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Lysophosphatidic Acid Inhibits Insulin Signaling in Primary Rat Hepatocytes via the LPA3 Receptor Subtype and is Increased in Obesity
Author(s) -
Susann Fayyaz,
Lukasz Japtok,
Fabian Schumacher,
Dominik Wigger,
Tim J. Schulz,
Kathrin Haubold,
Erich Gulbins,
Heinz Völler,
Burkhard Kleuser
Publication year - 2017
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.486
H-Index - 87
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.1159/000480470
Subject(s) - lysophosphatidic acid , autotaxin , endocrinology , medicine , insulin receptor , insulin resistance , protein kinase b , glycogen synthase , receptor , lysophosphatidylcholine , insulin , insulin receptor substrate , biology , chemistry , signal transduction , biochemistry , phospholipid , membrane , phosphatidylcholine
Obesity is a main risk factor for the development of hepatic insulin resistance and it is accompanied by adipocyte hypertrophy and an elevated expression of different adipokines such as autotaxin (ATX). ATX converts lysophosphatidylcholine to lysophosphatidic acid (LPA) and acts as the main producer of extracellular LPA. This bioactive lipid regulates a broad range of physiological and pathological responses by activation of LPA receptors (LPA1-6).

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