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Obesity GAd2 gene

Jai Prakash, Balraj Mittal, Shally Awasthi, Neena Srivastava
BACKGROUND: Obesity associated with type 2 diabetes, and hypertension increased mortality and morbidity. Glutamate decarboxylase 2 (GAD2) gene is associated with obesity and it regulate food intake and insulin level. We investigated the association of GAD-2gene -243A>G (rs2236418) and +61450C>A (rs992990) polymorphisms with obesity and related phenotypes. METHODS: Insulin, glucose and lipid levels were estimated using standard protocols. All subjects were genotyped (PCR-RFLP) method...
April 2016: Iranian Journal of Public Health
Ke-Chang Chen, Yi-Chen Lin, Wen-Chii Chao, Hsieh-Kun Chung, Su-Sheng Chi, Wen-Sheng Liu, Wen-Tung Wu
BACKGROUND AND OBJECTIVES: It has been proposed that glutamate decarboxylase 2 and the dopamine D2 receptor are involved in the brain reward cascade to increase carbohydrate craving and cause eating disorders. We investigated the association between the polymorphisms of the GAD2 and DRD2 genes and obesity with a higher body mass index (BMI) in Taiwanese patients. DESIGN AND SETTING: A retrospective, case-control study at Antai Tian-Sheng Memorial Hospital from 1 January to 31 December 2009...
March 2012: Annals of Saudi Medicine
Anne C Choquette, Simone Lemieux, Angelo Tremblay, Vicky Drapeau, Claude Bouchard, Marie-Claude Vohl, Louis Pérusse
The glutamate decarboxylase 2 (GAD2) gene encodes for the glutamic acid decarboxylase enzyme (GAD65), which is implicated in the formation of the gamma-aminobutyric acid (GABA), a neurotransmitter involved in the regulation of food intake. The objective of the present study was to test for association between GAD2 single-nucleotide polymorphisms (SNPs) and eating behaviors, dietary intake and obesity in subjects (n=873) from the Quebec Family Study (QFS). Energy and macronutrient intakes were measured using a 3-day dietary record and eating behaviors were assessed using the Three-Factor Eating Questionnaire (TFEQ)...
October 19, 2009: Physiology & Behavior
G H Goossens, L Petersen, E E Blaak, G Hul, P Arner, A Astrup, P Froguel, K Patel, O Pedersen, J Polak, J-M Oppert, J A Martinez, T I A Sørensen, W H M Saris
BACKGROUND: Part of the heterogeneity of the obesity phenotype may originate from genetic differences between obese individuals that may influence energy expenditure (EE). OBJECTIVE: To examine if common single-nucleotide polymorphisms (SNPs) in genes related to obesity-associated phenotypes are associated with postabsorptive resting energy expenditure (REE) and postprandial REE in obese individuals. DESIGN AND METHODS: Postabsorptive REE and 3-h postprandial REE (liquid test meal containing 95% fat, energy content 50% of estimated REE) were measured in 743 obese individuals from eight clinical centres in seven European countries...
June 2009: International Journal of Obesity: Journal of the International Association for the Study of Obesity
Selma Feldman Witchel, Carlie White, Ingrid Libman
OBJECTIVE: To test the a priori hypothesis that the frequency of a single-nucleotide polymorphism (SNP) located in the promoter region of the glutamate decarboxylase 2 (GAD2) gene (-243A-->G) would be overrepresented among children with higher body mass index (BMI) values. DESIGN: Genotype-phenotype correlation study. SETTING: University-based pediatric endocrinology practice. PATIENT(S): Eighty-seven girls with PP and 70 adolescent girls with hyperandrogenism...
May 2009: Fertility and Sterility
T W Boesgaard, S I Castella, G Andersen, A Albrechtsen, T Sparsø, K Borch-Johnsen, T Jørgensen, T Hansen, O Pedersen
AIMS: The glutamate decarboxylase gene (GAD2) encodes GAD65, an enzyme catalysing the production of the gamma-aminobutyric acid (GABA) which interacts with neuropeptide Y to stimulate food intake. It has been suggested that in pancreatic islets, GABA serves as a functional regulator of pancreatic hormone release. Conflicting results have been reported concerning the potential impact of GAD2 variation on estimates of energy metabolism. The aim of this study was to elucidate potential associations between the GAD2-243A-->G polymorphism and levels of body mass index (BMI) and estimates of glycaemia...
July 2007: Diabetic Medicine: a Journal of the British Diabetic Association
Christopher J Groves, Eleftheria Zeggini, Mark Walker, Graham A Hitman, Jonathan C Levy, Stephen O'Rahilly, Andrew T Hattersley, Mark I McCarthy, Steven Wiltshire
Obesity is a major health problem, and many family-based studies have suggested that it has a strong genetic basis. We performed a genome-wide quantitative trait linkage scan for loci influencing BMI in 573 pedigrees from the U.K. We identified genome-wide significant linkage (logarithm of odds = 3.74, between D10S208 and D10S196, genome-wide P=0.0186) on chromosome 10p. The size of our study population and the statistical significance of our findings provide substantial contributions to the body of evidence for a locus on chromosome 10p...
June 2006: Diabetes
Hemant K Tiwari, Luigi Bouchard, Louis Pérusse, David B Allison
Morbidly obese individuals represent one of the fastest growing subpopulations of obese individuals. Thus, it is of significant interest to broaden our understanding of the potential genetic causes of this public health concern. A recent study investigated a role of positional candidate gene GAD2 (the gene for glutamic acid decarboxylase) in the development of morbid obesity. This commentary carefully examines the genetic and functional arguments for and against the GAD2 gene as an influential gene for obesity...
September 2005: Nutrition Reviews
Michael M Swarbrick, Björn Waldenmaier, Len A Pennacchio, Denise L Lind, Martha M Cavazos, Frank Geller, Raphael Merriman, Anna Ustaszewska, Mary Malloy, André Scherag, Wen-Chi Hsueh, Winfried Rief, Franck Mauvais-Jarvis, Clive R Pullinger, John P Kane, Robert Dent, Ruth McPherson, Pui-Yan Kwok, Anke Hinney, Johannes Hebebrand, Christian Vaisse
The demonstration of association between common genetic variants and chronic human diseases such as obesity could have profound implications for the prediction, prevention, and treatment of these conditions. Unequivocal proof of such an association, however, requires independent replication of initial positive findings. Recently, three (-243 A>G, +61450 C>A, and +83897 T>A) single nucleotide polymorphisms (SNPs) within glutamate decarboxylase 2 (GAD2) were found to be associated with class III obesity (body mass index > 40 kg/m2)...
September 2005: PLoS Biology
David Meyre, Philippe Boutin, Agnès Tounian, Marianne Deweirder, Mounir Aout, Béatrice Jouret, Barbara Heude, Jacques Weill, Maite Tauber, Patrick Tounian, Philippe Froguel
Low birth weight is a risk factor for obesity and type 2 diabetes. The fetal insulin hypothesis proposes that low birth weight might be mediated partly by genetic factors that impair insulin secretion/sensitivity during the fetal stage, as shown for glucokinase, the ATP-sensitive K+ channel subunit Kir6.2, and the small heterodimer partner genes. Glutamic acid decarboxylase 2 gene (GAD2) overexpression impairs insulin secretion in animals. Recently, polymorphisms in the GAD2 gene were associated with adult morbid obesity...
April 2005: Journal of Clinical Endocrinology and Metabolism
Philippe Boutin, Christian Dina, Francis Vasseur, Séverine Dubois, Laetitia Corset, Karin Séron, Lynn Bekris, Janice Cabellon, Bernadette Neve, Valérie Vasseur-Delannoy, Mohamed Chikri, M Aline Charles, Karine Clement, Ake Lernmark, Philippe Froguel
The gene GAD2 encoding the glutamic acid decarboxylase enzyme (GAD65) is a positional candidate gene for obesity on Chromosome 10p11-12, a susceptibility locus for morbid obesity in four independent ethnic populations. GAD65 catalyzes the formation of gamma-aminobutyric acid (GABA), which interacts with neuropeptide Y in the paraventricular nucleus to contribute to stimulate food intake. A case-control study (575 morbidly obese and 646 control subjects) analyzing GAD2 variants identified both a protective haplotype, including the most frequent alleles of single nucleotide polymorphisms (SNPs) +61450 C>A and +83897 T>A (OR = 0...
December 2003: PLoS Biology
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