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PNPLA3 genetic variants determine hepatic steatosis in non-obese chronic hepatitis C patients.

Huang CF, Chen JJ, Yeh ML, Huang CI, Hsieh MY, Yang HL, Dai CY, Huang JF, Lin ZY, Chen SC, Chuang WL, Chen YL, Yu ML - Sci Rep (2015)

Bottom Line: PNPLA3 genetic variants had minimal effects on hepatic steatosis among overweight or obese patients.In conclusions, both PNPLA3 genetic variants and BMI played important roles in hepatic steatosis among Asian chronic hepatitis C patients.However, the genetic effect was mainly restricted to non-obese patients.

View Article: PubMed Central - PubMed

Affiliation: 1] Graguate Institute of Clinical Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan [2] Hepatobiliary Division, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan [3] Department of Occupational Medicine, Kaohsiung Municipal Ta-Tung Hospital, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan [4] Faculty of Internal Medicine, School of Medicine, College of Medicine, and Center for Lipid and Glycomedicine Research, Kaohsiung Medical University, Kaohsiung, Taiwan.

ABSTRACT
The influence of patatin-like phospholipase domain-containing 3 (PNPLA3) genetic variants in the development of liver steatosis in Asian chronic hepatitis C patients remains elusive. A total of 1018 biopsy-proven chronic hepatitis C patients were enrolled for evaluation. The proportions of PNPLA3 rs738409 GG genotype carriage were 7.8% (44/563), 15.8% (58/367) and 19.3% (17/88) in patients with no (liver fat content < 5%), mild (5-33%) and moderate/severe (> 66%) hepatic steatosis, respectively (trend P < 0.001). Stepwise logistic regression analysis revealed that the strongest factor independently associated with steatosis was the carriage of the PNPLA3 rs738409 GG genotype (odds ratio [OR]/95% confidence intervals [CI]:2.34/1.557-3.515, P < 0.001). Among the patients with BMI < 24 kg/m(2), carriage of the rs738409 GG genotype was the only factor associated with hepatic steatosis (OR/CI:3.44/1.824-6.500, P < 0.001). PNPLA3 genetic variants had minimal effects on hepatic steatosis among overweight or obese patients. Compared to patients with BMI < 24 kg/m(2)/non-GG genotype, those with BMI >24 kg/m(2)/GG genotype were more likely to have hepatic steatosis (OR/CI:3.87/2.292-6.524, P < 0.001). In conclusions, both PNPLA3 genetic variants and BMI played important roles in hepatic steatosis among Asian chronic hepatitis C patients. However, the genetic effect was mainly restricted to non-obese patients.

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Percentage of patients with hepatic steatosis <5%, 5–33% and >33%, respectively, stratified by body mass index and PNPLA3 rs38409 genotype.Supplementary Figure 1 Proportion of hepatic steatosis in patients with different PNPLA3 rs38409 genotypes, stratified by BMI.
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f2: Percentage of patients with hepatic steatosis <5%, 5–33% and >33%, respectively, stratified by body mass index and PNPLA3 rs38409 genotype.Supplementary Figure 1 Proportion of hepatic steatosis in patients with different PNPLA3 rs38409 genotypes, stratified by BMI.

Mentions: Both the PNPLA3 genetic variants and BMI determined hepatic steatosis. We further analyzed their interactions in contributing to fatty liver. There was a significantly increased proportion of mild and moderate/severe hepatic steatosis in patients with BMI>24 kg/m2 and the PNPLA3 rs738409 GG genotype compared to those with BMI<24 kg/m2 and/or non-GG genotype (P < 0.001) (fig. 2). The proportion of hepaticsteatosis was 30.5%, 51.8% and 63.5% in patients with BMI<24 kg/m2/non-GG genotype, BMI<24 kg/m2/GG genotype or BMI>24 kg/m2/non-GG genotype, and BMI>24 kg/m2/GG genotype, respectively. Compared to patients with BMI<24 kg/m2/non-GG genotype, those with BMI>24 kg/m2/GG genotype were more likely to have hepatic steatosis (OR/CI:3.87/2.292–6.524, P < 0.001), followed by those patients with BMI<24 kg/m2/GG genotype or BMI>24 kg/m2/non-GG genotype (OR/CI:2.43/1.849–3.202, P < 0.001) (Table 5).


PNPLA3 genetic variants determine hepatic steatosis in non-obese chronic hepatitis C patients.

Huang CF, Chen JJ, Yeh ML, Huang CI, Hsieh MY, Yang HL, Dai CY, Huang JF, Lin ZY, Chen SC, Chuang WL, Chen YL, Yu ML - Sci Rep (2015)

Percentage of patients with hepatic steatosis <5%, 5–33% and >33%, respectively, stratified by body mass index and PNPLA3 rs38409 genotype.Supplementary Figure 1 Proportion of hepatic steatosis in patients with different PNPLA3 rs38409 genotypes, stratified by BMI.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4490397&req=5

f2: Percentage of patients with hepatic steatosis <5%, 5–33% and >33%, respectively, stratified by body mass index and PNPLA3 rs38409 genotype.Supplementary Figure 1 Proportion of hepatic steatosis in patients with different PNPLA3 rs38409 genotypes, stratified by BMI.
Mentions: Both the PNPLA3 genetic variants and BMI determined hepatic steatosis. We further analyzed their interactions in contributing to fatty liver. There was a significantly increased proportion of mild and moderate/severe hepatic steatosis in patients with BMI>24 kg/m2 and the PNPLA3 rs738409 GG genotype compared to those with BMI<24 kg/m2 and/or non-GG genotype (P < 0.001) (fig. 2). The proportion of hepaticsteatosis was 30.5%, 51.8% and 63.5% in patients with BMI<24 kg/m2/non-GG genotype, BMI<24 kg/m2/GG genotype or BMI>24 kg/m2/non-GG genotype, and BMI>24 kg/m2/GG genotype, respectively. Compared to patients with BMI<24 kg/m2/non-GG genotype, those with BMI>24 kg/m2/GG genotype were more likely to have hepatic steatosis (OR/CI:3.87/2.292–6.524, P < 0.001), followed by those patients with BMI<24 kg/m2/GG genotype or BMI>24 kg/m2/non-GG genotype (OR/CI:2.43/1.849–3.202, P < 0.001) (Table 5).

Bottom Line: PNPLA3 genetic variants had minimal effects on hepatic steatosis among overweight or obese patients.In conclusions, both PNPLA3 genetic variants and BMI played important roles in hepatic steatosis among Asian chronic hepatitis C patients.However, the genetic effect was mainly restricted to non-obese patients.

View Article: PubMed Central - PubMed

Affiliation: 1] Graguate Institute of Clinical Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan [2] Hepatobiliary Division, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan [3] Department of Occupational Medicine, Kaohsiung Municipal Ta-Tung Hospital, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan [4] Faculty of Internal Medicine, School of Medicine, College of Medicine, and Center for Lipid and Glycomedicine Research, Kaohsiung Medical University, Kaohsiung, Taiwan.

ABSTRACT
The influence of patatin-like phospholipase domain-containing 3 (PNPLA3) genetic variants in the development of liver steatosis in Asian chronic hepatitis C patients remains elusive. A total of 1018 biopsy-proven chronic hepatitis C patients were enrolled for evaluation. The proportions of PNPLA3 rs738409 GG genotype carriage were 7.8% (44/563), 15.8% (58/367) and 19.3% (17/88) in patients with no (liver fat content < 5%), mild (5-33%) and moderate/severe (> 66%) hepatic steatosis, respectively (trend P < 0.001). Stepwise logistic regression analysis revealed that the strongest factor independently associated with steatosis was the carriage of the PNPLA3 rs738409 GG genotype (odds ratio [OR]/95% confidence intervals [CI]:2.34/1.557-3.515, P < 0.001). Among the patients with BMI < 24 kg/m(2), carriage of the rs738409 GG genotype was the only factor associated with hepatic steatosis (OR/CI:3.44/1.824-6.500, P < 0.001). PNPLA3 genetic variants had minimal effects on hepatic steatosis among overweight or obese patients. Compared to patients with BMI < 24 kg/m(2)/non-GG genotype, those with BMI >24 kg/m(2)/GG genotype were more likely to have hepatic steatosis (OR/CI:3.87/2.292-6.524, P < 0.001). In conclusions, both PNPLA3 genetic variants and BMI played important roles in hepatic steatosis among Asian chronic hepatitis C patients. However, the genetic effect was mainly restricted to non-obese patients.

No MeSH data available.


Related in: MedlinePlus