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Erschienen in: Endocrine 3/2009

01.06.2009 | Original Paper

Association of TRB3 gene Q84R polymorphism with type 2 diabetes mellitus in Chinese population

verfasst von: Zhiyong Shi, Jing Liu, Qian Guo, Xiaoqin Ma, Linna Shen, Sanni Xu, Hongxia Gao, Xinjian Yuan, Junling Zhang

Erschienen in: Endocrine | Ausgabe 3/2009

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Abstract

Background TRB3, a human homolog of Drosophila Tribbles, has been shown as a critical negative regulator of Akt (also known as protein kinase B), which is a key component in insulin signaling. In addition, TRB3 is another PPAR-target gene and functions as an important link between glucose and lipid metabolism. The Q84R polymorphic variant of TRB3 has been linked to insulin resistance and related clinical outcomes. However, it is unclear whether this polymorphism is associated with type 2 diabetes mellitus (T2DM) in the Chinese population. Methods In this study, we genotyped Q84R polymorphism in 177 patients with T2DM and 245 control subjects in Chinese population by using the polymerase chain reaction/ligase detection reaction (PCR/LDR) assay. Results No significant difference in the Q84R genotype frequency was observed between T2DM patients and controls (= 0.642). In T2DM group, the Q84R variant in cases was associated with higher FINS, higher HOMA-IR, and lower LnISI (= 0.003, 0.001, and 0.001, respectively). However, the changes in HOMA-IR and LnISI were not significant in controls (the P value is 0.098 and 0.203, respectively). In addition, FINS levels were also significantly increased from Q84Q to R84 in controls (= 0.036). Conclusion Our data indicate that the TRB3 Q84R polymorphism is not associated with T2DM in Chinese population. However, the Q84R variant is associated with insulin resistance among T2DM patients in Chinese population.
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Metadaten
Titel
Association of TRB3 gene Q84R polymorphism with type 2 diabetes mellitus in Chinese population
verfasst von
Zhiyong Shi
Jing Liu
Qian Guo
Xiaoqin Ma
Linna Shen
Sanni Xu
Hongxia Gao
Xinjian Yuan
Junling Zhang
Publikationsdatum
01.06.2009
Verlag
Springer US
Erschienen in
Endocrine / Ausgabe 3/2009
Print ISSN: 1355-008X
Elektronische ISSN: 1559-0100
DOI
https://doi.org/10.1007/s12020-009-9162-6

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