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Body fat and mobility are explained by common genetic and environmental influences in older women.

https://arctichealth.org/en/permalink/ahliterature157662
Source
Obesity (Silver Spring). 2008 Jul;16(7):1616-21
Publication Type
Article
Date
Jul-2008
Author
Alfredo Ortega-Alonso
Sarianna Sipilä
Urho M Kujala
Jaakko Kaprio
Taina Rantanen
Author Affiliation
Department of Health Sciences, University of Jyväskylä, Jyväskylä, Finland. alfredo.ortega@sport.jyu.fi
Source
Obesity (Silver Spring). 2008 Jul;16(7):1616-21
Date
Jul-2008
Language
English
Publication Type
Article
Keywords
Activities of Daily Living
Adiposity - genetics
Age Factors
Aged
Aging - genetics
Electric Impedance
Environment
Female
Finland
Genetic Predisposition to Disease
Humans
Locomotion - genetics
Middle Aged
Mobility Limitation
Models, Genetic
Obesity - genetics - physiopathology
Physical Endurance - genetics
Risk factors
Twins, Dizygotic - genetics
Twins, Monozygotic - genetics
Walking
Abstract
In older adults, mobility limitations often coexist with overweight or obesity, suggesting that similar factors may underlie both traits. This study examined the extent to which genetic and environmental influences explain the association between adiposity and mobility in older women. Body fat percentage (bioimpedance test), walking speed over 10 m, and distance walked in a 6-min test were evaluated in 92 monozygotic (MZ) and 104 dizygotic (DZ) pairs of twin sisters reared together, aged 63-76 years. Genetic and environmental influences on each trait were estimated using age-adjusted multivariate genetic modeling. The analyses showed that the means (and s.d.) for body fat percentage, walking speed, and walking endurance were 33.2+/-7.3%, 1.7+/-0.3 m/s and 529.7+/-75.4 m, respectively. The phenotypic correlation between adiposity and walking speed was -0.32 and between adiposity and endurance it was -0.33. Genetic influences explained 80% of the association between adiposity and speed, and 65% of adiposity and walking endurance. Cross-trait genetic influences accounted for 12% of the variability in adiposity, 56% in walking speed, and 34% in endurance. Trait-specific genetic influences were also detected for adiposity (54%) and walking endurance (13%), but not speed. In conclusion, among community-living older women, an inverse association was found between adiposity and mobility that was mostly due to the effect of shared genes. This result suggests that the identification of genetic variants for body fat metabolism may also provide understanding of the development of mobility limitations in older women.
PubMed ID
18421266 View in PubMed
Less detail

The common FTO variant rs9939609 is not associated with BMI in a longitudinal study on a cohort of Swedish men born 1920-1924.

https://arctichealth.org/en/permalink/ahliterature98623
Source
BMC Med Genet. 2009;10:131
Publication Type
Article
Date
2009
Author
Jacobsson JA
Risérus U
Axelsson T
Lannfelt L
Schiöth HB
Fredriksson R
Author Affiliation
Department of Neuroscience, Functional Pharmacology, Uppsala University, Uppsala, Sweden. Josefin.Jacobsson@neuro.uu.se
Source
BMC Med Genet. 2009;10:131
Date
2009
Language
English
Publication Type
Article
Keywords
Aged
Aged, 80 and over
Alleles
Body mass index
Genetic Association Studies
Genetic Variation
Genotype
Humans
Longitudinal Studies
Male
Middle Aged
Motor Activity
Obesity - genetics - physiopathology
Proteins - genetics
Risk factors
Sweden
Abstract
BACKGROUND: Common FTO (fat mass and obesity associated) gene variants have recently been strongly associated with body mass index and obesity in several large studies. Here we set out to examine the association of the FTO variant rs9939609 with BMI in a 32 year follow up study of men born 1920-1924. Moreover, we analyzed the effect of physical activity on the different genotypes. METHODS: The FTO rs9936609 was genotyped using an Illumina golden gate assay. BMI was calculated using standard methods and body fat was estimated by measuring skinfold thickness using a Harpenden caliper. Physical activity was assessed using a four question medical questionnaire. RESULTS: FTO rs9939609 was genotyped in 1153 elderly Swedish men taking part of a population-based cohort study, the ULSAM cohort. The risk of obesity and differences in BMI according to genotype at the ages of 50, 60, 70, 77 and 82 were investigated. We found no increased risk of obesity and no association with BMI at any age with the FTO rs9939609 variant. We found however interaction between physical activity at the age of 50 years and genotype on BMI levels (p = 0.039) and there was a clear trend towards larger BMI differences between the TT and AA carriers as well as between AT and AA carriers in the less physically active subjects. CONCLUSION: Here we found that the well established obesity risk allele for a common variant in FTO does not associate with increased BMI levels in a Swedish population of adult men which reached adulthood before the appearance of today's obesogenic enviroment. There is an interaction between physical activity and the effect of the FTO genotype on BMI levels suggesting that lack of physical activity is a requirement for an association of FTO gene variants to obesity.
PubMed ID
20003232 View in PubMed
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Common polymorphisms in the genes regulating the early insulin signalling pathway: effects on weight change and the conversion from impaired glucose tolerance to Type 2 diabetes. The Finnish Diabetes Prevention Study.

https://arctichealth.org/en/permalink/ahliterature180244
Source
Diabetologia. 2004 May;47(5):871-7
Publication Type
Article
Date
May-2004
Author
O. Laukkanen
J. Pihlajamäki
J. Lindström
J. Eriksson
T T Valle
H. Hämäläinen
P. Ilanne-Parikka
S. Keinänen-Kiukaanniemi
J. Tuomilehto
M. Uusitupa
M. Laakso
Author Affiliation
Department of Medicine, University of Kuopio, Finland.
Source
Diabetologia. 2004 May;47(5):871-7
Date
May-2004
Language
English
Publication Type
Article
Keywords
Body mass index
Body Weight - physiology
Diabetes Mellitus, Type 2 - epidemiology - genetics - physiopathology
Finland - epidemiology
Gene Frequency
Glucose Intolerance - genetics - physiopathology
Humans
Insulin - physiology
Life Style
Minisatellite Repeats
Obesity - genetics - physiopathology
Polymorphism, Genetic
Signal Transduction - genetics
Abstract
Type 2 diabetes is a complex disorder with strong heritability. The aim of our study was to investigate whether common polymorphisms in the genes regulating the early insulin signalling pathway (insulin; A-23T, insulin-like growth factor 1 receptor [IGF-1R]; GAG1013GAA, plasma cell membrane glycoprotein 1 [PC-1]; K121Q, insulin receptor substrate [IRS-1]; G972R, insulin receptor substrate 2 [IRS-2]; G1057D and phosphatidylinositol 3-kinase p85 alpha [PI3K]; M326I) affect the weight change and development of Type 2 diabetes in the Finnish Diabetes Prevention Study.
We screened for the polymorphisms in 490 overweight subjects with impaired glucose tolerance whose DNA was available from the Finnish Diabetes Prevention Study. These subjects were randomly allocated into a control group and an intervention group characterised by intensive, individualised diet and exercise.
In carriers of the GAA1013GAA genotype of IGF-1R, the R972 allele of IRS-1 and the D1057D genotype of IRS-2, lifestyle intervention did not lead to significant differences in weight loss between the intervention and control groups, implying a role of these risk genotypes in the regulation of body weight. We observed a statistically significant difference in the conversion rate from IGT to diabetes between the genotypes of the IGF-1R gene (GAG1013GAG: 18.6%, GAG1013GAA: 10.4%, GAA1013GAA: 19.5%, p=0.033). Common polymorphisms in the insulin, PC-1 and PI3K genes did not regulate weight change or conversion to diabetes.
The common polymorphisms of the IGF-1R, IRS-1 and IRS-2 genes may modify the weight change response to a lifestyle intervention but not the conversion from IGT to Type 2 diabetes, whereas IGF-1R may also regulate the risk of developing Type 2 diabetes.
PubMed ID
15127203 View in PubMed
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Effect of birth year on birth weight and obesity in adulthood: comparison between subjects born prior to and during the great depression in Iceland.

https://arctichealth.org/en/permalink/ahliterature120918
Source
PLoS One. 2012;7(9):e44551
Publication Type
Article
Date
2012
Author
Cindy Mari Imai
Thorhallur Ingi Halldorsson
Ingibjorg Gunnarsdottir
Vilmundur Gudnason
Thor Aspelund
Gudmundur Jonsson
Bryndis Eva Birgisdottir
Inga Thorsdottir
Author Affiliation
Unit for Nutrition Research, Landspitali University Hospital and Faculty of Food Science and Nutrition, School of Health Sciences, University of Iceland, Reykjavik, Iceland. cmi1@hi.is
Source
PLoS One. 2012;7(9):e44551
Date
2012
Language
English
Publication Type
Article
Keywords
Adult
Age Factors
Aged
Anthropometry
Birth weight
Body Composition
Body mass index
Cohort Studies
Economic Recession
Environmental Exposure
Female
Humans
Iceland
Male
Maternal Age
Middle Aged
Obesity - genetics - physiopathology
Outcome Assessment (Health Care)
Poverty
Pregnancy
Prenatal Exposure Delayed Effects
Sex Factors
Abstract
Many epidemiological studies have linked small size at birth to adverse adult health outcomes but the relative influence of environmental exposures is less well established.
The authors investigated the impact of prenatal environmental exposure by comparing 2750 participants born before (1925-1929) and during (1930-1934) the Great Depression in Reykjavik, Iceland. Calendar year served as proxy for environmental effects. Anthropometric measurements at birth and school-age (8-13 years) were collected from national registries. Participants were medically examined as adults (33-65 years).
Mean birth weight, adjusted for maternal age and parity, decreased by 97 g (95% confidence interval (CI): 39, 156) for men and 70 g (95% CI: 11, 129) for women from 1925 to 1934; growth at school-age was significantly reduced for participants growing during the Depression. As adults, women prenatally exposed to the Depression had higher body mass index (?0.6 kg/m(2), 95% CI: 0.2, 1.1), higher fasting blood glucose levels (?0.16 mmol/L, 95% CI: 0.07, 0.23) and greater odds of being obese 1.43 (95% CI: 1.01, 2.02) compared to unexposed counterparts. Non-significant associations were observed in men.
Reduction in birth weight due to rapid shifts in the economic environment appears to have a modest but significant association with later obesity for women while male offspring appear to be less affected by these conditions.
Notes
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PubMed ID
22957081 View in PubMed
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Genotype-phenotype associations in obesity dependent on definition of the obesity phenotype.

https://arctichealth.org/en/permalink/ahliterature159553
Source
Obes Facts. 2008;1(3):138-45
Publication Type
Article
Date
2008
Author
Sofia Inez Iqbal Kring
Lesli Hingstrup Larsen
Claus Holst
Søren Toubro
Torben Hansen
Arne Astrup
Oluf Pedersen
Thorkild I A Sørensen
Author Affiliation
Institute of Preventive Medicine, Copenhagen University Hospital, Centre for Health and Society, Copenhagen, Denmark. SI@ipm.regionh.dk
Source
Obes Facts. 2008;1(3):138-45
Date
2008
Language
English
Publication Type
Article
Keywords
Adult
Alleles
Body Fat Distribution
Body mass index
Case-Control Studies
Cohort Studies
Denmark
Follow-Up Studies
Genetic Association Studies
Humans
Ion Channels - genetics
Logistic Models
Male
Middle Aged
Mitochondrial Proteins - genetics
Obesity - genetics - physiopathology
Phenotype
Polymorphism, Genetic - genetics
Receptors, Cytoplasmic and Nuclear - genetics
Receptors, Somatostatin - genetics
Waist Circumference
Abstract
In previous studies of associations of variants in the genes UCP2, UCP3, PPARG2, CART, GRL, MC4R, MKKS, SHP, GHRL, and MCHR1 with obesity, we have used a case-control approach with cases defined by a threshold for BMI. In the present study, we assess the association of seven abdominal, peripheral, and overall obesity phenotypes, which were analyzed quantitatively, and thirteen candidate gene polymorphisms in these ten genes in the same cohort.
Obese Caucasian men (n = 234, BMI >or= 31.0 kg/m(2)) and a randomly sampled non-obese group (n = 323), originally identified at the draft board examinations, were re-examined at median ages of 47.0 or 49.0 years by anthropometry and DEXA scanning. Obesity phenotypes included BMI, fat body mass index, waist circumference, waist for given BMI, intra-abdominal adipose tissue, hip circumference and lower body fat mass (%). Using logistic regression models, we estimated the odds for defined genotypes (dominant or recessive genetic transmission) in relation to z-scores of the phenotypes.
The minor (rare) allele for SHP 512G>C (rs6659176) was associated with increased hip circumference. The minor allele for UCP2 Ins45bp was associated with increased BMI, increased abdominal obesity, and increased hip circumference. The minor allele for UCP2 -866G>A (rs6593669) was associated with borderline increased fat body mass index. The minor allele for MCHR1 100213G>A (rs133072) was associated with reduced abdominal obesity. None of the other genotype-phenotype combinations showed appreciable associations.
If replicated in independent studies with focus on the specific phenotypes, our explorative studies suggest significant associations between some candidate gene polymorphisms and distinct obesity phenotypes, predicting beneficial and detrimental effects, depending on compartments for body fat accumulation.
PubMed ID
20054173 View in PubMed
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Haplotypes in the phospholipid transfer protein gene are associated with obesity-related phenotypes: the Qu├ębec Family Study.

https://arctichealth.org/en/permalink/ahliterature174330
Source
Int J Obes (Lond). 2005 Nov;29(11):1338-45
Publication Type
Article
Date
Nov-2005
Author
Y. Bossé
L. Bouchard
J-P Després
C. Bouchard
L. Pérusse
M-C Vohl
Author Affiliation
Lipid Research Center, CHUL Research Center, Laval University, Québec, Canada.
Source
Int J Obes (Lond). 2005 Nov;29(11):1338-45
Date
Nov-2005
Language
English
Publication Type
Article
Keywords
Adult
Body Composition
Body mass index
Female
Haplotypes
Health Surveys
Humans
Introns
Linkage Disequilibrium
Male
Middle Aged
Obesity - genetics - physiopathology
Phenotype
Phospholipid Transfer Proteins - genetics
Polymorphism, Single Nucleotide
Quebec
Abstract
The phospholipid transfer protein (PLTP) may play a role in body fat regulation.
To investigate the association between PLTP genetic variants and obesity-related phenotypes.
Two intronic variants, one in intron 1 (c.-87G>A) and the other in intron 12 (c.1175+68T>G), were genotyped in 811 participants of the Québec Family Study. Nine obesity-related phenotypes were investigated, including body mass index (BMI), obesity (BMI> or =30 kg/m(2)), and waist circumference, percentage of fat, fat mass and fat-free mass measured by hydrostatic weighing as well as total, visceral and subcutaneous abdominal adipose tissue areas assessed by computed tomography. Single markers and haplotypes were tested for associations in family-based designs using the FBAT program.
The SNP located in intron 1 showed significant associations with obesity, BMI, waist circumference and fat-free mass (P
PubMed ID
15953936 View in PubMed
Less detail

Insulin resistance syndrome in Australian aboriginal people.

https://arctichealth.org/en/permalink/ahliterature207549
Source
Clin Exp Pharmacol Physiol. 1997 Sep-Oct;24(9-10):776-81
Publication Type
Article
Author
K G Rowley
J D Best
R. McDermott
E A Green
L S Piers
K. O'Dea
Author Affiliation
Deakin Institute of Human Nutrition, Deakin University, Malvern, Australia. rols@deakin.edu.au
Source
Clin Exp Pharmacol Physiol. 1997 Sep-Oct;24(9-10):776-81
Language
English
Publication Type
Article
Keywords
Female
Humans
Insulin Resistance - genetics - physiology
Male
Obesity - genetics - physiopathology
Oceanic Ancestry Group - genetics
Abstract
1. Like many indigenous populations, Australian Aboriginal people have developed high rates of obesity, non-insulin-dependent diabetes mellitus (NIDDM) and cardiovascular and renal disease following the transition from a traditional to an 'urbanized' lifestyle. These conditions tend to cluster as part of the insulin resistance syndrome. 2. The prevalence of overweight people and obesity in Australian Aboriginal populations ranges from 0% in communities with a traditionally orientated lifestyle to well over 50% in the worst affected communities. There is a predominantly central pattern of fat deposition in both men and women, which is associated with greater insulin resistance and cardiovascular risk than is peripheral fat deposition. 3. Data from four previously published, population-based surveys in Aboriginal communities were combined to give a cohort of 1079 subjects of 15 years and older. Several conditions of the insulin resistance syndrome had a strong, positive association with increasing body mass index (BMI): NIDDM (both cross-sectionally and longitudinally), hypertension, dyslipidaemia and albuminuria. Remaining lean (BMI
PubMed ID
9315388 View in PubMed
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Meal frequencies modify the effect of common genetic variants on body mass index in adolescents of the northern Finland birth cohort 1986.

https://arctichealth.org/en/permalink/ahliterature107228
Source
PLoS One. 2013;8(9):e73802
Publication Type
Article
Date
2013
Author
Anne Jääskeläinen
Ursula Schwab
Marjukka Kolehmainen
Marika Kaakinen
Markku J Savolainen
Philippe Froguel
Stéphane Cauchi
Marjo-Riitta Järvelin
Jaana Laitinen
Author Affiliation
Department of Clinical Nutrition, Institute of Public Health and Clinical Nutrition, University of Eastern Finland, Kuopio, Finland.
Source
PLoS One. 2013;8(9):e73802
Date
2013
Language
English
Publication Type
Article
Keywords
Adolescent
Alleles
Body mass index
Cohort Studies
Feeding Behavior
Female
Finland
Gene Frequency
Genetic Predisposition to Disease - genetics
Genotype
Humans
Male
Meals
Obesity - genetics - physiopathology
Polymorphism, Single Nucleotide
Population Surveillance - methods
Proteins - genetics
Receptor, Melanocortin, Type 4 - genetics
Risk factors
Sex Factors
Abstract
Recent studies suggest that meal frequencies influence the risk of obesity in children and adolescents. It has also been shown that multiple genetic loci predispose to obesity already in youth. However, it is unknown whether meal frequencies could modulate the association between single nucleotide polymorphisms (SNPs) and the risk of obesity. We examined the effect of two meal patterns on weekdays -5 meals including breakfast (regular) and = 4 meals with or without breakfast (meal skipping) - on the genetic susceptibility to increased body mass index (BMI) in Finnish adolescents. Eight variants representing 8 early-life obesity-susceptibility loci, including FTO and MC4R, were genotyped in 2215 boys and 2449 girls aged 16 years from the population-based Northern Finland Birth Cohort 1986. A genetic risk score (GRS) was calculated for each individual by summing the number of BMI-increasing alleles across the 8 loci. Weight and height were measured and dietary data were collected using self-administered questionnaires. Among meal skippers, the difference in BMI between high-GRS and low-GRS (
Notes
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PubMed ID
24040077 View in PubMed
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Neurosystems linking corticolimbic and hypothalamic pathways in energy balance: view from the Chair.

https://arctichealth.org/en/permalink/ahliterature150243
Source
Int J Obes (Lond). 2009 Jun;33 Suppl 2:S3-7
Publication Type
Conference/Meeting Material
Date
Jun-2009
Author
S. Fulton
Author Affiliation
Department of Nutrition, CRCHUM & Montreal Diabetes Research Center, Université de Montréal, Montréal, Québec, Canada. stephanie.fulton@umontreal.ca
Source
Int J Obes (Lond). 2009 Jun;33 Suppl 2:S3-7
Date
Jun-2009
Language
English
Publication Type
Conference/Meeting Material
Keywords
Appetite Regulation - genetics - physiology
Energy Metabolism
Feeding Behavior
Homeostasis - genetics - physiology
Humans
Hypothalamus - metabolism - physiology
Motivation - genetics
Neural Pathways - physiology
Obesity - genetics - physiopathology - psychology
Quebec
Reward
Signal Transduction
Abstract
Recent work has advanced our knowledge of the neural pathways interfacing corticolimbic substrates of food motivation and reward with hypothalamic controls of food intake. As a neuroanatomical interface between limbic motivational processes, energy-sensing mechanisms in the mediobasal hypothalamus and motor output pathways, several studies draw attention to the lateral hypothalamus. Reviewed here are some highlights of the first session of the 11th International Symposium of the Merck-Frosst/CIHR Obesity Research Chair held in Quebec City on 5 November 2008 describing the neuroanatomical and neurochemical crosstalk between hypothalamic, midbrain and limbic sites and their role in energy balance.
PubMed ID
19528976 View in PubMed
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Obesity and insulin resistance in Swedish subjects.

https://arctichealth.org/en/permalink/ahliterature48265
Source
Diabet Med. 1996 Sep;13(9 Suppl 6):S85-6
Publication Type
Article
Date
Sep-1996
Author
P. Arner
Author Affiliation
Department of Medicine, Huddinge Hospital, Sweden.
Source
Diabet Med. 1996 Sep;13(9 Suppl 6):S85-6
Date
Sep-1996
Language
English
Publication Type
Article
Keywords
Adipose Tissue - metabolism
Aged
Diabetes Mellitus - genetics - physiopathology
Glucose Intolerance - genetics - physiopathology
Humans
Insulin - secretion
Insulin Resistance
Male
Middle Aged
Muscle, Skeletal - metabolism
Obesity - genetics - physiopathology
Receptor, Insulin - metabolism
Reference Values
Sweden
Tumor Necrosis Factor-alpha - biosynthesis - physiology
Abstract
Insulin resistance and secretory defects seem to be present in Swedish obese elderly, NIDDM subjects. A defect in insulin secretion seems to dominate in lean elderly male Swedish subjects with NIDDM. Furthermore, TNF alpha expression and secretion are increased in adipose tissue from obese subjects and correlates with insulin resistance roughly measured as elevated fasting plasma insulin in spite of normal fasting blood glucose.
PubMed ID
8894488 View in PubMed
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13 records – page 1 of 2.