Possible role of TCF7L2 in the pathogenesis of type 2 diabetes mellitus

With people's changing life style and dietary habits, the prevalence of type 2 diabetes mellitus (T2DM) has become much more serious than ever before. T2DM is a polygenic metabolic disorder, resulting from the interaction of genetic and various environmental factors. Among all the T2DM related...

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Main Authors: Zhi-qiu Huang, Yao-qi Liao, Run-ze Huang, Jin-peng Chen, Hui-lin Sun
Format: Article
Language:English
Published: Taylor & Francis Group 2018-07-01
Series:Biotechnology & Biotechnological Equipment
Subjects:
Online Access:http://dx.doi.org/10.1080/13102818.2018.1438211
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spelling doaj-43575129d19e478390cfaac41a9f75e62020-11-25T00:16:06ZengTaylor & Francis GroupBiotechnology & Biotechnological Equipment1310-28181314-35302018-07-0132483083410.1080/13102818.2018.14382111438211Possible role of TCF7L2 in the pathogenesis of type 2 diabetes mellitusZhi-qiu Huang0Yao-qi Liao1Run-ze Huang2Jin-peng Chen3Hui-lin Sun4The First Affiliated Hospital of Guangdong Pharmaceutical UniversityThe First Affiliated Hospital of Guangdong Pharmaceutical UniversityThe First Affiliated Hospital of Guangdong Pharmaceutical UniversityThe First Affiliated Hospital of Guangdong Pharmaceutical UniversityThe First Affiliated Hospital of Guangdong Pharmaceutical UniversityWith people's changing life style and dietary habits, the prevalence of type 2 diabetes mellitus (T2DM) has become much more serious than ever before. T2DM is a polygenic metabolic disorder, resulting from the interaction of genetic and various environmental factors. Among all the T2DM related genes, the transcription factor 7 like 2 (TCF7L2) gene is one of the most relevant risk-related genes for T2DM. However, the role of TCF7L2 in T2DM pathogenesis has not yet been interpreted thoroughly. Based on the experimental studies in recent years, this review discusses several possible mechanisms of T2DM pathogenesis induced by TCF7L2.http://dx.doi.org/10.1080/13102818.2018.1438211T2DMTCF7L2genetic mutationWnt signaling pathwayβ-cell apoptosisproinsulin conversionβ-cell responsiveness
collection DOAJ
language English
format Article
sources DOAJ
author Zhi-qiu Huang
Yao-qi Liao
Run-ze Huang
Jin-peng Chen
Hui-lin Sun
spellingShingle Zhi-qiu Huang
Yao-qi Liao
Run-ze Huang
Jin-peng Chen
Hui-lin Sun
Possible role of TCF7L2 in the pathogenesis of type 2 diabetes mellitus
Biotechnology & Biotechnological Equipment
T2DM
TCF7L2
genetic mutation
Wnt signaling pathway
β-cell apoptosis
proinsulin conversion
β-cell responsiveness
author_facet Zhi-qiu Huang
Yao-qi Liao
Run-ze Huang
Jin-peng Chen
Hui-lin Sun
author_sort Zhi-qiu Huang
title Possible role of TCF7L2 in the pathogenesis of type 2 diabetes mellitus
title_short Possible role of TCF7L2 in the pathogenesis of type 2 diabetes mellitus
title_full Possible role of TCF7L2 in the pathogenesis of type 2 diabetes mellitus
title_fullStr Possible role of TCF7L2 in the pathogenesis of type 2 diabetes mellitus
title_full_unstemmed Possible role of TCF7L2 in the pathogenesis of type 2 diabetes mellitus
title_sort possible role of tcf7l2 in the pathogenesis of type 2 diabetes mellitus
publisher Taylor & Francis Group
series Biotechnology & Biotechnological Equipment
issn 1310-2818
1314-3530
publishDate 2018-07-01
description With people's changing life style and dietary habits, the prevalence of type 2 diabetes mellitus (T2DM) has become much more serious than ever before. T2DM is a polygenic metabolic disorder, resulting from the interaction of genetic and various environmental factors. Among all the T2DM related genes, the transcription factor 7 like 2 (TCF7L2) gene is one of the most relevant risk-related genes for T2DM. However, the role of TCF7L2 in T2DM pathogenesis has not yet been interpreted thoroughly. Based on the experimental studies in recent years, this review discusses several possible mechanisms of T2DM pathogenesis induced by TCF7L2.
topic T2DM
TCF7L2
genetic mutation
Wnt signaling pathway
β-cell apoptosis
proinsulin conversion
β-cell responsiveness
url http://dx.doi.org/10.1080/13102818.2018.1438211
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