AI Article Synopsis
- The study identifies a link between glutathione transferase Kappa (GSTK1-1) levels, obesity, and gene polymorphisms related to insulin secretion and fat deposition.
- Two significant single nucleotide polymorphisms (SNPs) in the GSTK1 promoter were discovered, with one SNP (-1308) affecting transcription differently in liver and kidney cells, suggesting tissue-specific effects.
- Another SNP (-1032) reduces transcription by affecting methylation, offering new insights into how genetic factors regulate GSTK1 expression, which may influence metabolic processes like insulin secretion and fat accumulation.
Article Abstract
The level of glutathione transferase Kappa (GSTK1-1) has been correlated with obesity (Liu et.al. 2008 PNAS 105: 18302-7) and a polymorphism in the hGSTK1 promoter has been associated with insulin secretion and fat deposition (Gao et al 2009 Endocr J 56: 487-94). We searched for additional polymorphisms that may influence GSTK1-1 function or expression. Two SNPs were identified in the 5' non-coding region. A SNP at -1308 that occurs in Chinese subjects is predicted to eliminate a FXR/RXR transcription factor-binding site and causes a 55% increase in transcription rate in HepG2 cells and a 59% decrease in HEK293 cells. These data suggest that the impact of this polymorphism is complex and tissue specific. A SNP at -1032 alters a methylation site and represses transcription by 38%. These observations provide the first functional insight into genetic factors that regulate hGSTK1 expression and may directly influence insulin secretion and fat deposition.
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| http://dx.doi.org/10.1016/j.ygeno.2010.02.007 | DOI Listing |
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