Document Detail


The G/G genotype of a resistin single-nucleotide polymorphism at -420 increases type 2 diabetes mellitus susceptibility by inducing promoter activity through specific binding of Sp1/3.
MedLine Citation:
PMID:  15338456     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Insulin resistance is a major cause of type 2 diabetes mellitus (T2DM). Resistin, an adipocyte-secreted hormone, antagonizes insulin. Transgenic mice that overexpress the resistin gene (Retn) in adipose tissue are insulin-resistant, whereas Retn (-/-) mice show lower fasting blood glucose, suggesting that the altered Retn promoter function could cause diabetes. To determine the role of RETN in human T2DM, we analyzed polymorphisms in its 5' flanking region. We found that the -420G/G genotype was associated with T2DM (397 cases and 406 controls) (P=.008; adjusted odds ratio = 1.97 [by logistic regression analysis]) and could accelerate the onset of disease by 4.9 years (P=.006 [by multiple regression analysis]). Meta-analysis of 1,888 cases and 1,648 controls confirmed this association (P=.013). Linkage disequilibrium analysis revealed that the -420G/G genotype itself was a primary variant determining T2DM susceptibility. Functionally, Sp1 and Sp3 transcription factors bound specifically to the susceptible DNA element that included -420G. Overexpression of Sp1 or Sp3 enhanced RETN promoter activity with -420G in Drosophila Schneider line 2 cells that lacked endogenous Sp family members. Consistent with these findings, fasting serum resistin levels were higher in subjects with T2DM who carried the -420G/G genotype. Therefore, the specific recognition of -420G by Sp1/3 increases RETN promoter activity, leading to enhanced serum resistin levels, thereby inducing human T2DM.
Authors:
Haruhiko Osawa; Kazuya Yamada; Hiroshi Onuma; Akiko Murakami; Masaaki Ochi; Hiroko Kawata; Tatsuya Nishimiya; Toshiyuki Niiya; Ikki Shimizu; Wataru Nishida; Mitsuru Hashiramoto; Azuma Kanatsuka; Yasuhisa Fujii; Jun Ohashi; Hideichi Makino
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't     Date:  2004-08-26
Journal Detail:
Title:  American journal of human genetics     Volume:  75     ISSN:  0002-9297     ISO Abbreviation:  Am. J. Hum. Genet.     Publication Date:  2004 Oct 
Date Detail:
Created Date:  2004-08-31     Completed Date:  2004-12-16     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  0370475     Medline TA:  Am J Hum Genet     Country:  United States    
Other Details:
Languages:  eng     Pagination:  678-86     Citation Subset:  IM    
Affiliation:
Department of Laboratory Medicine, Ehime University School of Medicine, Ehime, Japan.
Data Bank Information
Bank Name/Acc. No.:
RefSeq/NT_020415;  NT_077812
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MeSH Terms
Descriptor/Qualifier:
Aged
Base Sequence
DNA-Binding Proteins / genetics,  metabolism
Diabetes Mellitus, Type 2 / genetics*
Female
Gene Frequency
Genetic Predisposition to Disease*
Genotype
Hormones, Ectopic / blood,  genetics*
Humans
Japan
Linkage Disequilibrium
Logistic Models
Male
Middle Aged
Molecular Sequence Data
Polymorphism, Single Nucleotide / genetics*
Promoter Regions, Genetic / genetics
Resistin
Sequence Analysis, DNA
Sp1 Transcription Factor / genetics,  metabolism
Sp3 Transcription Factor
Transcription Factors / genetics,  metabolism
Chemical
Reg. No./Substance:
0/DNA-Binding Proteins; 0/Hormones, Ectopic; 0/RETN protein, human; 0/Resistin; 0/SP3 protein, human; 0/Sp1 Transcription Factor; 0/Transcription Factors; 148710-94-5/Sp3 Transcription Factor
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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