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JCI online early table of contents: April 13, 2009
Date:4/13/2009

s, they developed atherosclerotic lesions with massive nanoparticle accumulation. The authors therefore conclude from these results that targeting lipoprotein pintocytosis should be considered when developing novel atherosclerotic therapies that prevent macrophage uptake of lipoproteins.

TITLE: Fluorescent pegylated nanoparticles demonstrate fluid-phase pinocytosis by macrophages in mouse atherosclerotic lesions

AUTHOR CONTACT:
Howard S. Kruth
NHLBI, National Institutes of Health, Bethesda, Maryland, USA.
Phone: (301) 496-4826; Fax: (301) 402-4359; E-mail: kruthh@nhlbi.nih.gov.

View the PDF of this article at: https://www.the-jci.org/article.php?id=35548


METABOLIC DISEASE: Adding insight into nonalcoholic fatty liver disease

Nonalcoholic fatty liver disease (NAFLD) is a common chronic liver disease associated with conditions such as obesity, type 2 diabetes, and high blood pressure. It covers a spectrum of disease states, beginning with hepatic steatosis, which leads to steatohepatitis, cirrhosis, and ultimately liver cancer. Fabienne Foufelle and colleagues, at INSERM UMRS 872, Paris, have now provided new insight into the mechanisms underlying hepatic steatosis in obese insulin-resistant rodents. Specifically, they find that ER stress activates the protein SREBP-1c, which is intimately involved in hepatic lipogenesis (and thereby hepatic steatosis), explaining why ER stress has a role in hepatic steatosis. Further, they show that overexpression of the protein GRP78 inhibits both insulin and ER stressinduced activation of SREBP-1c.

TITLE: GRP78 expression inhibits insulin and ER stressinduced SREBP-1c activation and reduces hepatic steatosis in mice

AUTHOR CONTACT:
Fabienne Foufelle
INSERM UMR-S 872, Centre de Recherche des Cordeliers, Paris, France.
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Contact: Karen Honey
press_releases@the-jci.org
215-573-1850
Journal of Clinical Investigation
Source:Eurekalert

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