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The -238 and -308 G-->A polymorphisms of the tumor necrosis factor alpha gene promoter are not associated with features of the insulin resistance syndrome or altered birth weight in Danish Caucasians.

https://arctichealth.org/en/permalink/ahliterature47878
Source
J Clin Endocrinol Metab. 2000 Apr;85(4):1731-4
Publication Type
Article
Date
Apr-2000
Author
S K Rasmussen
S A Urhammer
J N Jensen
T. Hansen
K. Borch-Johnsen
O. Pedersen
Author Affiliation
Steno Diabetes Center and Hagedorn Research Institute, Gentofte, Denmark.
Source
J Clin Endocrinol Metab. 2000 Apr;85(4):1731-4
Date
Apr-2000
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Birth Weight - genetics
Body constitution
Body mass index
Denmark
Diabetes Mellitus, Type 2 - genetics
Female
Genotype
Humans
Insulin - blood
Insulin Resistance - genetics
Lipids - blood
Male
Obesity - genetics
Polymorphism, Restriction Fragment Length
Promoter Regions (Genetics)
Research Support, Non-U.S. Gov't
Tumor Necrosis Factor-alpha - genetics
Abstract
Recently, two G-->A polymorphisms at positions -308 and -238, in the promoter of the tumor necrosis factor alpha (TNF-alpha) gene, have been identified. These variants have, in different ethnic groups, been linked to estimates of insulin resistance and obesity. The objective of the present study was to investigate whether these genetic variants of TNF-alpha were associated with features of the insulin resistance syndrome or alterations in birth weight in two Danish study populations comprising 380 unrelated young healthy subjects and 249 glucose-tolerant relatives of type 2 diabetic patients, respectively. All study participants underwent an iv glucose tolerance test with the addition of tolbutamide after 20 min. In addition, a number of biochemical and anthropometric measures were performed on each subject. The subjects were genotyped for the polymorphisms by applying PCR restriction fragment length polymorphism. Neither of the variants was related to altered insulin sensitivity index or other features of the insulin resistance syndrome (body mass index, waist to hip ratio, fat mass, fasting serum lipids or fasting serum insulin or C-peptide). Birth weight and the ponderal index were also not associated with the polymorphisms. In conclusion, although the study was carried out on sufficiently large study samples, the study does not support a major role of the -308 or -238 substitutions of the TNF-alpha gene in the pathogenesis of insulin resistance or altered birth weight among Danish Caucasian subjects.
PubMed ID
10770222 View in PubMed
Less detail

2000 EASD/Sankyo Insulin Resistance Project Award.

https://arctichealth.org/en/permalink/ahliterature47796
Source
Diabetologia. 2000 Oct;43(10):42-3
Publication Type
Article
Date
Oct-2000
Source
Diabetologia. 2000 Oct;43(10):42-3
Date
Oct-2000
Language
English
Publication Type
Article
Keywords
Awards and Prizes
Diabetes Mellitus, Type 2 - genetics
History, 20th Century
Insulin Resistance - genetics
Portraits
Sweden
PubMed ID
11079763 View in PubMed
Less detail

Archaeology of NIDDM. Excavation of the "thrifty" genotype.

https://arctichealth.org/en/permalink/ahliterature3237
Source
Diabetes. 1991 Feb;40(2):161-5
Publication Type
Article
Date
Feb-1991
Author
M. Wendorf
I D Goldfine
Author Affiliation
Archaeological Research Facility, University of California, Berkeley.
Source
Diabetes. 1991 Feb;40(2):161-5
Date
Feb-1991
Language
English
Publication Type
Article
Keywords
Archaeology
Diabetes Mellitus, Type 2 - genetics - history
Genotype
History, Ancient
Humans
Indians, North American - genetics - history
Insulin Resistance - genetics
North America
Paleontology
Research Support, U.S. Gov't, P.H.S.
Abstract
Since the 1940s, numerous cases of non-insulin-dependent diabetes mellitus (NIDDM) have been observed in certain American Indian populations. Extremely high prevalence rates of NIDDM occur most strikingly in several tribes of Paleo-Indians, whose ancestors migrated to North America greater than 11,000 yr ago. Archaeological evidence from that period indicates that certain groups of Paleo-Indians maintained an arctic-like hunter-gatherer life-style in an area in temperate North America ranging from Wyoming to Arizona. This life-style featured a reliance on unpredictable big game species as a major food source. However, at this time, big game species were becoming extinct. It is hypothesized that those Paleo-Indians who relied on big game as a food source developed a "thrifty" genotype that allowed a selective advantage during the periods of fasting that occurred between big game kills. It also is hypothesized that this thrifty genotype in these Indians may contribute to NIDDM when a sedentary life-style is adopted and food sources are constant. Because insulin resistance in muscle is a major feature of NIDDM, it is possible that insulin resistance per se is the phenotypic expression of the thrifty genotype.
PubMed ID
1991567 View in PubMed
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Association between features of the insulin resistance syndrome and Alzheimer's disease independently of apolipoprotein E4 phenotype: cross sectional population based study.

https://arctichealth.org/en/permalink/ahliterature207319
Source
BMJ. 1997 Oct 25;315(7115):1045-9
Publication Type
Article
Date
Oct-25-1997
Author
J. Kuusisto
K. Koivisto
L. Mykkänen
E L Helkala
M. Vanhanen
T. Hänninen
K. Kervinen
Y A Kesäniemi
P J Riekkinen
M. Laakso
Author Affiliation
Department of Medicine, Kuopio University Hospital, Finland.
Source
BMJ. 1997 Oct 25;315(7115):1045-9
Date
Oct-25-1997
Language
English
Publication Type
Article
Keywords
Aged
Alzheimer Disease - epidemiology - genetics
Apolipoprotein E4
Apolipoproteins E - genetics
Cross-Sectional Studies
Female
Finland - epidemiology
Follow-Up Studies
Humans
Hyperinsulinism - epidemiology - genetics
Insulin Resistance - genetics
Logistic Models
Male
Phenotype
Risk factors
Abstract
To determine the association between features of the insulin resistance syndrome and Alzheimer's disease.
Cross sectional population based study.
980 people aged 69 to 78 (349 men, 631 women).
Population of Kuopio, eastern Finland.
Presence of features of the insulin resistance syndrome and diagnosis of Alzheimer's disease by detailed neurological and neuropsychological evaluation.
46 (4.7%) subjects were classified as having probable or possible Alzheimer's disease. In univariate analyses, apolipoprotein E4 phenotype (odds ratio; 95% confidence interval 3.24: 1.77 to 5.92), age (1.16; 1.05 to 1.29), low level of education (0.82; 0.72 to 0.93), low total cholesterol concentration (0.77; 0.59 to 1.00), high systolic blood pressure (1.01; 1.00 to 1.03), high fasting and 2 hour plasma glucose concentrations (1.11; 1.01 to 1.23 and 1.08; 1.03 to 1.13, respectively), high fasting and 2 hour insulin concentrations (1.05; 1.02 to 1.08 and 1.003; 1.00 to 1.01, respectively), and abnormal glucose tolerance (1.86; 1.23 to 2.80) were significantly associated with Alzheimer's disease. In multivariate analysis including apolipoprotein E4 phenotype, age, education, systolic blood pressure, total cholesterol concentration, fasting glucose concentration, and insulin concentration, apolipoprotein E4 phenotype, age, education, total cholesterol, and insulin were significantly associated with Alzheimer's disease. In 532 non-diabetic subjects without the e4 allele hyperinsulinaemia was associated with an increased risk for Alzheimer's disease (prevalence of disease 7.5% v 1.4% in normoinsulinaemic subjects, P = 0.0004). In contrast, in the 228 with the e4 allele hyperinsulinaemia had no effect on the risk of disease (7.0% v 7.1%, respectively).
Features of the insulin resistance syndrome are associated with Alzheimer's disease independently of apolipoprotein E4 phenotype.
PubMed ID
9366728 View in PubMed
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Association between mu-opioid receptor-1 102T>C polymorphism and intermediate type 2 diabetes phenotypes: results from the Quebec Family Study (QFS).

https://arctichealth.org/en/permalink/ahliterature156912
Source
Clin Exp Pharmacol Physiol. 2008 Sep;35(9):1018-22
Publication Type
Article
Date
Sep-2008
Author
Stephanie-May Ruchat
Martine Girard
S John Weisnagel
Claude Bouchard
Marie-Claude Vohl
Louis Pérusse
Author Affiliation
Department of Preventive Medicine, Division of Kinesiology, Laval University, Quebec, Canada.
Source
Clin Exp Pharmacol Physiol. 2008 Sep;35(9):1018-22
Date
Sep-2008
Language
English
Publication Type
Article
Keywords
Adult
Diabetes Mellitus, Type 2 - genetics
Female
Gene Frequency
Genetic Linkage
Genetic Predisposition to Disease
Glucose Intolerance - genetics
Glucose Tolerance Test
Humans
Insulin Resistance - genetics
Male
Middle Aged
Phenotype
Polymorphism, Single Nucleotide
Quebec
Receptors, Opioid, mu - genetics
Risk factors
Abstract
It has been suggested recently that molecules expressed both in the pancreas and hypothalamus, such as mu-opioid receptor 1 (OPRM1), could form an integrated brain-liver system, which may sense glucose levels and therefore contribute to the development of type 2 diabetes mellitus (T2DM). In the present study, we tested associations between OPRM1 gene polymorphisms (rs1799971, 102T/C and rs0648007G/A) and indices of glucose tolerance, insulin sensitivity (IS) and insulin secretion derived from plasma measures obtained in a fasting state and following a 75 g oral glucose tolerance test (OGTT) in 749 subjects from the Quebec Family Study (QFS). Polymorphisms were tested for association with glucose tolerance (normal vs IFG and T2DM combined) by calculating a chi(2) statistic and corresponding P values, whereas associations with quantitative measures of glucose tolerance, IS and insulin secretion were tested using mixed linear models implemented in the MIXED procedure of sas (SAS Institute, Cary, NC, USA). Associations were found between 102T/C OPRM1 and indices of glucose tolerance and IS. Compared with T/T homozygotes, carriers of the OPRM1 C-102 variant exhibited a better glucose tolerance with a lower (P = 0.006) glucose area under the curve (AUC) following the OGTT and a better IS with a higher (P = 0.03) value of the Cederholm index, a numerical index of the curve relating glucose uptake to the log(10) plasma insulin levels during the OGTT. The results of the present study reveal that the 102T/C OPRM1 gene polymorphism is associated with a better glucose tolerance and improved IS, both of which suggest a potential protective effect of this variant on T2DM risk.
PubMed ID
18518884 View in PubMed
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Association of 18 confirmed susceptibility loci for type 2 diabetes with indices of insulin release, proinsulin conversion, and insulin sensitivity in 5,327 nondiabetic Finnish men.

https://arctichealth.org/en/permalink/ahliterature150518
Source
Diabetes. 2009 Sep;58(9):2129-36
Publication Type
Article
Date
Sep-2009
Author
Alena Stancáková
Teemu Kuulasmaa
Jussi Paananen
Anne U Jackson
Lori L Bonnycastle
Francis S Collins
Michael Boehnke
Johanna Kuusisto
Markku Laakso
Author Affiliation
Department of Medicine, University of Kuopio and Kuopio University Hospital, Kuopio, Finland.
Source
Diabetes. 2009 Sep;58(9):2129-36
Date
Sep-2009
Language
English
Publication Type
Article
Keywords
Aged
Diabetes Mellitus, Type 2 - epidemiology - genetics - metabolism
Finland - epidemiology
Gene Expression Profiling
Genetic Predisposition to Disease - epidemiology
Genotype
Glucose Tolerance Test
Humans
Insulin - metabolism
Insulin Resistance - genetics
Male
Middle Aged
Obesity - epidemiology - genetics - metabolism
Polymorphism, Single Nucleotide
Proinsulin - metabolism
Risk factors
Abstract
We investigated the effects of 18 confirmed type 2 diabetes risk single nucleotide polymorphisms (SNPs) on insulin sensitivity, insulin secretion, and conversion of proinsulin to insulin.
A total of 5,327 nondiabetic men (age 58 +/- 7 years, BMI 27.0 +/- 3.8 kg/m(2)) from a large population-based cohort were included. Oral glucose tolerance tests and genotyping of SNPs in or near PPARG, KCNJ11, TCF7L2, SLC30A8, HHEX, LOC387761, CDKN2B, IGF2BP2, CDKAL1, HNF1B, WFS1, JAZF1, CDC123, TSPAN8, THADA, ADAMTS9, NOTCH2, KCNQ1, and MTNR1B were performed. HNF1B rs757210 was excluded because of failure to achieve Hardy-Weinberg equilibrium.
Six SNPs (TCF7L2, SLC30A8, HHEX, CDKN2B, CDKAL1, and MTNR1B) were significantly (P or=11 vs.
Notes
Cites: Diabetes Care. 1999 Sep;22(9):1462-7010480510
Cites: Diabetes. 2009 May;58(5):1212-2119223598
Cites: Diabetes. 2006 Dec;55(12):3630-417130514
Cites: Nature. 2007 Feb 22;445(7130):881-517293876
Cites: Diabetologia. 2007 Jun;50(6):1192-20017437080
Cites: Science. 2007 May 11;316(5826):889-9417434869
Cites: Nat Genet. 2007 Jun;39(6):770-517460697
Cites: Science. 2007 Jun 1;316(5829):1331-617463246
Cites: Science. 2007 Jun 1;316(5829):1341-517463248
Cites: Science. 2007 Jun 1;316(5829):1336-4117463249
Cites: Diabetes. 2007 Jul;56(7):1943-717416797
Cites: Nat Genet. 2007 Aug;39(8):951-317603484
Cites: Nat Genet. 2007 Aug;39(8):977-8317603485
Cites: Diabetologia. 2007 Sep;50(9):1852-717618413
Cites: PLoS One. 2007;2(9):e83217786204
Cites: Diabetologia. 2007 Dec;50(12):2443-5017661009
Cites: Diabetes. 2007 Dec;56(12):3101-417804762
Cites: Diabetes. 2007 Dec;56(12):3105-1117827400
Cites: J Clin Endocrinol Metab. 2008 Jan;93(1):304-917971425
Cites: Diabetes. 2008 Feb;57(2):514-718039816
Cites: Diabetologia. 2008 Mar;51(3):451-718060660
Cites: Diabetologia. 2008 Apr;51(4):597-60118264689
Cites: Diabetes. 2008 Apr;57(4):1093-10018252897
Cites: Diabetes. 2008 May;57(5):1419-2618346983
Cites: Nat Genet. 2008 May;40(5):638-4518372903
Cites: Dtsch Med Wochenschr. 2001 May 18;126(20):580-411402923
Cites: Diabetologia. 2001 Sep;44(9):1170-611596673
Cites: Diabetes. 2003 Feb;52(2):573-712540638
Cites: Diabetologia. 2003 Sep;46(9):1276-8312898014
Cites: J Clin Endocrinol Metab. 2008 May;93(5):1924-3018285412
Cites: Curr Opin Clin Nutr Metab Care. 2008 Jul;11(4):371-718541994
Cites: Diabetologia. 2008 Sep;51(9):1646-5218568334
Cites: Diabetologia. 2008 Sep;51(9):1659-6318618095
Cites: PLoS One. 2008;3(8):e301918714373
Cites: Diabetes. 2008 Sep;57(9):2503-1018544707
Cites: Diabetes. 2008 Sep;57(9):2534-4018567820
Cites: Diabetologia. 2008 Nov;51(11):1993-718712344
Cites: Diabetologia. 2008 Nov;51(11):1989-9218719881
Cites: J Clin Endocrinol Metab. 2008 Oct;93(10):4013-918611970
Cites: PLoS One. 2008;3(12):e396219088850
Cites: Nat Genet. 2009 Jan;41(1):77-8119060907
Cites: Nat Genet. 2009 Jan;41(1):82-819060908
Cites: Nat Genet. 2009 Jan;41(1):25-3419079261
Cites: Nat Genet. 2008 Sep;40(9):1092-718711367
Cites: Nat Genet. 2008 Sep;40(9):1098-10218711366
Cites: Diabetes. 2009 Feb;58(2):478-8819008344
Cites: Diabetologia. 2009 Apr;52(4):614-2019183934
Cites: Diabetes. 2006 Oct;55(10):2890-517003358
PubMed ID
19502414 View in PubMed
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Association of a microsatellite in FASL to type II diabetes and of the FAS-670G>A genotype to insulin resistance.

https://arctichealth.org/en/permalink/ahliterature82231
Source
Genes Immun. 2006 Jun;7(4):316-21
Publication Type
Article
Date
Jun-2006
Author
Nolsøe R L
Hamid Y H
Pociot F.
Paulsen S.
Andersen K M
Borch-Johnsen K.
Drivsholm T.
Hansen T.
Pedersen O.
Mandrup-Poulsen T.
Author Affiliation
Steno Diabetes Center, Gentofte, Denmark.
Source
Genes Immun. 2006 Jun;7(4):316-21
Date
Jun-2006
Language
English
Publication Type
Article
Keywords
3' Untranslated Regions - genetics
Adult
Aged
Antigens, CD95
Apoptosis
Denmark
Diabetes Mellitus, Type 2 - genetics
Fas Ligand Protein
Female
Humans
Insulin Resistance - genetics
Insulin-Secreting Cells - cytology
Male
Membrane Glycoproteins - genetics
Microsatellite Repeats
Middle Aged
Polymorphism, Genetic
Promoter Regions (Genetics) - genetics
Quantitative Trait, Heritable
Receptors, Tumor Necrosis Factor - genetics
Tumor Necrosis Factors - genetics
Abstract
Type II diabetes is caused by a failure of the pancreatic beta-cells to compensate for insulin resistance leading to hyperglycaemia. There is evidence for an essential role of an increased beta-cell apoptosis in type II diabetes. High glucose concentrations induce IL-1beta production in human beta-cells, Fas expression and concomitant apoptosis owing to a constitutive expression of FasL. FASL and FAS map to loci linked to type II diabetes and estimates of insulin resistance, respectively. We have tested two functional promoter polymorphisms, FAS-670 G>A and FASL-844C>T as well as a microsatellite in the 3' UTR of FASL for association to type II diabetes in 549 type II diabetic patients and 525 normal-glucose-tolerant (NGT) control subjects. Furthermore, we have tested these polymorphisms for association to estimates of beta-cell function and insulin resistance in NGT subjects. We found significant association to type II diabetes for the allele distribution of the FASL microsatellite (P-value 0.02, Bonferroni corrected). The FAS-670G>A was associated with homeostasis model assessment insulin resistance index and body mass index (P-values 0.02 and 0.02). We conclude that polymorphisms of FASL and FAS associate with type II diabetes and estimates of insulin resistance in Danish white subjects.
PubMed ID
16691186 View in PubMed
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Association of angiotensin converting enzyme and plasminogen activator inhibitor-1 promoter gene polymorphisms with features of the insulin resistance syndrome in patients with premature coronary heart disease.

https://arctichealth.org/en/permalink/ahliterature194221
Source
Atherosclerosis. 2001 Jul;157(1):57-64
Publication Type
Article
Date
Jul-2001
Author
L. Viitanen
J. Pihlajamäki
P. Halonen
M. Lehtonen
A. Kareinen
S. Lehto
M. Laakso
Author Affiliation
Department of Medicine, University of Kuopio, PO Box 1627, 70 211 Kuopio, Finland.
Source
Atherosclerosis. 2001 Jul;157(1):57-64
Date
Jul-2001
Language
English
Publication Type
Article
Keywords
Aged
Alleles
Coronary Disease - etiology - genetics
Female
Finland
Humans
Insulin Resistance - genetics
Male
Middle Aged
Peptidyl-Dipeptidase A - genetics
Plasminogen Activator Inhibitor 1 - genetics
Polymorphism, Genetic
Promoter Regions, Genetic
Abstract
Polymorphisms of the angiotensin-converting enzyme (ACE) (insertion/deletion (I/D) in intron 16) and of the plasminogen activator inhibitor-1 (PAI-1) (promoter 4G/5G) genes have been linked with coronary heart disease (CHD) and/or myocardial infarction (MI). We studied the association of polymorphisms in these genes with CHD with linkage and association analyses in 118 families with premature and severe CHD and in 110 healthy controls. In linkage analysis there was no evidence for a linkage of the ACE or PAI-1 loci with CHD. However, in quantitative linkage analysis the ACE locus was linked with fasting glucose (P=0. 047) and fasting free fatty acid levels (P=0.029). In association analysis the ACE genotype frequencies of probands with CHD did not differ from those of healthy controls. Normoglycemic probands with MI and with the ACE polymorphism DD genotype had characteristics of the insulin resistance syndrome. They had higher levels of 1-h glucose (P=0.008) and 2-h free fatty acids (P=0.011) in an oral glucose tolerance test and higher levels of total (P=0.005) and very-low-density lipoprotein triglycerides (P=0.006) than probands with the ID or the II genotypes. The PAI-1 gene polymorphism was not associated with any of the variables of glucose or lipid metabolism. In conclusion, the ACE and PAI-1 gene polymorphisms are not linked with early-onset CHD. However, the ACE gene polymorphism is associated with features of the insulin resistance syndrome.
Notes
Comment In: Atherosclerosis. 2002 Jan;160(1):257-811755945
PubMed ID
11427204 View in PubMed
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Association of a polymorphism in the beta 3-adrenergic-receptor gene with features of the insulin resistance syndrome in Finns.

https://arctichealth.org/en/permalink/ahliterature214559
Source
N Engl J Med. 1995 Aug 10;333(6):348-51
Publication Type
Article
Date
Aug-10-1995
Author
E. Widén
M. Lehto
T. Kanninen
J. Walston
A R Shuldiner
L C Groop
Author Affiliation
Department of Endocrinology, University of Lund, Sweden.
Source
N Engl J Med. 1995 Aug 10;333(6):348-51
Date
Aug-10-1995
Language
English
Publication Type
Article
Keywords
Age of Onset
Aged
Base Sequence
Blood Glucose - metabolism
Diabetes Mellitus, Type 2 - genetics - metabolism
Female
Finland
Gene Frequency
Humans
Insulin - metabolism
Insulin Resistance - genetics - physiology
Male
Middle Aged
Molecular Sequence Data
Obesity - genetics - metabolism
Point Mutation
Polymorphism, Genetic
Random Allocation
Receptors, Adrenergic, beta - genetics
Receptors, Adrenergic, beta-3
Abstract
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:
Notes
Comment In: N Engl J Med. 1995 Aug 10;333(6):382-37609759
PubMed ID
7609751 View in PubMed
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Association of indices of liver and adipocyte insulin resistance with 19 confirmed susceptibility loci for type 2 diabetes in 6,733 non-diabetic Finnish men.

https://arctichealth.org/en/permalink/ahliterature138653
Source
Diabetologia. 2011 Mar;54(3):563-71
Publication Type
Article
Date
Mar-2011
Author
J. Vangipurapu
A. Stancáková
J. Pihlajamäki
T M Kuulasmaa
T. Kuulasmaa
J. Paananen
J. Kuusisto
E. Ferrannini
M. Laakso
Author Affiliation
Department of Medicine, University of Eastern Finland, Kuopio University Hospital, 70210, Kuopio, Finland.
Source
Diabetologia. 2011 Mar;54(3):563-71
Date
Mar-2011
Language
English
Publication Type
Article
Keywords
ADAM Proteins - genetics
Adipocytes - metabolism - physiology
Antigens, Neoplasm - genetics
Cation Transport Proteins - genetics
Cell Cycle Proteins - genetics
Cyclin-Dependent Kinase 5 - genetics
Cyclin-Dependent Kinase Inhibitor p15 - genetics
Diabetes Mellitus, Type 2 - genetics - physiopathology
Finland
Genetic Predisposition to Disease - genetics
Hepatocyte Nuclear Factor 1-beta - genetics
Homeodomain Proteins - genetics
Humans
Insulin Resistance - genetics - physiology
Liver - metabolism - physiopathology
Male
Membrane Glycoproteins - genetics
Membrane Proteins - genetics
Middle Aged
Neoplasm Proteins - genetics
PPAR gamma - genetics
Polymorphism, Single Nucleotide
Potassium Channels, Inwardly Rectifying - genetics
RNA-Binding Proteins - genetics
Receptor, Notch2 - genetics
Tetraspanins
Transcription Factor 7-Like 2 Protein - genetics
Transcription Factors - genetics
Abstract
Of the confirmed type 2 diabetes susceptibility loci only a few are known to affect insulin sensitivity. We examined the association of indices of hepatic and adipocyte insulin resistance (IR) with 19 confirmed type 2 diabetes risk loci in a large population-based study.
Non-diabetic participants (n?=?8,460, age 57.3?±?7.0 years, BMI 26.8?±?3.8 kg/m(2); mean ± SD) from a population-based cohort underwent an OGTT. Of them, 6,733 non-diabetic men were genotyped for single nucleotide polymorphisms (SNPs) in or near PPARG2 (also known as PPARG), KCNJ11, TCF7L2, SLC30A8, HHEX, CDKN2B, IGF2BP2, CDKAL1, HNF1B, WFS1, JAZF1, CDC123, TSPAN8, THADA, ADAMTS9, NOTCH2, KCNQ1, MTNR1B and SNP rs7480010. We investigated hepatic IR with a new index of liver IR. The adipocyte IR index was defined as a product of fasting NEFA and plasma insulin levels.
Type 2 diabetes risk SNPs in or near KCNJ11 and HHEX were significantly (p?
PubMed ID
21153532 View in PubMed
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92 records – page 1 of 10.