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1H-MRS Measured Ectopic Fat in Liver and Muscle in Danish Lean and Obese Children and Adolescents.

https://arctichealth.org/en/permalink/ahliterature273208
Source
PLoS One. 2015;10(8):e0135018
Publication Type
Article
Date
2015
Author
Cilius Esmann Fonvig
Elizaveta Chabanova
Ehm Astrid Andersson
Johanne Dam Ohrt
Oluf Pedersen
Torben Hansen
Henrik S Thomsen
Jens-Christian Holm
Source
PLoS One. 2015;10(8):e0135018
Date
2015
Language
English
Publication Type
Article
Keywords
Adolescent
Anthropometry
Blood Glucose - analysis
Blood pressure
Body mass index
Body Weight
Cardiovascular Diseases - physiopathology
Child
Cross-Sectional Studies
Denmark
Dyslipidemias - blood
Fatty Liver - pathology
Female
Humans
Insulin - blood
Insulin Resistance
Intra-Abdominal Fat - pathology
Linear Models
Lipids - blood
Liver - metabolism - pathology
Male
Muscles - pathology
Overweight
Pediatric Obesity - blood - pathology
Proton Magnetic Resonance Spectroscopy
Puberty
Sex Factors
Subcutaneous Fat - pathology
Abstract
This cross sectional study aims to investigate the associations between ectopic lipid accumulation in liver and skeletal muscle and biochemical measures, estimates of insulin resistance, anthropometry, and blood pressure in lean and overweight/obese children.
Fasting plasma glucose, serum lipids, serum insulin, and expressions of insulin resistance, anthropometry, blood pressure, and magnetic resonance spectroscopy of liver and muscle fat were obtained in 327 Danish children and adolescents aged 8-18 years.
In 287 overweight/obese children, the prevalences of hepatic and muscular steatosis were 31% and 68%, respectively, whereas the prevalences in 40 lean children were 3% and 10%, respectively. A multiple regression analysis adjusted for age, sex, body mass index z-score (BMI SDS), and pubertal development showed that the OR of exhibiting dyslipidemia was 4.2 (95%CI: [1.8; 10.2], p = 0.0009) when hepatic steatosis was present. Comparing the simultaneous presence of hepatic and muscular steatosis with no presence of steatosis, the OR of exhibiting dyslipidemia was 5.8 (95%CI: [2.0; 18.6], p = 0.002). No significant associations between muscle fat and dyslipidemia, impaired fasting glucose, or blood pressure were observed. Liver and muscle fat, adjusted for age, sex, BMI SDS, and pubertal development, associated to BMI SDS and glycosylated hemoglobin, while only liver fat associated to visceral and subcutaneous adipose tissue and intramyocellular lipid associated inversely to high density lipoprotein cholesterol.
Hepatic steatosis is associated with dyslipidemia and liver and muscle fat depositions are linked to obesity-related metabolic dysfunctions, especially glycosylated hemoglobin, in children and adolescents, which suggest an increased cardiovascular disease risk.
Notes
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PubMed ID
26252778 View in PubMed
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Common variants in LEPR, IL6, AMD1, and NAMPT do not associate with risk of juvenile and childhood obesity in Danes: a case-control study.

https://arctichealth.org/en/permalink/ahliterature272210
Source
BMC Med Genet. 2015;16:105
Publication Type
Article
Date
2015
Author
Mette Hollensted
Tarunveer S Ahluwalia
Christian Theil Have
Niels Grarup
Cilius Esmann Fonvig
Tenna Ruest Haarmark Nielsen
Cæcilie Trier
Lavinia Paternoster
Oluf Pedersen
Jens-Christian Holm
Thorkild I A Sørensen
Torben Hansen
Source
BMC Med Genet. 2015;16:105
Date
2015
Language
English
Publication Type
Article
Keywords
Adenosylmethionine Decarboxylase - genetics
Body mass index
Case-Control Studies
Cytokines - genetics
Denmark
Female
Genetic Predisposition to Disease
Humans
Interleukin-6 - genetics
Male
Middle Aged
Nicotinamide Phosphoribosyltransferase - genetics
Pediatric Obesity - genetics
Polymorphism, Single Nucleotide
Receptors, Leptin - genetics
Young Adult
Abstract
Childhood obesity is a highly heritable disorder, for which the underlying genetic architecture is largely unknown. Four common variants involved in inflammatory-adipokine triggering (IL6 rs2069845, LEPR rs1137100, NAMPT rs3801266, and AMD1 rs2796749) have recently been associated with obesity and related traits in Indian children. The current study aimed to examine the effect of these variants on risk of childhood/juvenile onset obesity and on obesity-related quantitative traits in two Danish cohorts.
Genotype information was obtained for 1461 young Caucasian men from the Genetics of Overweight Young Adults (GOYA) study (overweight/obese: 739 and normal weight: 722) and the Danish Childhood Obesity Biobank (TDCOB; overweight/obese: 1022 and normal weight: 650). Overweight/obesity was defined as having a body mass index (BMI) =25 kg/m(2); among children and youths, this cut-off was defined using age and sex-specific cut-offs corresponding to an adult body mass index =25 kg/m(2). Risk of obesity was assessed using a logistic regression model whereas obesity-related quantitative measures were analyzed using a general linear model (based on z-scores) stratifying on the case status and adjusting for age and gender. Meta-analyses were performed using the fixed effects model.
No statistically significant association with childhood/juvenile obesity was found for any of the four gene variants among the individual or combined analyses (rs2069845 OR: 0.94 CI: 0.85-1.04; rs1137100 OR: 1.01 CI: 0.90-1.14; rs3801266: 0.96 CI: 0.84-1.10; rs2796749 OR: 1.02 CI: 0.90-1.15; p?>?0.05). However, among normal weight children and juvenile men, the LEPR rs1137100 A-allele significantly associated with lower BMI (ß?=?-0.12, p?=?0.0026).
The IL6, LEPR, NAMPT, and AMD1 gene variants previously found to associate among Indian children did not associate with risk of obesity or obesity-related quantitative measures among Caucasian children and juvenile men from Denmark.
Notes
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PubMed ID
26558825 View in PubMed
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Development of a type 2 diabetes risk model from a panel of serum biomarkers from the Inter99 cohort.

https://arctichealth.org/en/permalink/ahliterature150000
Source
Diabetes Care. 2009 Jul;32(7):1207-12
Publication Type
Article
Date
Jul-2009
Author
Janice A Kolberg
Torben Jørgensen
Robert W Gerwien
Sarah Hamren
Michael P McKenna
Edward Moler
Michael W Rowe
Mickey S Urdea
Xiaomei M Xu
Torben Hansen
Oluf Pedersen
Knut Borch-Johnsen
Author Affiliation
Tethys Bioscience, Emeryville, California, USA. jkolberg@tethysbio.com
Source
Diabetes Care. 2009 Jul;32(7):1207-12
Date
Jul-2009
Language
English
Publication Type
Article
Keywords
Adiponectin - blood
Adult
Biological Markers - blood
Blood Glucose - metabolism
Body mass index
C-Reactive Protein - metabolism
Case-Control Studies
Cohort Studies
Denmark - epidemiology
Diabetes Mellitus, Type 2 - blood - epidemiology
Female
Ferritins - blood
Hemoglobin A, Glycosylated - metabolism
Humans
Immunoassay
Insulin - blood
Male
Middle Aged
Receptors, Interleukin-2 - blood
Risk assessment
Risk factors
Abstract
The purpose of this study was to develop a model for assessing the 5-year risk of developing type 2 diabetes from a panel of 64 circulating candidate biomarkers.
Subjects were selected from the Inter99 cohort, a longitudinal population-based study of approximately 6,600 Danes in a nested case-control design with the primary outcome of 5-year conversion to type 2 diabetes. Nondiabetic subjects, aged >or=39 years, with BMI >or=25 kg/m(2) at baseline were selected. Baseline fasting serum samples from 160 individuals who developed type 2 diabetes and from 472 who did not were tested. An ultrasensitive immunoassay was used to measure of 58 candidate biomarkers in multiple diabetes-associated pathways, along with six routine clinical variables. Statistical learning methods and permutation testing were used to select the most informative biomarkers. Risk model performance was estimated using a validated bootstrap bias-correction procedure.
A model using six biomarkers (adiponectin, C-reactive protein, ferritin, interleukin-2 receptor A, glucose, and insulin) was developed for assessing an individual's 5-year risk of developing type 2 diabetes. This model has a bootstrap-estimated area under the curve of 0.76, which is greater than that for A1C, fasting plasma glucose, fasting serum insulin, BMI, sex-adjusted waist circumference, a model using fasting glucose and insulin, and a noninvasive clinical model.
A model incorporating six circulating biomarkers provides an objective and quantitative estimate of the 5-year risk of developing type 2 diabetes, performs better than single risk indicators and a noninvasive clinical model, and provides better stratification than fasting plasma glucose alone.
Notes
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Comment In: Diabetes Care. 2010 Feb;33(2):e28; author reply e2920103554
PubMed ID
19564473 View in PubMed
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Dietary ascorbic acid and subsequent change in body weight and waist circumference: associations may depend on genetic predisposition to obesity--a prospective study of three independent cohorts.

https://arctichealth.org/en/permalink/ahliterature259633
Source
Nutr J. 2014;13:43
Publication Type
Article
Date
2014
Author
Sofus C Larsen
Lars Angquist
Tarunveer Singh Ahluwalia
Tea Skaaby
Nina Roswall
Anne Tjønneland
Jytte Halkjær
Kim Overvad
Oluf Pedersen
Torben Hansen
Allan Linneberg
Lise Lotte N Husemoen
Ulla Toft
Berit L Heitmann
Thorkild I A Sørensen
Source
Nutr J. 2014;13:43
Date
2014
Language
English
Publication Type
Article
Keywords
Ascorbic Acid - administration & dosage
Body mass index
Body Weight
Cohort Studies
Denmark
Diet
Female
Genetic Predisposition to Disease
Humans
Male
Middle Aged
Obesity - genetics
Polymorphism, Single Nucleotide
Prospective Studies
Waist Circumference
Waist-Hip Ratio
Abstract
Cross-sectional data suggests that a low level of plasma ascorbic acid positively associates with both Body Mass Index (BMI) and Waist Circumference (WC). This leads to questions about a possible relationship between dietary intake of ascorbic acid and subsequent changes in anthropometry, and whether such associations may depend on genetic predisposition to obesity. Hence, we examined whether dietary ascorbic acid, possibly in interaction with the genetic predisposition to a high BMI, WC or waist-hip ratio adjusted for BMI (WHR), associates with subsequent annual changes in weight (?BW) and waist circumference (?WC).
A total of 7,569 participants' from MONICA, the Diet Cancer and Health study and the INTER99 study were included in the study. We combined 50 obesity associated single nucleotide polymorphisms (SNPs) in four genetic scores: a score of all SNPs and a score for each of the traits (BMI, WC and WHR) with which the SNPs associate. Linear regression was used to examine the association between ascorbic acid intake and ?BW or ?WC. SNP-score?×?ascorbic acid interactions were examined by adding product terms to the models.
We found no significant associations between dietary ascorbic acid and ?BW or ?WC. Regarding SNP-score?×?ascorbic acid interactions, each additional risk allele of the 14 WHR associated SNPs associated with a ?WC of 0.039?cm/year (P?=?0.02, 95% CI: 0.005 to 0.073) per 100?mg/day higher ascorbic acid intake. However, the association to ?WC only remained borderline significant after adjustment for ?BW.
In general, our study does not support an association between dietary ascorbic acid and ?BW or ?WC, but a diet with a high content of ascorbic acid may be weakly associated to higher WC gain among people who are genetically predisposed to a high WHR. However, given the quite limited association any public health relevance is questionable.
Notes
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PubMed ID
24886192 View in PubMed
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Do gene variants influencing adult adiposity affect birth weight? A population-based study of 24 loci in 4,744 Danish individuals.

https://arctichealth.org/en/permalink/ahliterature138658
Source
PLoS One. 2010;5(12):e14190
Publication Type
Article
Date
2010
Author
Ehm A Andersson
Kasper Pilgaard
Charlotta Pisinger
Marie N Harder
Niels Grarup
Kristine Færch
Camilla Sandholt
Pernille Poulsen
Daniel R Witte
Torben Jørgensen
Allan Vaag
Oluf Pedersen
Torben Hansen
Author Affiliation
Hagedorn Research Institute, Gentofte, Denmark.
Source
PLoS One. 2010;5(12):e14190
Date
2010
Language
English
Publication Type
Article
Keywords
Adiposity - genetics
Alleles
Birth weight
Body Composition
Body mass index
Denmark
Female
Genetic Variation
Genome-Wide Association Study
Genotype
Humans
Infant, Newborn
Infant, Premature
Models, Genetic
Obesity - genetics
Polymorphism, Single Nucleotide
Pregnancy
Abstract
Several obesity risk alleles affecting adult adiposity have been identified by the recent wave of genome wide association studies. We aimed to examine the potential effect of these variants on fetal body composition by investigating the variants in relation to birth weight and ponderal index of the newborn.
Midwife records from the Danish State Archives provided information on mother's age, parity, as well as birth weight, birth length and prematurity of the newborn in 4,744 individuals of the population-based Inter99 study. Twenty-four risk alleles showing genome-wide associations with adult BMI and/or waist circumference were genotyped. None of the 24 risk variants tested showed an association with birth weight or ponderal index after correction for multiple testing. Birth weight was divided into three categories low (=10(th) percentile), normal (10(th)-90(th) percentile) and high birth weight (=90th percentile) to allow for non-linear associations. There was no difference in the number of risk alleles between the groups (p?=?0.57). No interactions between each risk allele and birth weight in the prediction of adult BMI were observed. An obesity risk score was created by summing up risk alleles. The risk score did not associate with fetal body composition. Moreover there was no interaction between the risk score and birth weight/ponderal index in the prediction of adult BMI.
24 common variants associated with adult adiposity did not affect or interact with birth weight among Danes suggesting that the effects of these variants predominantly arise in the post-natal life.
Notes
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PubMed ID
21152014 View in PubMed
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The functional Pro129Thr variant of the FAAH gene is not associated with various fat accumulation phenotypes in a population-based cohort of 5,801 whites.

https://arctichealth.org/en/permalink/ahliterature165694
Source
J Mol Med (Berl). 2007 May;85(5):445-9
Publication Type
Article
Date
May-2007
Author
Dorit P Jensen
Camilla H Andreasen
Mette K Andersen
Lars Hansen
Hans Eiberg
Knut Borch-Johnsen
Torben Jørgensen
Torben Hansen
Oluf Pedersen
Author Affiliation
Steno Diabetes Center, Niels Steensens Vej 2, 2820, Gentofte, Denmark. dpaj@steno.dk
Source
J Mol Med (Berl). 2007 May;85(5):445-9
Date
May-2007
Language
English
Publication Type
Article
Keywords
Adult
Amidohydrolases - genetics - metabolism
Body mass index
Case-Control Studies
Cohort Studies
Denmark
European Continental Ancestry Group - genetics
Female
Gene Frequency
Genotype
Humans
Male
Middle Aged
Mutation
Obesity - enzymology - genetics - physiopathology
Phenotype
Population Surveillance
Proline
Threonine
Abstract
Food intake and weight gain are influenced by endocannabinoids whose actions are regulated by the fatty acid amide hydrolase (FAAH) enzyme. The homozygous Thr/Thr genotype of the functional Pro129Thr variant (rs324420) in the gene encoding FAAH was recently reported to associate with overweight and obesity in white and black populations. We investigated the Pro129Thr variant in relation to overweight and obesity in a relatively large population-based study sample of Danish whites (n=5,801). In case-control studies of obesity, a borderline association with the major Pro allele was identified; however, after correction for multiple testing, no association was found. Furthermore, a possible association between the major Pro allele and obesity was not supported by studies of obesity-related quantitative traits. In conclusion, in a large study sample, we were unable to find robust evidence of an association of the Pro129Thr FAAH variant with overweight, obesity, and any related quantitative traits among the examined whites.
PubMed ID
17216208 View in PubMed
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Genetic risk score of 46 type 2 diabetes risk variants associates with changes in plasma glucose and estimates of pancreatic ß-cell function over 5 years of follow-up.

https://arctichealth.org/en/permalink/ahliterature112415
Source
Diabetes. 2013 Oct;62(10):3610-7
Publication Type
Article
Date
Oct-2013
Author
Ehm A Andersson
Kristine H Allin
Camilla H Sandholt
Anders Borglykke
Cathrine J Lau
Rasmus Ribel-Madsen
Thomas Sparsø
Johanne M Justesen
Marie N Harder
Marit E Jørgensen
Torben Jørgensen
Torben Hansen
Oluf Pedersen
Author Affiliation
Novo Nordisk Foundation Center for Basic Metabolic Research, Section of Metabolic Genetics.
Source
Diabetes. 2013 Oct;62(10):3610-7
Date
Oct-2013
Language
English
Publication Type
Article
Keywords
Adult
Blood Glucose - genetics - metabolism
Body mass index
Denmark - epidemiology
Diabetes Mellitus, Type 2 - blood - epidemiology - genetics
Female
Follow-Up Studies
Genetic Predisposition to Disease
Genetic Variation
Genome-Wide Association Study
Genotype
Glucose Tolerance Test
Hemoglobin A, Glycosylated - genetics - metabolism
Humans
Incidence
Insulin-Secreting Cells - metabolism
Life Style
Male
Middle Aged
Polymorphism, Single Nucleotide
Risk factors
Time Factors
Abstract
More than 40 genetic risk variants for type 2 diabetes have been validated. We aimed to test whether a genetic risk score associates with the incidence of type 2 diabetes and with 5-year changes in glycemic traits and whether the effects were modulated by changes in BMI and lifestyle. The Inter99 study population was genotyped for 46 variants, and a genetic risk score was constructed. During a median follow-up of 11 years, 327 of 5,850 individuals developed diabetes. Physical examinations and oral glucose tolerance tests were performed at baseline and after 5 years (n = 3,727). The risk of incident type 2 diabetes was increased with a hazard ratio of 1.06 (95% CI 1.03-1.08) per risk allele. While the population in general had improved glucose regulation during the 5-year follow-up period, each additional allele in the genetic risk score was associated with a relative increase in fasting, 30-min, and 120-min plasma glucose values and a relative decrease in measures of ß-cell function over the 5-year period, whereas indices of insulin sensitivity were unaffected. The effect of the genetic risk score on 5-year changes in fasting plasma glucose was stronger in individuals who increased their BMI. In conclusion, a genetic risk score based on 46 variants associated strongly with incident type 2 diabetes and 5-year changes in plasma glucose and ß-cell function. Individuals who gain weight may be more susceptible to the cumulative impact of type 2 diabetes risk variants on fasting plasma glucose.
PubMed ID
23835328 View in PubMed
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Genetic variation in GIPR influences the glucose and insulin responses to an oral glucose challenge.

https://arctichealth.org/en/permalink/ahliterature98334
Source
Nat Genet. 2010 Feb;42(2):142-8
Publication Type
Article
Date
Feb-2010
Author
Richa Saxena
Marie-France Hivert
Claudia Langenberg
Toshiko Tanaka
James S Pankow
Peter Vollenweider
Valeriya Lyssenko
Nabila Bouatia-Naji
Josée Dupuis
Anne U Jackson
W H Linda Kao
Man Li
Nicole L Glazer
Alisa K Manning
Jian'an Luan
Heather M Stringham
Inga Prokopenko
Toby Johnson
Niels Grarup
Trine W Boesgaard
Cécile Lecoeur
Peter Shrader
Jeffrey O'Connell
Erik Ingelsson
David J Couper
Kenneth Rice
Kijoung Song
Camilla H Andreasen
Christian Dina
Anna Köttgen
Olivier Le Bacquer
François Pattou
Jalal Taneera
Valgerdur Steinthorsdottir
Denis Rybin
Kristin Ardlie
Michael Sampson
Lu Qi
Mandy van Hoek
Michael N Weedon
Yurii S Aulchenko
Benjamin F Voight
Harald Grallert
Beverley Balkau
Richard N Bergman
Suzette J Bielinski
Amelie Bonnefond
Lori L Bonnycastle
Knut Borch-Johnsen
Yvonne Böttcher
Eric Brunner
Thomas A Buchanan
Suzannah J Bumpstead
Christine Cavalcanti-Proença
Guillaume Charpentier
Yii-Der Ida Chen
Peter S Chines
Francis S Collins
Marilyn Cornelis
Gabriel J Crawford
Jerome Delplanque
Alex Doney
Josephine M Egan
Michael R Erdos
Mathieu Firmann
Nita G Forouhi
Caroline S Fox
Mark O Goodarzi
Jürgen Graessler
Aroon Hingorani
Bo Isomaa
Torben Jørgensen
Mika Kivimaki
Peter Kovacs
Knut Krohn
Meena Kumari
Torsten Lauritzen
Claire Lévy-Marchal
Vladimir Mayor
Jarred B McAteer
David Meyre
Braxton D Mitchell
Karen L Mohlke
Mario A Morken
Narisu Narisu
Colin N A Palmer
Ruth Pakyz
Laura Pascoe
Felicity Payne
Daniel Pearson
Wolfgang Rathmann
Annelli Sandbaek
Avan Aihie Sayer
Laura J Scott
Stephen J Sharp
Eric Sijbrands
Andrew Singleton
David S Siscovick
Nicholas L Smith
Thomas Sparsø
Amy J Swift
Holly Syddall
Gudmar Thorleifsson
Anke Tönjes
Tiinamaija Tuomi
Jaakko Tuomilehto
Timo T Valle
Gérard Waeber
Andrew Walley
Dawn M Waterworth
Eleftheria Zeggini
Jing Hua Zhao
Thomas Illig
H Erich Wichmann
James F Wilson
Cornelia van Duijn
Frank B Hu
Andrew D Morris
Timothy M Frayling
Andrew T Hattersley
Unnur Thorsteinsdottir
Kari Stefansson
Peter Nilsson
Ann-Christine Syvänen
Alan R Shuldiner
Mark Walker
Stefan R Bornstein
Peter Schwarz
Gordon H Williams
David M Nathan
Johanna Kuusisto
Markku Laakso
Cyrus Cooper
Michael Marmot
Luigi Ferrucci
Vincent Mooser
Michael Stumvoll
Ruth J F Loos
David Altshuler
Bruce M Psaty
Jerome I Rotter
Eric Boerwinkle
Torben Hansen
Oluf Pedersen
Jose C Florez
Mark I McCarthy
Michael Boehnke
Inês Barroso
Robert Sladek
Philippe Froguel
James B Meigs
Leif Groop
Nicholas J Wareham
Richard M Watanabe
Author Affiliation
Broad Institute of Harvard and Massachusetts Institute of Technology, Cambridge, Massachusetts, USA.
Source
Nat Genet. 2010 Feb;42(2):142-8
Date
Feb-2010
Language
English
Geographic Location
Denmark
Publication Type
Article
Keywords
Adenylate Cyclase - genetics
Body mass index
Denmark
Diabetes Mellitus, Type 2 - genetics
Female
Gene Expression Profiling
Gene Expression Regulation
Genetic Loci - genetics
Genetic Variation
Genome-Wide Association Study
Glucose - metabolism
Glucose Tolerance Test
Humans
Incretins - genetics
Insulin - metabolism
Male
Meta-Analysis as Topic
Polymorphism, Single Nucleotide - genetics
Proteins - genetics
RNA, Messenger - genetics - metabolism
Receptors, Gastrointestinal Hormone - genetics - metabolism
Abstract
Glucose levels 2 h after an oral glucose challenge are a clinical measure of glucose tolerance used in the diagnosis of type 2 diabetes. We report a meta-analysis of nine genome-wide association studies (n = 15,234 nondiabetic individuals) and a follow-up of 29 independent loci (n = 6,958-30,620). We identify variants at the GIPR locus associated with 2-h glucose level (rs10423928, beta (s.e.m.) = 0.09 (0.01) mmol/l per A allele, P = 2.0 x 10(-15)). The GIPR A-allele carriers also showed decreased insulin secretion (n = 22,492; insulinogenic index, P = 1.0 x 10(-17); ratio of insulin to glucose area under the curve, P = 1.3 x 10(-16)) and diminished incretin effect (n = 804; P = 4.3 x 10(-4)). We also identified variants at ADCY5 (rs2877716, P = 4.2 x 10(-16)), VPS13C (rs17271305, P = 4.1 x 10(-8)), GCKR (rs1260326, P = 7.1 x 10(-11)) and TCF7L2 (rs7903146, P = 4.2 x 10(-10)) associated with 2-h glucose. Of the three newly implicated loci (GIPR, ADCY5 and VPS13C), only ADCY5 was found to be associated with type 2 diabetes in collaborating studies (n = 35,869 cases, 89,798 controls, OR = 1.12, 95% CI 1.09-1.15, P = 4.8 x 10(-18)).
Notes
RefSource: Curr Diab Rep. 2010 Aug;10(4):249-51
PubMed ID
20081857 View in PubMed
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Genome wide association study identifies KCNMA1 contributing to human obesity.

https://arctichealth.org/en/permalink/ahliterature133416
Source
BMC Med Genomics. 2011;4:51
Publication Type
Article
Date
2011
Author
Hong Jiao
Peter Arner
Johan Hoffstedt
David Brodin
Beatrice Dubern
Sébastien Czernichow
Ferdinand van't Hooft
Tomas Axelsson
Oluf Pedersen
Torben Hansen
Thorkild I A Sørensen
Johannes Hebebrand
Juha Kere
Karin Dahlman-Wright
Anders Hamsten
Karine Clement
Ingrid Dahlman
Author Affiliation
Department of Biosciences and Nutrition, Karolinska Institutet, SE-141 83 Huddinge, Sweden. hong.jiao@ki.se
Source
BMC Med Genomics. 2011;4:51
Date
2011
Language
English
Publication Type
Article
Keywords
Alleles
Body mass index
Case-Control Studies
Cohort Studies
Female
France
Genetic Predisposition to Disease - genetics
Genome, Human
Genome-Wide Association Study
Germany
Humans
Large-Conductance Calcium-Activated Potassium Channel alpha Subunits - genetics
Male
Middle Aged
Obesity, Morbid - genetics
Polymorphism, Single Nucleotide
Sweden
Abstract
Recent genome-wide association (GWA) analyses have identified common single nucleotide polymorphisms (SNPs) that are associated with obesity. However, the reported genetic variation in obesity explains only a minor fraction of the total genetic variation expected to be present in the population. Thus many genetic variants controlling obesity remain to be identified. The aim of this study was to use GWA followed by multiple stepwise validations to identify additional genes associated with obesity.
We performed a GWA analysis in 164 morbidly obese subjects (BMI:body mass index>40 kg/m2) and 163 Swedish subjects (>45 years) who had always been lean. The 700 SNPs displaying the strongest association with obesity in the GWA were analyzed in a second cohort comprising 460 morbidly obese subjects and 247 consistently lean Swedish adults. 23 SNPs remained significantly associated with obesity (nominal P
Notes
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PubMed ID
21708048 View in PubMed
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A genome-wide association study of thyroid stimulating hormone and free thyroxine in Danish children and adolescents.

https://arctichealth.org/en/permalink/ahliterature285215
Source
PLoS One. 2017;12(3):e0174204
Publication Type
Article
Date
2017
Author
Tenna Ruest Haarmark Nielsen
Emil Vincent Rosenbaum Appel
Mathilde Svendstrup
Johanne Dam Ohrt
Maria Dahl
Cilius Esmann Fonvig
Mette Hollensted
Christian Theil Have
Haja N Kadarmideen
Oluf Pedersen
Torben Hansen
Jens-Christian Holm
Niels Grarup
Source
PLoS One. 2017;12(3):e0174204
Date
2017
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Age Factors
Body mass index
Child
Child, Preschool
Denmark
Female
Genetic Loci - genetics - physiology
Genetic Markers - genetics
Genetic Predisposition to Disease - genetics
Humans
Male
Pediatric Obesity - blood - genetics
Polymorphism, Single Nucleotide - genetics
Thyrotropin - blood
Thyroxine - blood
Young Adult
Abstract
Hypothyroidism is associated with obesity, and thyroid hormones are involved in the regulation of body composition, including fat mass. Genome-wide association studies (GWAS) in adults have identified 19 and 6 loci associated with plasma concentrations of thyroid stimulating hormone (TSH) and free thyroxine (fT4), respectively.
This study aimed to identify and characterize genetic variants associated with circulating TSH and fT4 in Danish children and adolescents and to examine whether these variants associate with obesity.
Genome-wide association analyses of imputed genotype data with fasting plasma concentrations of TSH and fT4 from a population-based sample of Danish children, adolescents, and young adults, and a group of children, adolescents, and young adults with overweight and obesity were performed (N = 1,764, mean age = 12.0 years [range 2.5-24.7]). Replication was performed in additional comparable samples (N = 2,097, mean age = 11.8 years [1.2-22.8]). Meta-analyses, using linear additive fixed-effect models, were performed on the results of the discovery and replication analyses.
No novel loci associated with TSH or fT4 were identified. Four loci previously associated with TSH in adults were confirmed in this study population (PDE10A (rs2983511: ß = 0.112SD, p = 4.8 · 10-16), FOXE1 (rs7847663: ß = 0.223SD, p = 1.5 · 10-20), NR3C2 (rs9968300: ß = 0.194SD), p = 2.4 · 10-11), VEGFA (rs2396083: ß = 0.088SD, p = 2.2 · 10-10)). Effect sizes of variants known to associate with TSH or fT4 in adults showed a similar direction of effect in our cohort of children and adolescents, 11 of which were associated with TSH or fT4 in our study (p
Notes
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PubMed ID
28333968 View in PubMed
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