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Publication
Expression of the human apoE2 isoform in adipocytes: altered cellular processing
and impaired adipocyte lipogenesis.
Authors
Huang ZH, Maeda N, Mazzone T
Submitted By
Submitted Externally on 3/4/2015
Status
Published
Journal
Journal of lipid research
Year
2011
Date Published
9/1/2011
Volume : Pages
52 : 1733 - 1741
PubMed Reference
Abstract
Expression of apoE in adipocytes has been shown to have an important role in
modulating adipocyte triglyceride (TG) metabolism and gene expression that is
independent of circulating and extracellular apoE. The impact of adipocyte
expression of common human apoE isoforms was evaluated using adipocytes
harvested from human apoE2, -3, and -4 knock-in mice. Expression of the apoE2
isoform was associated with an increase in adipocyte apoE gene expression and
apoE synthesis. Newly synthesized apoE2 was unstable in adipocytes and
demonstrated increased degradation and decreased secretion. ApoE2-expressing
mice were hyperlipidemic, and had increased size of gonadal fat pads and of
adipocytes, compared with apoE3 mice. In isolated cells, however, expression of
the apoE2 isoform produced defective lipogenesis and increased TG hydrolysis.
Incubation of adipose tissue with apoE3-containing TG-rich lipoproteins resulted
in a significant increase in TG in adipose tissue from apoE3 and -E4 mice, but
not apoE2 mice. Reduced capacity to internalize FFA as lipogenic substrate
contributed to defective lipogenesis. Newly synthesized apoE2 is unstable in
adipocytes and results in decreased adipocyte TG synthesis and defective FA
uptake. These changes recapitulate those observed in apoE knockout adipocytes
and have implications for understanding metabolic disturbances in humans
expressing the E2 isoform.
Investigators with authorship
Name
Institution
Nobuyo Maeda
University of North Carolina
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Please acknowledge all posters, manuscripts or scientific materials that were generated in part or whole using funds from the Diabetic Complications Consortium(看片视频) using the following text:
Financial support for this work provided by the NIDDK Diabetic Complications Consortium (RRID:SCR_001415, www.diacomp.org), grants DK076169 and DK115255
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