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Lipoprotein metabolism in liver diseases

Perez-Matos, Maria Camilaa; Sandhu, Bynvantb; Bonder, Alana; Jiang, Zhenghui Gordona

doi: 10.1097/MOL.0000000000000569
NUTRITION AND METABOLISM: Edited by Frank M. Sacks and Majken K. Jensen
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Purpose of review The liver is the central hub of lipoprotein metabolism. A complex relationship exists between dyslipidemia and chronic liver diseases (CLDs). Recent advances in the genetics of nonalcoholic fatty liver disease (NAFLD) and alcoholic liver disease (ALD) exemplify the pivotal role of lipoprotein metabolism in the pathogenesis of CLD. We review these relationships in four quintessential forms of CLD: NAFLD, ALD, cholestatic liver disease and cirrhosis, with a focus on recent discoveries.

Recent findings An I148 M variant in patatin-like phospholipase domain-containing protein 3 (PNPLA3) and an E167K variant in transmembrane 6 superfamily 2 (TM6SF2) are major genetic risk factors for the development and progression of NAFLD. These genetic variants also increase the risk of ALD. Both PNPLA3 and TM6SF2 are involved in the hepatic assembly of very low-density lipoprotein. The discovery of these two genetic variants highlights the risk of CLD when environmental factors are combined with functional modifications in the lipoprotein metabolism pathway.

Summary The relationship between CLD and lipoprotein metabolism is reciprocal. On the one hand, the progression of CLD impairs lipoprotein metabolism; on the other hand, modifications in lipoprotein metabolism can substantially increase the risk of CLD. These relationships are at play among the most common forms of CLD affecting a significant proportion of the population.

aDivision of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA

bDepartment of Surgery and Cancer, Imperial College London, London, UK

Correspondence to Zhenghui Gordon Jiang, Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Liver Center, 110 Francis St. Suite 8E, Boston, MA 02115, USA. Tel: +1 617-632-1070; fax: +1 617-623-1065; e-mail: zgjiang@bidmc.harvard.edu

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