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Role of the Lipolysis Stimulated Lipoprotein Receptor in Hepatic Lipid Homeostasis during the Postprandial Phase
Author(s) -
Yen Frances,
Akbar Samina,
Layeghkhavidaki Hamed,
Pinçon Anthony,
Lanhers MarieClaire,
Oster Thierry,
Gregory Pauron Lynn,
Corbier Catherine
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.743.2
Subject(s) - medicine , endocrinology , postprandial , lipolysis , lipid metabolism , biology , glucose homeostasis , lipoprotein , adipose tissue , insulin resistance , insulin , cholesterol
Elevated postprandial lipemia (PPL) as an important risk factor for cardiovascular disease has been attributed to the accumulation of atherogenic remnant lipoproteins in the circulation. The hepatic lipolysis stimulated lipoprotein receptor, LSR, participates in the removal of these particles in the liver during the postprandial phase. LSR expression is regulated by leptin, and is reduced in obese mouse models which also display high PPL, suggesting a role of LSR in the regulation of lipid homeostasis. To determine the effect of reduced LSR expression on hepatic lipid metabolism, pathway‐specific qPCR arrays were used to determine mRNA expression profiles of genes related to lipid metabolism in livers from female 6‐month old LSR +/‐ mice and LSR +/+ littermates after 6 weeks on a standard (STD) or high‐fat diet (60 % kcal, HFD). Of the 84 genes studied, 32 were significantly down‐regulated in STD‐LSR +/‐ mice as compared to STD‐LSR +/+ , a majority of which were involved in insulin and adipokine‐signaling pathways and were PPAR‐a target genes. Of these genes, 70% were also modified in HFD‐LSR +/+ , suggesting that STD‐LSR +/‐ demonstrated a propensity towards a “high‐fat”‐like profile. Interestingly, the expression of 3 genes related to the inflammatory pathway: Ilβ, TNF‐α, and Il10 was increased in HFD‐LSR +/‐ mice, which could contribute to PPL‐associated inflammation. Our results show similar profiles of genes affected by either LSR heterozygosity or by HFD, pointing towards a significant contribution of LSR in the regulation of lipid homeostasis during the postprandial phase. Grant source: French Ministry MESR, Région Lorraine