<?xml version="1.0" encoding="utf-8"?>
<export-example>
  <doc>
    <id>1995</id>
    <completedYear>2009</completedYear>
    <publishedYear/>
    <thesisYearAccepted/>
    <language>eng</language>
    <pageFirst>1040</pageFirst>
    <pageLast>1049</pageLast>
    <pageNumber/>
    <edition/>
    <issue>5</issue>
    <volume>58</volume>
    <type>article</type>
    <publisherName>American Diabetes Association</publisherName>
    <publisherPlace/>
    <creatingCorporation/>
    <contributingCorporation/>
    <belongsToBibliography>1</belongsToBibliography>
    <completedDate>--</completedDate>
    <publishedDate>--</publishedDate>
    <thesisDateAccepted>--</thesisDateAccepted>
    <title language="eng">Liver-specific loss of lipolysis-stimulated lipoprotein receptor triggers systemic hyperlipidemia in mice</title>
    <abstract language="eng">In mammals, proper storage and distribution of lipids in and between tissues is essential for the maintenance of energy homeostasis. In contrast, aberrantly high levels of triglycerides in the blood ("hypertriglyceridemia") represent a hallmark of the metabolic syndrome and type 2 diabetes. As hypertriglyceridemia has been identified as an important risk factor for cardiovascular complications, in this study we aimed to identify molecular mechanisms in aberrant triglyceride elevation under these conditions.&#13;
To determine the importance of hepatic lipid handling for systemic dyslipidemia, we profiled the expression patterns of various hepatic lipid transporters and receptors under healthy and type 2 diabetic conditions. A differentially expressed lipoprotein receptor was functionally characterized by generating acute, liver-specific loss- and gain-of-function animal models.&#13;
We show that the hepatic expression of lipid transporter lipolysis-stimulated lipoprotein receptor (LSR) is specifically impaired in mouse models of obesity and type 2 diabetes and can be restored by leptin replacement. Experimental imitation of this pathophysiological situation by liver-specific knockdown of LSR promotes hypertriglyceridemia and elevated apolipoprotein (Apo)B and E serum levels in lean wild-type and ApoE knockout mice. In contrast, genetic restoration of LSR expression in obese animals to wild-type levels improves serum triglyceride levels and serum profiles in these mice.&#13;
The dysregulation of hepatic LSR under obese and diabetic conditions may provide a molecular rationale for systemic dyslipidemia in type 2 diabetes and the metabolic syndrome and represent a novel target for alternative treatment strategies in these patients.</abstract>
    <parentTitle language="eng">Diabetes</parentTitle>
    <identifier type="urn">urn:nbn:de:kobv:526-opus4-19954</identifier>
    <enrichment key="opus.import.date">2025-02-10T10:25:49+00:00</enrichment>
    <enrichment key="opus.source">sword</enrichment>
    <enrichment key="opus.import.user">sword</enrichment>
    <enrichment key="DOI_VoR">https://doi.org/10.2337/db08-1184</enrichment>
    <enrichment key="SourceTitle">Prachiti Narvekar, Mauricio Berriel Diaz, Anja Krones-Herzig, Ulrike Hardeland, Daniela Strzoda, Sigrid Stöhr, Marcus Frohme, Stephan Herzig; Liver-Specific Loss of Lipolysis-Stimulated Lipoprotein Receptor Triggers Systemic Hyperlipidemia in Mice. Diabetes 1 May 2009; 58 (5): 1040–1049. https://doi.org/10.2337/db08-1184</enrichment>
    <licence>Creative Commons - CC BY-NC-ND 3.0 - Namensnennung - Nicht-kommerziell - Keine Bearbeitung 3.0 Unported</licence>
    <author>Prachiti Narvekar</author>
    <author>Mauricio Berriel Diaz</author>
    <author>Anja Krones-Herzig</author>
    <author>Ulrike Hardeland</author>
    <author>Daniela Strzoda</author>
    <author>Sigrid Stöhr</author>
    <author>Marcus Frohme</author>
    <author>Stephan Herzig</author>
    <collection role="ddc" number="612">Humanphysiologie</collection>
    <collection role="ddc" number="616">Krankheiten</collection>
    <collection role="institutes" number="">Fachbereich Ingenieurwesen / Wirtschaftsingenieurwesen (bis 8/2014)</collection>
    <collection role="open_access" number="">open_access</collection>
    <collection role="Import" number="import">Import</collection>
    <thesisPublisher>Technische Hochschule Wildau</thesisPublisher>
    <file>https://opus4.kobv.de/opus4-th-wildau/files/1995/zdb00509001040.pdf</file>
  </doc>
</export-example>
