Clinical and genetic associations with hypertriglyceridemic waist in a Canadian aboriginal population.

Clinical and genetic associations with hypertriglyceridemic waist in a Canadian aboriginal population. Research Abstract Details 

Research Abstract Table of Contents

Jump to the:

Clinical and genetic associations with hypertriglyceridemic waist in a Canadian aboriginal population. Abstract Text:

OBJECTIVES: To determine the prevalence of 'hypertriglyceridemic waist' (HTGW) in Oji-Cree, to examine its interaction with hepatic nuclear factor-1alpha (HNF1A) in association with type 2 diabetes, and to characterize its putative genetic determinants. METHOD: The presence or absence of HTGW was determined in 522 Oji-Cree subjects (223 males, 299 females), >or=18 years of age, in whom physical measurements and fasting plasma analyte concentrations were gathered, and a 75-g oral glucose tolerance test was administered, as part of a cross-sectional study. Subjects were genotyped for HNF1A codon 319, angiotensinogen (AGT) codons 174 and 235, G-protein beta3-subunit (GNB3) nucleotide 825, fatty acid-binding protein (FABP2) codon 54, nucleotides -455 and -482 of the apolipoprotein (apo) C-III (APOC3) promoter, and a 5-bp insertion/deletion polymorphism within the 3'-untranslated region of protein phosphatase 1 regulatory subunit 3 (PPP1R3). RESULTS: The unadjusted prevalence of HTGW in Oji-Cree adults was 20.5%, with more males affected than females (27.8 vs 15.1%, P=0.0004). Logistic regression analysis, adjusted for age and gender, showed type 2 diabetes was associated with both HNF1A G319S (odds ratio (OR) 4.85, 95% CI 2.45, 9.58) and HTGW (OR 4.96, 95% CI 2.49, 9.88). When the HNF1A mutation and HTGW were present in combination, the OR for type 2 diabetes was markedly increased (OR 43.2, 95% CI 12.4, 150). In women only, both GNB3 825C>T and FABP2 A54T genotypes were significantly associated with HTGW (OR 2.02, 95% CI 1.01, 4.05 and OR 1.95, 95% CI 1.01, 3.74, respectively). CONCLUSIONS: HTGW is prevalent in Oji-Cree, especially in men. The ORs for type 2 diabetes were similar ( approximately 5-fold) for subjects with either the presence of HTGW or the private HNF1A G319S mutation. These two independent risk factors acted synergistically to confer an even greater increased risk of type 2 diabetes.

Clinical and genetic associations with hypertriglyceridemic waist in a Canadian aboriginal population. Publishing Authors By Initials

For similar epidemiologic factors: sex factors research abstracts see: epidemiologic factors: sex factors research

PUBMED ID PMID:

MEDLINE DATE:

Clinical and genetic associations with hypertriglyceridemic waist in a Canadian aboriginal population. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: International journal of obesity (2005)

VOLUME: 30

Page Numbers: 484-91

Journal Abbreviation:

ISSN: 0307-0565

DAY: 14

MONTH: Mar

YEAR: 2006

Clinical and genetic associations with hypertriglyceridemic waist in a Canadian aboriginal population. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 101256108

Clinical and genetic associations with hypertriglyceridemic waist in a Canadian aboriginal population. Keywords Mesh Terms:

KEYWORDS: Sex Factors

MESH TERMS: genetics

Chemical & Substance for Abstract: Clinical and genetic associations with hypertriglyceridemic waist in a Canadian aboriginal population. Information

Substance Name: Hepatocyte Nuclear Factor 1-alpha

Registry Number: 0

Grant and Affiliation Information for Clinical and genetic associations with hypertriglyceridemic waist in a Canadian aboriginal population.

AFFILIATION: Blackburn Cardiovascular Genetics Laboratory, Robarts Research Institute and University of Western Ontario, London, Ontario, Canada.

Country: England

AGENCY:

GRANT:

ACRONYM:

MEDLINETA: Int J Obes (Lond)

REFSOURCE:

DATABASENAME:

ACCESSION NUMBER:

Number Hits: 0

Clinical and genetic associations with hypertriglyceridemic waist in a Canadian aboriginal population Related Publications

• A Glimpse at HDL-based Therapy for Atherosclerosis.
• Abetalipoproteinemia: two case reports and literature review.
• Adaptation to visuomotor rotations in younger and older adults.
• Association between the -455T>C promoter polymorphism of the APOC3 gene and the metabolic syndrome in a multi-ethnic sample.
• Association between the FTO rs9939609 polymorphism and the metabolic syndrome in a non-Caucasian multi-ethnic sample.
• Clinical and genetic associations with hypertriglyceridemic waist in a Canadian aboriginal population.
• Common variants APOC3, APOA5, APOE and PON1 are associated with variation in plasma lipoprotein traits in Greenlanders.
• Effect of change in posture and exercise on repolarization in patients with long QT syndrome with HERG channel mutations.
• Efficacy and safety of pioglitazone in treatment of a patient with an atypical partial lipodystrophy syndrome.
• Emerging antidyslipidemic drugs.
• GCK and HNF1A mutations in Canadian families with maturity onset diabetes of the young (MODY).
• Gene-environment interactions in atherosclerosis.
• Gene-environment interactions in atherosclerosis: animal models.
• Genetic determinants of plasma lipoproteins.
• Genetics of metabolic syndrome.
• Genetics of metabolic syndrome: is there a role for phenomics?
• HIV-associated dyslipidaemia: pathogenesis and treatment.
• Heterozygous CAV1 frameshift mutations (MIM 601047) in patients with atypical partial lipodystrophy and hypertriglyceridemia.
• Human hepatocyte nuclear factor-1 beta (HNF1B) 1968A/G polymorphism.
• Is raising HDL a futile strategy for atheroprotection?
• Lipoprotein (a): an emerging risk factor for atherosclerosis.
• Lipoprotein(a) and apolipoproteins B and A-I after acute myocardial infarction.
• Lipoprotein(a) and fibrinolysis.
• Lipoprotein(a): biochemistry and genetics.
• Microsomal triglyceride transfer protein inhibition-friend or foe?
• Monogenic pediatric dyslipidemias: Classification, genetics and clinical spectrum.
• Phenomics, lamin A/C, and metabolic disease.
• Single nucleotide polymorphisms of the fukutin gene.
• Spectrum of HNF1A and GCK mutations in Canadian families with maturity-onset diabetes of the young (MODY).
• The failure of torcetrapib: what have we learned?