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The common variant in the FTO gene did not modify the effect of lifestyle changes on body weight: the Finnish Diabetes Prevention Study.

https://arctichealth.org/en/permalink/ahliterature152890
Source
Obesity (Silver Spring). 2009 Apr;17(4):832-6
Publication Type
Article
Date
Apr-2009
Author
Lappalainen TJ
Tolppanen A-M
Kolehmainen M
Schwab U
Lindström J
Tuomilehto J
Pulkkinen L
Eriksson JG
Laakso M
Gylling H
Uusitupa M
Author Affiliation
School of Public Health and Clinical Nutrition, Department of Clinical Nutrition, Food and Health Research Centre, University of Kuopio, Kuopio, Finland.
Source
Obesity (Silver Spring). 2009 Apr;17(4):832-6
Date
Apr-2009
Language
English
Publication Type
Article
Keywords
Adult
Aged
Blood Glucose - metabolism
Body mass index
Body Weight - ethnology - genetics
Cross-Sectional Studies
Diabetes Mellitus - ethnology - prevention & control
Female
Finland
Follow-Up Studies
Genetic Predisposition to Disease - genetics
Genotype
Humans
Life Style
Male
Middle Aged
Obesity - ethnology - genetics
Polymorphism, Single Nucleotide - genetics
Proteins - genetics
Abstract
The common single-nucleotide polymorphism in the FTO (fat mass and obesity associated) gene is consistently associated with an increased risk of obesity. However, the knowledge of a potential modifying effect of the FTO gene on changes in body weight achieved by lifestyle intervention is limited. We examined whether the FTO gene variant (rs9939609, T/A) is associated with body weight and BMI and long-term weight changes in the Finnish Diabetes Prevention Study (DPS). Altogether, 522 (aged 40-65 years; BMI >or=25 kg/m(2)) subjects with impaired glucose tolerance (IGT) were randomized to control and lifestyle intervention groups. SNP rs9939609 was genotyped from 502 subjects. At baseline, those with the AA genotype had higher BMI than subjects with other genotypes (P = 0.006). The association was observed in women (P = 0.016) but not in men. During the 4-year follow-up, the subjects with the AA genotype had consistently the highest BMI (P = 0.009) in the entire study population. The magnitude of weight reduction was greater in the intervention group, but the risk allele did not modify weight change in either of the groups. Our results confirm the association between the common FTO variant and BMI in a cross-sectional setting and during the long-term lifestyle intervention. We did not observe association between FTO variant and the magnitude of weight reduction achieved by long-term lifestyle intervention. Based on the results from the DPS, it is unlikely that the common variant of the FTO gene affects the success of lifestyle modification on weight loss.
PubMed ID
19180072 View in PubMed
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A health examination trial among males in northern Finland.

https://arctichealth.org/en/permalink/ahliterature76770
Source
Pages 442-444 in H. Linderholm et al., eds. Circumpolar Health 87. Proceedings of the Seventh International Congress on Circumpolar Health, Umeå, Sweden, 1987. Arctic Medical Research. 1988;47 Supp 1.
Publication Type
Article
Date
1988
  1 document  
Author
Näyhä, S.
Nayha, S
Laakso, M.
Haasi, J.
Kolivuori, T.
Author Affiliation
Department of Public Health Science, University of Oulu
Regional Institute of Occupational Health, Oulu, Finland
Source
Pages 442-444 in H. Linderholm et al., eds. Circumpolar Health 87. Proceedings of the Seventh International Congress on Circumpolar Health, Umeå, Sweden, 1987. Arctic Medical Research. 1988;47 Supp 1.
Date
1988
Language
English
Geographic Location
Finland
Publication Type
Article
Digital File Format
Text - PDF
Physical Holding
Alaska Medical Library
Keywords
Finland
General health status
Lapps
Reindeer herding districts
Documents
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Insulin sensitivity, insulin release and glucagon-like peptide-1 levels in persons with impaired fasting glucose and/or impaired glucose tolerance in the EUGENE2 study.

https://arctichealth.org/en/permalink/ahliterature86776
Source
Diabetologia. 2008 Mar;51(3):502-11
Publication Type
Article
Date
Mar-2008
Author
Laakso M.
Zilinskaite J.
Hansen T.
Boesgaard T Welløv
Vänttinen M.
Stancáková A.
Jansson P-A
Pellmé F.
Holst J J
Kuulasmaa T.
Hribal M L
Sesti G.
Stefan N.
Fritsche A.
Häring H.
Pedersen O.
Smith U.
Author Affiliation
Department of Medicine, University of Kuopio, Kuopio, Finland.
Source
Diabetologia. 2008 Mar;51(3):502-11
Date
Mar-2008
Language
English
Publication Type
Article
Keywords
Adult
Blood Glucose - metabolism
Diabetes Mellitus, Type 2 - blood - genetics
Family
Fasting
Female
Gastric Inhibitory Polypeptide - blood
Glucagon-Like Peptide 1 - blood
Glucose Intolerance - blood - genetics
Glucose Tolerance Test
Humans
Insulin - blood - secretion
Male
Middle Aged
Reference Values
Abstract
AIMS/HYPOTHESIS: We examined the phenotype of individuals with impaired fasting glucose (IFG) and/or impaired glucose tolerance (IGT) with regard to insulin release and insulin resistance. METHODS: Non-diabetic offspring (n=874; mean age 40+/-10.4 years; BMI 26.6+/-4.9 kg/m(2)) of type 2 diabetic patients from five different European Centres (Denmark, Finland, Germany, Italy and Sweden) were examined with regard to insulin sensitivity (euglycaemic clamps), insulin release (IVGTT) and glucose tolerance (OGTT). The levels of glucagon-like peptide-1 (GLP-1) and gastric inhibitory polypeptide (GIP) were measured during the OGTT in 278 individuals. RESULTS: Normal glucose tolerance was found in 634 participants, while 110 had isolated IFG, 86 had isolated IGT and 44 had both IFG and IGT, i.e. about 28% had a form of reduced glucose tolerance. Participants with isolated IFG had lower glucose-corrected first-phase (0-10 min) and higher second-phase insulin release (10-60 min) during the IVGTT, while insulin sensitivity was reduced in all groups with abnormal glucose tolerance. Similarly, GLP-1 but not GIP levels were reduced in individuals with abnormal glucose tolerance. CONCLUSIONS/INTERPRETATION: The primary mechanism leading to hyperglycaemia in participants with isolated IFG is likely to be impaired basal and first-phase insulin secretion, whereas in isolated IGT the primary mechanism leading to postglucose load hyperglycaemia is insulin resistance. Reduced GLP-1 levels were seen in all groups with abnormal glucose tolerance and were unrelated to the insulin release pattern during an IVGTT.
PubMed ID
18080106 View in PubMed
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Polymorphisms in the SLC2A2 (GLUT2) gene are associated with the conversion from impaired glucose tolerance to type 2 diabetes: the Finnish Diabetes Prevention Study.

https://arctichealth.org/en/permalink/ahliterature174146
Source
Diabetes. 2005 Jul;54(7):2256-60
Publication Type
Article
Date
Jul-2005
Author
Laukkanen O
Lindström J
Eriksson J
Valle TT
Hämäläinen H
Ilanne-Parikka P
Keinänen-Kiukaanniemi S
Tuomilehto J
Uusitupa M
Laakso M
Author Affiliation
Department of Medicine, University of Kuopio, 70210 Kuopio, Finland.
Source
Diabetes. 2005 Jul;54(7):2256-60
Date
Jul-2005
Language
English
Publication Type
Article
Keywords
Analysis of Variance
Diabetes Mellitus, Type 2 - genetics - prevention & control
Disease Progression
Finland
Genotype
Glucose Intolerance - genetics
Glucose Transporter Type 2
Humans
Monosaccharide Transport Proteins - genetics
Multivariate Analysis
Obesity - genetics
Polymorphism, Single Nucleotide
Risk factors
Abstract
Impaired insulin secretion is a fundamental defect in type 2 diabetes. The aim of this study was to investigate whether single nucleotide polymorphisms (SNPs) in the genes regulating insulin secretion (SLC2A2 [encoding GLUT2], GCK, TCF1 [encoding HNF-1alpha], HNF4A, GIP, and GLP1R) are associated with the conversion from impaired glucose tolerance (IGT) to type 2 diabetes in participants of the Finnish Diabetes Prevention Study. With the exception of SLC2A2, other genes were not associated with the risk of type 2 diabetes. All four SNPs of SLC2A2 predicted the conversion to diabetes, and rs5393 (AA genotype) increased the risk of type 2 diabetes in the entire study population by threefold (odds ratio 3.04, 95% CI 1.34-6.88, P = 0.008). The risk for type 2 diabetes in the AA genotype carriers was increased in the control group (5.56 [1.78-17.39], P = 0.003) but not in the intervention group. We conclude that the SNPs of SLC2A2 predict the conversion to diabetes in obese subjects with IGT.
PubMed ID
15983230 View in PubMed
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