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Branched chain amino acid supplementation modulates the effect of inflammatory mediators on the function of a hepatoma cell line

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TitleInfo
Title
Branched chain amino acid supplementation modulates the effect of inflammatory mediators on the function of a hepatoma cell line
Name (type = personal)
NamePart (type = family)
Hashemi
NamePart (type = given)
Sharareh
NamePart (type = date)
1972-
DisplayForm
Sharareh Hashemi
Role
RoleTerm (authority = RULIB)
author
Name (type = personal)
NamePart (type = family)
Berthiaume
NamePart (type = given)
Francois
DisplayForm
Francois Berthiaume
Affiliation
Advisory Committee
Role
RoleTerm (authority = RULIB)
chair
Name (type = personal)
NamePart (type = family)
Androulakis
NamePart (type = given)
Ioannis P
DisplayForm
Ioannis P Androulakis
Affiliation
Advisory Committee
Role
RoleTerm (authority = RULIB)
co-chair
Name (type = personal)
NamePart (type = family)
Ierapetritou
NamePart (type = given)
Marianthi
DisplayForm
Marianthi Ierapetritou
Affiliation
Advisory Committee
Role
RoleTerm (authority = RULIB)
co-chair
Name (type = corporate)
NamePart
Rutgers University
Role
RoleTerm (authority = RULIB)
degree grantor
Name (type = corporate)
NamePart
Graduate School - New Brunswick
Role
RoleTerm (authority = RULIB)
school
TypeOfResource
Text
Genre (authority = marcgt)
theses
OriginInfo
DateCreated (qualifier = exact)
2013
DateOther (qualifier = exact); (type = degree)
2013-05
Place
PlaceTerm (type = code)
xx
Language
LanguageTerm (authority = ISO639-2b); (type = code)
eng
Abstract (type = abstract)
Severe trauma injuries often lead to a prolonged inflammatory response associated with metabolic abnormalities. These abnormalities lead to persistent skeletal muscle proteolysis and rapid loss of lean body mass, which may lead to multiple organ dysfunction and death. The liver plays an important role in this systemic response to injury by modulating the inflammatory processes, immune functions, and metabolic pathways. The acute phase of the response is characterized by the release of inflammatory mediators, including proinflammatory cytokines and reactive oxygen species (ROS), as well as a change in the protein secretion pattern and increased amino acid utilization by the liver. When these changes persist for long periods of time, they likely contribute to the body’s negative nitrogen balance as well as loss of lean body mass (LBM). Among all proteins secreted by the liver, albumin is the most abundant one and its secretion rate significantly decreases in inflammatory states, and results in a lower circulating concentration in patients. Albumin provides the critical colloid osmotic pressure to regulate the passage of water and diffusible solutes through the capillaries. Increased utilization of amino acids in trauma is thought to be important for defense against diseases; however, it reduces body stores of proteins and free amino acids to supply amino acid needs for tissue repair, acute phase protein production, and gluconeogenesis. Nutritional supplementation is currently being used to alleviate endogenous nitrogen depletion and to maximize protein synthesis for optimal wound healing and immune function. Among nutritional supplements, there has been increased interest in using branched chain amino acids (BCAAs), and clinical studies suggest that BCAAs can enhance liver function in inflammatory states. The mechanism whereby BCAAs impact the liver function during inflammation is unclear. The purpose of this research is to investigate the effect of proinflammatory mediators (more specifically the cytokines interleukin-1ß & interleukin-6) and reactive oxygen species H₂O₂, and BCAAs on a cell culture model of liver consisting of HepG2/C3A hepatoma cells. It was found that these mediators reversibly suppressed albumin and urea production in a dose-dependent manner, and also decreased the amount of the intracellular antioxidant reduced glutathione. BCAA supplementation mitigated the effect of these inflammatory mediators; however, this effect was maximized at a relatively low concentration of BCAAs, above which no further benefit was observed. Therefore, BCAAs are potentially beneficial to support liver function during inflammation.
Subject (authority = RUETD)
Topic
Biomedical Engineering
Subject (authority = ETD-LCSH)
Topic
Branched chain amino acids
RelatedItem (type = host)
TitleInfo
Title
Rutgers University Electronic Theses and Dissertations
Identifier (type = RULIB)
ETD
Identifier
ETD_4533
PhysicalDescription
Form (authority = gmd)
electronic resource
InternetMediaType
application/pdf
InternetMediaType
text/xml
Extent
xi, 89 p. : ill.
Note (type = degree)
M.S.
Note (type = bibliography)
Includes bibliographical references
Note (type = statement of responsibility)
by Sharareh Hashemi
Subject (authority = ETD-LCSH)
Topic
Wounds and injuries--Complications
Subject (authority = ETD-LCSH)
Topic
Inflammation--Mediators
Identifier (type = hdl)
http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000068877
RelatedItem (type = host)
TitleInfo
Title
Graduate School - New Brunswick Electronic Theses and Dissertations
Identifier (type = local)
rucore19991600001
Location
PhysicalLocation (authority = marcorg); (displayLabel = Rutgers, The State University of New Jersey)
NjNbRU
Identifier (type = doi)
doi:10.7282/T3SX6BTQ
Genre (authority = ExL-Esploro)
ETD graduate
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Rights

RightsDeclaration (ID = rulibRdec0006)
The author owns the copyright to this work.
RightsHolder (type = personal)
Name
FamilyName
Hashemi
GivenName
Sharareh
Role
Copyright Holder
RightsEvent
Type
Permission or license
DateTime (encoding = w3cdtf); (qualifier = exact); (point = start)
2013-03-06 15:39:25
AssociatedEntity
Name
Sharareh Hashemi
Role
Copyright holder
Affiliation
Rutgers University. Graduate School - New Brunswick
AssociatedObject
Type
License
Name
Author Agreement License
Detail
I hereby grant to the Rutgers University Libraries and to my school the non-exclusive right to archive, reproduce and distribute my thesis or dissertation, in whole or in part, and/or my abstract, in whole or in part, in and from an electronic format, subject to the release date subsequently stipulated in this submittal form and approved by my school. I represent and stipulate that the thesis or dissertation and its abstract are my original work, that they do not infringe or violate any rights of others, and that I make these grants as the sole owner of the rights to my thesis or dissertation and its abstract. I represent that I have obtained written permissions, when necessary, from the owner(s) of each third party copyrighted matter to be included in my thesis or dissertation and will supply copies of such upon request by my school. I acknowledge that RU ETD and my school will not distribute my thesis or dissertation or its abstract if, in their reasonable judgment, they believe all such rights have not been secured. I acknowledge that I retain ownership rights to the copyright of my work. I also retain the right to use all or part of this thesis or dissertation in future works, such as articles or books.
Copyright
Status
Copyright protected
Availability
Status
Open
Reason
Permission or license
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RULTechMD (ID = TECHNICAL1)
ContentModel
ETD
OperatingSystem (VERSION = 5.1)
windows xp
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