charts represent a cross-section of children who live in the United States; breastfed infants are represented on the basis of their distribution in the US population. The 2000 CDC growth charts more closely match the national distribution of birth weights than did the 1977 NCHS growth charts, and the disjunction between weight-for-length and weight-for-stature or length-for-age and stature-for-age found in the 1977 charts has been corrected. Moreover, the 2000 CDC growth charts can be used to obtain both percentiles and z scores. Finally, body mass index-for-age charts are available for children and adolescents 2 to 20 years of age. The 2000 CDC growth charts are recommended for use in the United States. Pediatric clinics should make the transition from the 1977 NCHS to the 2000 CDC charts for routine monitoring of growth in infants, children, and adolescents.
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            Association of a polymorphism in the beta 3-adrenergic-receptor gene with features of the insulin resistance syndrome in Finns.

            Because visceral obesity predicts insulin resistance, we studied whether alterations in the gene encoding for the beta 3-adrenergic receptor in visceral fat are associated with insulin resistance. We studied the frequency of a cytosine-to-thymidine mutation that results in the replacement of tryptophan by arginine at position 64 (Trp64Arg) of the beta 3-adrenergic receptor by restriction-enzyme digestion with BstOl in 335 subjects from western Finland, 207 of whom were nondiabetic and 128 of whom had non-insulin-dependent diabetes mellitus (NIDDM). We also determined the frequency of the mutation in 156 subjects from southern Finland. Sensitivity to insulin was measured by the hyperinsulinemic-euglycemic clamp technique in 66 randomly selected nondiabetic subjects. In the subjects from western Finland, the frequency of the mutated allele was similar in the nondiabetic subjects and the subjects with NIDDM (12 vs. 11 percent). The mean age of the subjects at the onset of diabetes was lower among those with the mutation than those without it (56 vs. 61 years, P = 0.04). Among the nondiabetic subjects, those with the mutation had a higher ratio of waist to hip circumference (P = 0.02), a greater increase in the serum insulin response after the oral administration of glucose (P = 0.05), a higher diastolic blood pressure (82 vs. 78 mm Hg, P = 0.01), and a lower rate of glucose disposal during the clamp study (5.3 vs. 6.5 mg [29 vs. 36 mumol] per kilogram of body weight per minute; P = 0.04) than the subjects without the mutated allele. In an analysis of sibling pairs, the siblings with the mutation generally had higher waist:hip ratios (P = 0.05) and higher responses of blood glucose and serum insulin after the oral administration of glucose than their siblings without the mutation (P = 0.02 and P = 0.005, respectively). The Trp64Arg allele of the beta 3-adrenergic receptor is associated with abdominal obesity and resistance to insulin and may contribute to the early onset of NIDDM:
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              A gain-of-function polymorphism in a G-protein coupling domain of the human beta1-adrenergic receptor.

              The beta1-adrenergic receptor (beta1AR) is a key cell surface signaling protein expressed in the heart and other organs that mediates the actions of catecholamines of the sympathetic nervous system. A polymorphism in the intracellular cytoplasmic tail near the seventh transmembrane-spanning segment of the human beta1AR has been identified in a cohort of normal individuals. At amino acid position 389, Gly or Arg can be found (allele frequencies 0.26 and 0. 74, respectively), the former previously considered as the human wild-type beta1AR. Using site-directed mutagenesis to mimic the two variants, CHW-1102 cells were permanently transfected to express the Gly-389 and Arg-389 receptors. In functional studies with matched expression, the Arg-389 receptors had slightly higher basal levels of adenylyl cyclase activities (10.7 +/- 1.2 versus 6.1 +/- 0.4 pmol/min/mg). However, maximal isoproterenol-stimulated levels were markedly higher for the Arg-389 as compared to the Gly-389 receptor (63.3 +/- 6.1 versus 20.9 +/- 2.0 pmol/min/mg). Agonist-promoted [35S]guanosine 5'-O-(thiotriphosphate) binding was also increased with the Arg-389 receptor consistent with enhanced coupling to Gs and increased adenylyl cyclase activation. In agonist competition studies carried out in the absence of guanosine 5'-(beta, gamma-imido)triphosphate, high affinity binding could not be resolved with the Gly-389 receptor, whereas Arg-389 displayed an accumulation of the agonist high affinity receptor complex (RH = 26%). Taken together, these data indicate that this polymorphic variation of the human beta1AR results in alterations of receptor-Gs interaction with functional signal transduction consequences, consistent with its localization in a putative G-protein binding domain. The genetic variation of beta1AR at this locus may be the basis of interindividual differences in pathophysiologic characteristics or in the response to therapeutic betaAR agonists and antagonists in cardiovascular and other diseases.
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                Author and article information

                Journal
                J Biomed Res
                J Biomed Res
                JBR
                Journal of Biomedical Research
                Editorial Department of Journal of Biomedical Research
                1674-8301
                2352-4685
                January 2017
                29 September 2016
                : 31
                : 1
                : 40-46
                Affiliations
                [ 1]Faculty of Medicine of the Autonomous University of San Luis Potosí , México, CIACYT-Faculty of Medicine, Av. Sierra Leona 550, Col. Lomas 2a. Sección, C.P. 78210, San Luis Potosí, S.L.P., México
                [ 2]Medical Research Unit in Biochemistry, Hospital de Especialidades, Centro Médico Nacional Siglo XXI del Instituto Mexicano del Seguro Social , México City, C.P. 06720, México
                [ 3]Department of Medical Sciences, Campus León, University of Guanajuato. León , C.P. 37320, México
                [ 4]Chronic Infection and Cancer Division, Research Center on Infectious Diseases, Instituto Nacional de Salud Pública , C.P. 62100, Cuernavaca, Morelos, México
                [ 5]Department of Pharmacy, Campus Guanajuato, University of Guanajuato , Noria Alta C.P. 36050, Guanajuato, México
                Author notes
                [ ]Corresponding author: Jorge A. Alegría-Torres, Ph.D. Department of Pharmacy, Campus Guanajuato, University of Guanajuato, Noria Alta C.P. 36050, Guanajuato, México. Email: giorgio_alegretto@ 123456hotmail.com .

                CLC number: R587.1, Document code: A

                The authors reported no conflict of interests.

                Article
                jbr-31-01-040
                10.7555/JBR.30.20150169
                5274511
                8a11ae9a-f05e-4b26-85e5-19388cf0cbf1
                © 2017 by the Journal of Biomedical Research. All rights reserved.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited

                History
                : 12 December 2015
                : 02 April 2016
                : 23 June 2016
                Page count
                Figures: 0, Tables: 3, References: 41, Pages: 7
                Categories
                Original Article

                childhood obesity,β-adrenergic receptor (adrb) gene,polymorphisms,mexican children

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