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Low hepatic copper content and PNPLA3 polymorphism in non-alcoholic fatty liver disease in patients without metabolic syndrome.
J Trace Elem Med Biol. 2017 Jan; 39:100-107.JT

Abstract

INTRODUCTION

The pathogenesis of non-alcoholic fatty liver disease (NAFLD) is multifactorial including metabolic, genetic (e.g. PNPLA3 [patatin-like phospholipase domain-containing 3 gene]), viral factors and drugs. Besides, there is evidence for a role of copper deficiency. Aim of the study was to evaluate the role of hepatic copper content, PNPLA3 in NAFLD patients with and without metabolic syndrome (MetS).

METHODS

One-hundred seventy-four NAFLD patients, who underwent liver biopsy for diagnostic work-up, were studied. Diagnosis of MetS was based on the WHO Clinical Criteria. Steatosis was semiquantified as percentage of fat containing hepatocytes and was graded according to Brunt. Histological features of non-alcoholic steatohepatitis (NASH) were assessed using the Bedossa classification. Hepatic copper content (in μg/g dry weight) was measured by flame atomic absorption spectroscopy. SNP rs738409 in PNPLA3 was investigated by RT-PCR.

RESULTS

Mean hepatic copper content was 22.3 (19.6-25.1) μg/g. The mean percentage of histologically lipid containing hepatocytes was 42.2% (38.3-46.0) and correlated inversely with hepatic copper content (ρ=-0.358, P<0.001). By subgroup analysis this inverse correlation remained significant only in patients without MetS (OR: 0.959 [CI95%: 0.926-0.944], P=0.020). Presence of minor allele (G) of PNPLA3 was also associated with moderate/severe steatosis (≥33%) both in patients with (OR: 2.405 [CI95%: 1.220-4.744], P=0.011) and without MetS (OR: 2.481 [CI95%: 1.172-5.250], P=0.018), but was only associated with NASH (OR: 2.002 [CI95%: 1.062-3.772], P=0.032) and liver fibrosis (OR: 2.646 [CI95%: 1.299-5.389], P=0.007) in patients without MetS.

CONCLUSION

Hepatic copper content and PNPLA3 mutations are associated with disease activity in NAFLD patients without MetS. Presence of MetS appears to mask the effects of hepatic copper and PNPLA3.

Authors+Show Affiliations

Department of Internal Medicine III, Division of Gastroenterology and Hepatology, Medical University of Vienna, Vienna, Austria.Department of Internal Medicine III, Division of Gastroenterology and Hepatology, Medical University of Vienna, Vienna, Austria.Department of Internal Medicine I, Paracelsus Private Medical University, Salzburg, Austria.Department of Internal Medicine III, Division of Gastroenterology and Hepatology, Medical University of Vienna, Vienna, Austria.Department of Internal Medicine, KH Oberndorf, Oberndorf, Austria.Department of Internal Medicine III, Division of Gastroenterology and Hepatology, Medical University of Vienna, Vienna, Austria.Department of Internal Medicine, KH Oberndorf, Oberndorf, Austria.Institute of Clinical Pathology, Medical University of Vienna, Vienna, Austria.Department of Internal Medicine III, Division of Gastroenterology and Hepatology, Medical University of Vienna, Vienna, Austria.Department of Internal Medicine, KH Oberndorf, Oberndorf, Austria.Department of Internal Medicine III, Division of Gastroenterology and Hepatology, Medical University of Vienna, Vienna, Austria. Electronic address: peter.ferenci@meduniwien.ac.at.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

27908400

Citation

Stättermayer, Albert Friedrich, et al. "Low Hepatic Copper Content and PNPLA3 Polymorphism in Non-alcoholic Fatty Liver Disease in Patients Without Metabolic Syndrome." Journal of Trace Elements in Medicine and Biology : Organ of the Society for Minerals and Trace Elements (GMS), vol. 39, 2017, pp. 100-107.
Stättermayer AF, Traussnigg S, Aigner E, et al. Low hepatic copper content and PNPLA3 polymorphism in non-alcoholic fatty liver disease in patients without metabolic syndrome. J Trace Elem Med Biol. 2017;39:100-107.
Stättermayer, A. F., Traussnigg, S., Aigner, E., Kienbacher, C., Huber-Schönauer, U., Steindl-Munda, P., Stadlmayr, A., Wrba, F., Trauner, M., Datz, C., & Ferenci, P. (2017). Low hepatic copper content and PNPLA3 polymorphism in non-alcoholic fatty liver disease in patients without metabolic syndrome. Journal of Trace Elements in Medicine and Biology : Organ of the Society for Minerals and Trace Elements (GMS), 39, 100-107. https://doi.org/10.1016/j.jtemb.2016.08.006
Stättermayer AF, et al. Low Hepatic Copper Content and PNPLA3 Polymorphism in Non-alcoholic Fatty Liver Disease in Patients Without Metabolic Syndrome. J Trace Elem Med Biol. 2017;39:100-107. PubMed PMID: 27908400.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Low hepatic copper content and PNPLA3 polymorphism in non-alcoholic fatty liver disease in patients without metabolic syndrome. AU - Stättermayer,Albert Friedrich, AU - Traussnigg,Stefan, AU - Aigner,Elmar, AU - Kienbacher,Christian, AU - Huber-Schönauer,Ursula, AU - Steindl-Munda,Petra, AU - Stadlmayr,Andreas, AU - Wrba,Friedrich, AU - Trauner,Michael, AU - Datz,Christian, AU - Ferenci,Peter, Y1 - 2016/08/20/ PY - 2016/06/06/received PY - 2016/08/02/revised PY - 2016/08/18/accepted PY - 2016/12/3/entrez PY - 2016/12/3/pubmed PY - 2017/4/30/medline KW - Copper KW - Fibrosis KW - Metabolic syndrome KW - NAFLD KW - NASH KW - PNPLA3 SP - 100 EP - 107 JF - Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) JO - J Trace Elem Med Biol VL - 39 N2 - INTRODUCTION: The pathogenesis of non-alcoholic fatty liver disease (NAFLD) is multifactorial including metabolic, genetic (e.g. PNPLA3 [patatin-like phospholipase domain-containing 3 gene]), viral factors and drugs. Besides, there is evidence for a role of copper deficiency. Aim of the study was to evaluate the role of hepatic copper content, PNPLA3 in NAFLD patients with and without metabolic syndrome (MetS). METHODS: One-hundred seventy-four NAFLD patients, who underwent liver biopsy for diagnostic work-up, were studied. Diagnosis of MetS was based on the WHO Clinical Criteria. Steatosis was semiquantified as percentage of fat containing hepatocytes and was graded according to Brunt. Histological features of non-alcoholic steatohepatitis (NASH) were assessed using the Bedossa classification. Hepatic copper content (in μg/g dry weight) was measured by flame atomic absorption spectroscopy. SNP rs738409 in PNPLA3 was investigated by RT-PCR. RESULTS: Mean hepatic copper content was 22.3 (19.6-25.1) μg/g. The mean percentage of histologically lipid containing hepatocytes was 42.2% (38.3-46.0) and correlated inversely with hepatic copper content (ρ=-0.358, P<0.001). By subgroup analysis this inverse correlation remained significant only in patients without MetS (OR: 0.959 [CI95%: 0.926-0.944], P=0.020). Presence of minor allele (G) of PNPLA3 was also associated with moderate/severe steatosis (≥33%) both in patients with (OR: 2.405 [CI95%: 1.220-4.744], P=0.011) and without MetS (OR: 2.481 [CI95%: 1.172-5.250], P=0.018), but was only associated with NASH (OR: 2.002 [CI95%: 1.062-3.772], P=0.032) and liver fibrosis (OR: 2.646 [CI95%: 1.299-5.389], P=0.007) in patients without MetS. CONCLUSION: Hepatic copper content and PNPLA3 mutations are associated with disease activity in NAFLD patients without MetS. Presence of MetS appears to mask the effects of hepatic copper and PNPLA3. SN - 1878-3252 UR - https://www.unboundmedicine.com/medline/citation/27908400/Low_hepatic_copper_content_and_PNPLA3_polymorphism_in_non_alcoholic_fatty_liver_disease_in_patients_without_metabolic_syndrome_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0946-672X(16)30221-8 DB - PRIME DP - Unbound Medicine ER -