Abstract
Background: Environmental and genetic factors play a role in the pathogenesis and natural history of non-alcoholic fatty liver disease (NAFLD). Methods: In 114 subjects with NAFLD we report the prevalence and correlation with clinical parameters of three polymorphisms: interleukin-6 (-174G/C), plasma cell differentiation antigen (K121Q) and microsomal transfer protein (-493G/T). In 59 biopsied patients with NAFLD the polymorphisms were also related to histological features. Results: IL-6 -174C variant was more prevalent (p <0.01) in NAFLD compared to controls. In the NAFLD group, C carriers had higher HOMA-IR and fasting insulin than G carriers (p <0.05). The prevalence of IL-6/C variant was higher (83%) in biopsied than in not biopsied subjects (66%) (p <0.05). In biopsied subjects, C carriers had higher HOMA and fasting insulin (p <0.05) compared than those with G allele. The prevalence of IL-6 -174G/C polymorphism was significantly higher in NASH than in NAFLD (p = 0.048). At logistic regression analysis IL-6 -174C was an independent predictor of both NAFLD (OR 4.116, C.I. 1.126-15.048) and NASH (OR 7.035, C.I. 1.167-42.394). Conversely, the distribution of PC-1 and MTP polymorphisms was not significantly different compared to the control group, nor associated with clinical or histological characteristics. Conclusions: Our data suggest that IL-6 -174C genetic polymorphisms, involved in inflammation and insulin resistance, are associated with NASH. These data may contribute to the understanding of the genetic susceptibility to NAFLD.
| Original language | English |
|---|---|
| Pages (from-to) | 823-828 |
| Number of pages | 6 |
| Journal | Digestive and Liver Disease |
| Volume | 41 |
| Issue number | 11 |
| DOIs | |
| Publication status | Published - Nov 2009 |
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Keywords
- Genes
- IL-6
- Inflammation
- Insulin resistance
- Steatohepatitis
- Steatosis
ASJC Scopus subject areas
- Gastroenterology
- Hepatology
Cite this
Genetic polymorphisms in non-alcoholic fatty liver disease : Interleukin-6-174G/C polymorphism is associated with non-alcoholic steatohepatitis. / Carulli, L.; Canedi, I.; Rondinella, S.; Lombardini, S.; Ganazzi, D.; Fargion, S.; De Palma, M.; Lonardo, A.; Ricchi, M.; Bertolotti, M.; Carulli, N.; Loria, P.
In: Digestive and Liver Disease, Vol. 41, No. 11, 11.2009, p. 823-828.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Genetic polymorphisms in non-alcoholic fatty liver disease
T2 - Interleukin-6-174G/C polymorphism is associated with non-alcoholic steatohepatitis
AU - Carulli, L.
AU - Canedi, I.
AU - Rondinella, S.
AU - Lombardini, S.
AU - Ganazzi, D.
AU - Fargion, S.
AU - De Palma, M.
AU - Lonardo, A.
AU - Ricchi, M.
AU - Bertolotti, M.
AU - Carulli, N.
AU - Loria, P.
PY - 2009/11
Y1 - 2009/11
N2 - Background: Environmental and genetic factors play a role in the pathogenesis and natural history of non-alcoholic fatty liver disease (NAFLD). Methods: In 114 subjects with NAFLD we report the prevalence and correlation with clinical parameters of three polymorphisms: interleukin-6 (-174G/C), plasma cell differentiation antigen (K121Q) and microsomal transfer protein (-493G/T). In 59 biopsied patients with NAFLD the polymorphisms were also related to histological features. Results: IL-6 -174C variant was more prevalent (p <0.01) in NAFLD compared to controls. In the NAFLD group, C carriers had higher HOMA-IR and fasting insulin than G carriers (p <0.05). The prevalence of IL-6/C variant was higher (83%) in biopsied than in not biopsied subjects (66%) (p <0.05). In biopsied subjects, C carriers had higher HOMA and fasting insulin (p <0.05) compared than those with G allele. The prevalence of IL-6 -174G/C polymorphism was significantly higher in NASH than in NAFLD (p = 0.048). At logistic regression analysis IL-6 -174C was an independent predictor of both NAFLD (OR 4.116, C.I. 1.126-15.048) and NASH (OR 7.035, C.I. 1.167-42.394). Conversely, the distribution of PC-1 and MTP polymorphisms was not significantly different compared to the control group, nor associated with clinical or histological characteristics. Conclusions: Our data suggest that IL-6 -174C genetic polymorphisms, involved in inflammation and insulin resistance, are associated with NASH. These data may contribute to the understanding of the genetic susceptibility to NAFLD.
AB - Background: Environmental and genetic factors play a role in the pathogenesis and natural history of non-alcoholic fatty liver disease (NAFLD). Methods: In 114 subjects with NAFLD we report the prevalence and correlation with clinical parameters of three polymorphisms: interleukin-6 (-174G/C), plasma cell differentiation antigen (K121Q) and microsomal transfer protein (-493G/T). In 59 biopsied patients with NAFLD the polymorphisms were also related to histological features. Results: IL-6 -174C variant was more prevalent (p <0.01) in NAFLD compared to controls. In the NAFLD group, C carriers had higher HOMA-IR and fasting insulin than G carriers (p <0.05). The prevalence of IL-6/C variant was higher (83%) in biopsied than in not biopsied subjects (66%) (p <0.05). In biopsied subjects, C carriers had higher HOMA and fasting insulin (p <0.05) compared than those with G allele. The prevalence of IL-6 -174G/C polymorphism was significantly higher in NASH than in NAFLD (p = 0.048). At logistic regression analysis IL-6 -174C was an independent predictor of both NAFLD (OR 4.116, C.I. 1.126-15.048) and NASH (OR 7.035, C.I. 1.167-42.394). Conversely, the distribution of PC-1 and MTP polymorphisms was not significantly different compared to the control group, nor associated with clinical or histological characteristics. Conclusions: Our data suggest that IL-6 -174C genetic polymorphisms, involved in inflammation and insulin resistance, are associated with NASH. These data may contribute to the understanding of the genetic susceptibility to NAFLD.
KW - Genes
KW - IL-6
KW - Inflammation
KW - Insulin resistance
KW - Steatohepatitis
KW - Steatosis
UR - http://www.scopus.com/inward/record.url?scp=70349898246&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=70349898246&partnerID=8YFLogxK
U2 - 10.1016/j.dld.2009.03.005
DO - 10.1016/j.dld.2009.03.005
M3 - Article
VL - 41
SP - 823
EP - 828
JO - Digestive and Liver Disease
JF - Digestive and Liver Disease
SN - 1590-8658
IS - 11
ER -