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Article

Dissociation of Fatty Liver and Insulin Resistance in I148M PNPLA3 Carriers: Differences in Diacylglycerol (DAG) FA18:1 Lipid Species as a Possible Explanation

1
Department of Internal Medicine IV, Division of Endocrinology, Diabetology, Angiology, Nephrology and Clinical Chemistry, University Hospital Tübingen, 72076 Tübingen, Germany
2
Institute for Diabetes Research and Metabolic Diseases of the Helmholtz Center Munich, University of Tübingen, 72076 Tübingen, Germany
3
German Center for Diabetes Research (DZD e.V.), 85764 Neuherberg, Germany
4
Sciex Germany GmbH, 64293 Darmstadt, Germany
5
Department of General, Visceral and Transplant Surgery, University Hospital Tübingen, 72076 Tübingen, Germany
6
Institute for Clinical Biochemistry and Pathobiochemistry of DDZ, University of Düsseldorf, 40225 Düsseldorf, Germany
*
Author to whom correspondence should be addressed.
Nutrients 2018, 10(9), 1314; https://doi.org/10.3390/nu10091314
Received: 6 August 2018 / Revised: 12 September 2018 / Accepted: 13 September 2018 / Published: 17 September 2018
Fatty liver is tightly associated with insulin resistance and the development of type 2 diabetes. I148M variant in patatin-like phospholipase domain-containing protein 3 (PNPLA3) gene is associated with high liver fat but normal insulin sensitivity. The underlying mechanism of the disassociation between high liver fat but normal insulin sensitivity remains obscure. We investigated the effect of I148M variant on hepatic lipidome of subjects with or without fatty liver, using the Lipidyzer method. Liver samples of four groups of subjects consisting of normal liver fat with wild-type PNPLA3 allele (group 1); normal liver fat with variant PNPLA3 allele (group 2); high liver fat with wild-type PNPLA3 allele (group 3); high liver fat with variant PNPLA3 allele (group 4); were analyzed. When high liver fat to normal liver fat groups were compared, wild-type carriers (group 3 vs. group 1) showed similar lipid changes compared to I148M PNPLA3 carriers (group 4 vs. group 2). On the other hand, in wild-type carriers, increased liver fat significantly elevated the proportion of specific DAGs (diacylglycerols), mostly DAG (FA18:1) which, however, remained unchanged in I148M PNPLA3 carriers. Since DAG (FA18:1) has been implicated in hepatic insulin resistance, the unaltered proportion of DAG (FA18:1) in I148M PNPLA3 carriers with fatty liver may explain the normal insulin sensitivity in these subjects. View Full-Text
Keywords: NAFLD; liver; PNPLA3; diacylglycerol; lipidomics NAFLD; liver; PNPLA3; diacylglycerol; lipidomics
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MDPI and ACS Style

Franko, A.; Merkel, D.; Kovarova, M.; Hoene, M.; Jaghutriz, B.A.; Heni, M.; Königsrainer, A.; Papan, C.; Lehr, S.; Häring, H.-U.; Peter, A. Dissociation of Fatty Liver and Insulin Resistance in I148M PNPLA3 Carriers: Differences in Diacylglycerol (DAG) FA18:1 Lipid Species as a Possible Explanation. Nutrients 2018, 10, 1314. https://doi.org/10.3390/nu10091314

AMA Style

Franko A, Merkel D, Kovarova M, Hoene M, Jaghutriz BA, Heni M, Königsrainer A, Papan C, Lehr S, Häring H-U, Peter A. Dissociation of Fatty Liver and Insulin Resistance in I148M PNPLA3 Carriers: Differences in Diacylglycerol (DAG) FA18:1 Lipid Species as a Possible Explanation. Nutrients. 2018; 10(9):1314. https://doi.org/10.3390/nu10091314

Chicago/Turabian Style

Franko, Andras; Merkel, Dietrich; Kovarova, Marketa; Hoene, Miriam; Jaghutriz, Benjamin A.; Heni, Martin; Königsrainer, Alfred; Papan, Cyrus; Lehr, Stefan; Häring, Hans-Ulrich; Peter, Andreas. 2018. "Dissociation of Fatty Liver and Insulin Resistance in I148M PNPLA3 Carriers: Differences in Diacylglycerol (DAG) FA18:1 Lipid Species as a Possible Explanation" Nutrients 10, no. 9: 1314. https://doi.org/10.3390/nu10091314

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