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PPARG gene Pro12Ala variant contributes to the development of non-alcoholic fatty liver in middle-aged and older Chinese population

Yang, Zhen; Wen, Jie; Li, Qin; Tao, Xiaoming; Ye, Zi; He, Min; Zhang, Weiwei; Huang, Ying; Chen, Lili and Ling, Charlotte LU , et al. (2012) In Molecular and Cellular Endocrinology 348(1). p.255-259
Abstract
Oxidative stress has been suggested to contribute to the development of non-alcoholic fatty liver disease (NAFLD). Peroxisome proliferator-activated receptor gamma (PPAR-gamma) heterozygous mice and Pro12Ala (C/G) polymorphism in PPARG exhibited increased resistance to oxidative stress. Smoking increases the production of reactive oxygen species, which could accelerates oxidative stress under overnutrition. To explore whether the C/G polymorphism, alone or in combination with smoking, may promote the development of non-alcoholic fatty liver, a case-control study was performed in 903 Chinese subjects. Among the study population, 436 patients with B-mode ultrasound-proven NAFLD (318 with steatosis hepatis I degrees, 90 with steatosis hepatis... (More)
Oxidative stress has been suggested to contribute to the development of non-alcoholic fatty liver disease (NAFLD). Peroxisome proliferator-activated receptor gamma (PPAR-gamma) heterozygous mice and Pro12Ala (C/G) polymorphism in PPARG exhibited increased resistance to oxidative stress. Smoking increases the production of reactive oxygen species, which could accelerates oxidative stress under overnutrition. To explore whether the C/G polymorphism, alone or in combination with smoking, may promote the development of non-alcoholic fatty liver, a case-control study was performed in 903 Chinese subjects. Among the study population, 436 patients with B-mode ultrasound-proven NAFLD (318 with steatosis hepatis I degrees, 90 with steatosis hepatis II degrees and 28 with steatosis hepatis III degrees) and 467 controls were genotyped by using TaqMan allelic discrimination assays. After adjusting for confounders, the C/C genotype significantly associated with NAFLD (OR = 1.87, 95%CI 1.13-2.85, p = 0.009); smoking was also an independent risk factor for NAFLD (OR = 1.69, 95%CI 1.18-2.43, p = 0.025). In addition, we found possible synergistic effects, the higher risk group (smokers with the C/C genotype) showed 3.75 times higher risk of NAFLD than the low-risk group (non-smokers with C/G genotype) in a multiple logistic analysis after adjusting for the confounders (p < 0.001), but no departure from additivity was found. Our results indicated that the C/C genotype and smoking were significant independent risk factors for NAFLD. The possible synergistic effects of genotype and smoking may promote the development of NAFLD by aggravating oxidative stress, which supports the hypothesis that oxidative stress contributes to the development of NAFLD. (C) 2011 Elsevier Ireland Ltd. All rights reserved. (Less)
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keywords
Pro/Ala variant, PPARG gene, Smoking, Synergistic effect, Non-alcoholic, fatty liver
in
Molecular and Cellular Endocrinology
volume
348
issue
1
pages
255 - 259
publisher
Elsevier
external identifiers
  • wos:000297539400029
  • scopus:80755189999
ISSN
1872-8057
DOI
10.1016/j.mce.2011.09.001
language
English
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yes
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57e41155-52a1-4914-82fb-3059fe017e0e (old id 2295798)
date added to LUP
2012-01-18 11:43:54
date last changed
2017-04-09 03:08:26
@article{57e41155-52a1-4914-82fb-3059fe017e0e,
  abstract     = {Oxidative stress has been suggested to contribute to the development of non-alcoholic fatty liver disease (NAFLD). Peroxisome proliferator-activated receptor gamma (PPAR-gamma) heterozygous mice and Pro12Ala (C/G) polymorphism in PPARG exhibited increased resistance to oxidative stress. Smoking increases the production of reactive oxygen species, which could accelerates oxidative stress under overnutrition. To explore whether the C/G polymorphism, alone or in combination with smoking, may promote the development of non-alcoholic fatty liver, a case-control study was performed in 903 Chinese subjects. Among the study population, 436 patients with B-mode ultrasound-proven NAFLD (318 with steatosis hepatis I degrees, 90 with steatosis hepatis II degrees and 28 with steatosis hepatis III degrees) and 467 controls were genotyped by using TaqMan allelic discrimination assays. After adjusting for confounders, the C/C genotype significantly associated with NAFLD (OR = 1.87, 95%CI 1.13-2.85, p = 0.009); smoking was also an independent risk factor for NAFLD (OR = 1.69, 95%CI 1.18-2.43, p = 0.025). In addition, we found possible synergistic effects, the higher risk group (smokers with the C/C genotype) showed 3.75 times higher risk of NAFLD than the low-risk group (non-smokers with C/G genotype) in a multiple logistic analysis after adjusting for the confounders (p &lt; 0.001), but no departure from additivity was found. Our results indicated that the C/C genotype and smoking were significant independent risk factors for NAFLD. The possible synergistic effects of genotype and smoking may promote the development of NAFLD by aggravating oxidative stress, which supports the hypothesis that oxidative stress contributes to the development of NAFLD. (C) 2011 Elsevier Ireland Ltd. All rights reserved.},
  author       = {Yang, Zhen and Wen, Jie and Li, Qin and Tao, Xiaoming and Ye, Zi and He, Min and Zhang, Weiwei and Huang, Ying and Chen, Lili and Ling, Charlotte and Qu, Shen and Hu, Renming},
  issn         = {1872-8057},
  keyword      = {Pro/Ala variant,PPARG gene,Smoking,Synergistic effect,Non-alcoholic,fatty liver},
  language     = {eng},
  number       = {1},
  pages        = {255--259},
  publisher    = {Elsevier},
  series       = {Molecular and Cellular Endocrinology},
  title        = {PPARG gene Pro12Ala variant contributes to the development of non-alcoholic fatty liver in middle-aged and older Chinese population},
  url          = {http://dx.doi.org/10.1016/j.mce.2011.09.001},
  volume       = {348},
  year         = {2012},
}