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The role of enterocyte fatty acid-binding proteins in the intestine and whole-body energy homeostasis

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TitleInfo
Title
The role of enterocyte fatty acid-binding proteins in the intestine and whole-body energy homeostasis
Name (type = personal)
NamePart (type = family)
Lackey
NamePart (type = given)
Atreju Ian
NamePart (type = date)
1991-
DisplayForm
Atreju Ian Lackey
Role
RoleTerm (authority = RULIB)
author
Name (type = personal)
NamePart (type = family)
Storch
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Judith
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Judith Storch
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Advisory Committee
Role
RoleTerm (authority = RULIB)
chair
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Quadro
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Loredana
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Loredana Quadro
Affiliation
Advisory Committee
Role
RoleTerm (authority = RULIB)
internal member
Name (type = personal)
NamePart (type = family)
Watford
NamePart (type = given)
Malcolm
DisplayForm
Malcolm Watford
Affiliation
Advisory Committee
Role
RoleTerm (authority = RULIB)
internal member
Name (type = personal)
NamePart (type = family)
Joseph
NamePart (type = given)
Laurie B
DisplayForm
Laurie B Joseph
Affiliation
Advisory Committee
Role
RoleTerm (authority = RULIB)
outside member
Name (type = personal)
NamePart (type = family)
Verzi
NamePart (type = given)
Michael P
DisplayForm
Michael P Verzi
Affiliation
Advisory Committee
Role
RoleTerm (authority = RULIB)
outside member
Name (type = corporate)
NamePart
Rutgers University
Role
RoleTerm (authority = RULIB)
degree grantor
Name (type = corporate)
NamePart
School of Graduate Studies
Role
RoleTerm (authority = RULIB)
school
TypeOfResource
Text
Genre (authority = marcgt)
theses
OriginInfo
DateCreated (encoding = w3cdtf); (keyDate = yes); (qualifier = exact)
2019
DateOther (encoding = w3cdtf); (qualifier = exact); (type = degree)
2019-10
Language
LanguageTerm (authority = ISO 639-3:2007); (type = text)
English
Abstract (type = abstract)
The fatty acid binding protein (FABP) family consists of 14‐15 kDa cytoplasmic proteins which are abundantly expressed in various mammalian tissues. In the proximal small intestinal enterocyte, at least three FABPs are highly expressed: liver FABP (LFABP; FABP1), which is also expressed in the liver, intestinal FABP (IFABP; FABP2), which is only expressed in the small intestine, and cellular retinoid binding protein 2 (CRBP2), which is also only expressed in the small intestine. Previous studies in high fat (HF) fed mice null for either LFABP or IFABP revealed a divergent phenotype, with LFABP-/- mice displaying a metabolically healthy obese (MHO) phenotype, while IFABP-/- mice remained lean. Conditional knock out LFABP mice (LFABP-cKO) were generated to assess what role intestinal-LFABP may have in the MHO phenotype. Like HF fed whole-body LFABP-/- mice, intestine-specific LFABP-/- (LFABPint-/-) were found to have better capacity for endurance exercise when compared to their wild-type (WT) “floxed” controls (LFABPfl/fl). Additionally, female LFABPint-/- were found to be more obese after the HF feeding challenge, having greater BW gain and increased fat mass. Thus, the ablation of intestine-specific ablation of LFABP is enough to induce the MHO phenotype in female mice, and improved exercise capacity in male and female mice. To assess the intestinal phenotypic changes that might explain their lean phenotype, HF feeding studies were performed in IFABP-/- mice. Additionally, as it was observed that HF fed IFABP-/- mice had a more fragile small intestine, we hypothesized that the ablation of IFABP may result in alterations in intestinal morphology and structure. IFABP-/- mice were found to have reduced energy absorption, taking in fewer calories while excreting the same amount of calories as their WT counterparts. Additionally, IFABP-/- mice had more rapid intestinal transit, partly explaining the reduction in energy absorption. IFABP-/- mice were observed to have a shortened average villus length, a thinner muscularis layer, reduced goblet cell density, and reduced Paneth cell abundance. The ablation of IFABP also resulted in alterations in tissue retinoid levels, and mucosal vitamin A-related gene expression. Although IFABP-/- mice were found to have a drastic reduction in mucosal CRBP2 gene expression, no changes were observed in CRBP2 protein abundance. Taken together, this work has demonstrated a role for enterocyte lipid binding proteins in efficient uptake and trafficking of not only dietary lipid, but nutrients in general. These studies have also revealed a role for the enterocyte FABPs in modulating intestinal physiology, intestinal morphology, and the whole-body ramifications of such alterations.
Subject (authority = RUETD)
Topic
Nutritional Sciences
Subject (authority = local)
Topic
Lipids
Subject (authority = LCSH)
Topic
Fatty acid-binding proteins
RelatedItem (type = host)
TitleInfo
Title
Rutgers University Electronic Theses and Dissertations
Identifier (type = RULIB)
ETD
Identifier
ETD_10242
PhysicalDescription
Form (authority = gmd)
InternetMediaType
application/pdf
InternetMediaType
text/xml
Extent
1 online resource (xvii, 153 pages) : illustrations
Note (type = degree)
Ph.D.
Note (type = bibliography)
Includes bibliographical references
RelatedItem (type = host)
TitleInfo
Title
School of Graduate Studies Electronic Theses and Dissertations
Identifier (type = local)
rucore10001600001
Location
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NjNbRU
Identifier (type = doi)
doi:10.7282/t3-hsrs-jw34
Genre (authority = ExL-Esploro)
ETD doctoral
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Rights

RightsDeclaration (ID = rulibRdec0006)
The author owns the copyright to this work.
RightsHolder (type = personal)
Name
FamilyName
Lackey
GivenName
Atreju
Role
Copyright Holder
RightsEvent
Type
Permission or license
DateTime (encoding = w3cdtf); (qualifier = exact); (point = start)
2019-09-13 14:28:11
AssociatedEntity
Name
Atreju Lackey
Role
Copyright holder
Affiliation
Rutgers University. School of Graduate Studies
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Name
Author Agreement License
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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
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Copyright protected
Availability
Status
Open
Reason
Permission or license
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2019-09-13T14:21:07
DateCreated (point = end); (encoding = w3cdtf); (qualifier = exact)
2019-09-13T14:21:07
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