RUcore: Rutgers University Community Repository
The role of Period 2 gene in mediating alcohol effects on metabolic signals in proopiomelanocortin producing neurons
Descriptive
TitleInfo
Title
The role of Period 2 gene in mediating alcohol effects on metabolic signals in proopiomelanocortin producing neurons
Name
(type = personal)
NamePart
(type = family)
Agapito
NamePart
(type = given)
Maria
DisplayForm
Maria Agapito
Role
RoleTerm
(authority = RULIB)
author
Name
(type = personal)
NamePart
(type = family)
Pintar
NamePart
(type = given)
John
DisplayForm
John Pintar
Affiliation
Advisory Committee
Role
RoleTerm
(authority = RULIB)
internal member
Name
(type = personal)
NamePart
(type = family)
Edery
NamePart
(type = given)
Isaac
DisplayForm
Isaac Edery
Affiliation
Advisory Committee
Role
RoleTerm
(authority = RULIB)
internal member
Name
(type = personal)
NamePart
(type = family)
Shumyatsky
NamePart
(type = given)
Gleb
DisplayForm
Gleb Shumyatsky
Affiliation
Advisory Committee
Role
RoleTerm
(authority = RULIB)
internal member
Name
(type = personal)
NamePart
(type = family)
Sarkar
NamePart
(type = given)
Dipak
DisplayForm
Dipak Sarkar
Affiliation
Advisory Committee
Role
RoleTerm
(authority = RULIB)
internal member
Name
(type = personal)
NamePart
(type = family)
Rosenwasser
NamePart
(type = given)
Alan
DisplayForm
Alan Rosenwasser
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
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)
An increasing body of knowledge suggests that fetal alcohol exposure disrupts circadian homeostasis and metabolic functions. In order to determine the mechanism by which fetal alcohol exposure alters the metabolic functions, we determined the postnatal ethanol-induced changes in the function of Proopiomelanocortin (Pomc) neurons known to regulate metabolic homeostasis. Additionally, we evaluated the role of a clock regulatory gene, Period 2 (Per2), in mediation of alcohol effects on Pomc neurons. To determine the interaction between alcohol and Per2 on β-endorphin neuronal activity, we first measured the secretion of this peptide from mediobasal hypothalamic (MBH) cells of postnatal mice in primary cultures following treatment with ethanol for various time periods. We found that ethanol acutely stimulated but chronically inhibited β-endorphin secretion in vitro and these effects of ethanol on β-endorphin secretion were absent following Per2 mutation. We also evaluated the effect of the clock gene mutation on postnatal alcohol programming of Pomc and metabolic genes expression in the hypothalamus. For this, We measured the levels of Pomc and various metabolic genes (Stat3, Sirt1, Asb4 and Pgc1α) and Pomc gene products β-endorphin and α-melanocyte stimulating (α-MSH) hormone in the MBH of alcohol-treated Per2 mutant and wild type mice at postnatal day 7 and 90. Postnatal ethanol exposures suppressed Pomc and metabolic genes and Pomc-derived products β-endorphin and α-MSH in the MBH for a prolonged period of time. Per2 mutation prevented these effects of postnatal ethanol on Pomc and metabolic genes. Furthermore, in order to determine the effect of Per2 gene deletion on postnatal alcohol programming of the circadian expression of metabolic genes in Pomc neurons, we created an Egfp- Pomc -Per2 mutant mice and employed these mice to determine gene expression in Laser captured isolated Pomc expressing neurons. We found that postnatal ethanol exposures permanently altered circadian expression of Pomc and metabolic genes in Pomc neurons. Per2 mutation prevented the postnatal ethanol-induced alteration of metabolic genes in Pomc neurons. Together, these data suggest that early life exposure to ethanol alters metabolic sensing in Pomc expressing neurons possibly via regulation of Per2 gene.
Subject
(authority = RUETD)
Topic
Neuroscience
Subject
(authority = ETD-LCSH)
Topic
Proopiomelanocortin
Subject
(authority = ETD-LCSH)
Topic
Fetus--Metabolism
Subject
(authority = ETD-LCSH)
Topic
Fetal alcohol syndrome
RelatedItem
(type = host)
TitleInfo
Title
Rutgers University Electronic Theses and Dissertations
Identifier
(type = RULIB)
ETD
Identifier
ETD_4614
PhysicalDescription
Form
(authority = gmd)
electronic resource
InternetMediaType
application/pdf
InternetMediaType
text/xml
Extent
xiv, 151 p. : ill.
Note
(type = degree)
Ph.D.
Note
(type = bibliography)
Includes bibliographical references
Note
(type = vita)
Includes vita
Note
(type = statement of responsibility)
by Maria Agapito
Identifier
(type = hdl)
http://hdl.rutgers.edu/1782.1/rucore10001600001.ETD.000068807
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/T3JW8CGW
Genre
(authority = ExL-Esploro)
ETD doctoral
Back to the top
Rights
RightsDeclaration
(ID = rulibRdec0006)
The author owns the copyright to this work.
RightsHolder
(type = personal)
Name
FamilyName
Agapito
GivenName
Maria
Role
Copyright Holder
RightsEvent
Type
Permission or license
DateTime
(encoding = w3cdtf);
(qualifier = exact);
(point = start)
2013-04-10 07:20:06
AssociatedEntity
Name
Maria Agapito
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.
RightsEvent
DateTime
(encoding = w3cdtf);
(qualifier = exact);
(point = start)
2013-05-31
DateTime
(encoding = w3cdtf);
(qualifier = exact);
(point = end)
2014-05-31
Type
Embargo
Detail
Access to this PDF has been restricted at the author's request. It will be publicly available after May 31st, 2014.
Copyright
Status
Copyright protected
Availability
Status
Open
Reason
Permission or license
Back to the top
Technical
RULTechMD
(ID = TECHNICAL1)
ContentModel
ETD
OperatingSystem
(VERSION = 5.1)
windows xp
Back to the top
Statistical Profile