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Phytoecdysteroids
Descriptive
TypeOfResource
Text
TitleInfo
(ID = T-1)
Title
Phytoecdysteroids
SubTitle
understanding their anabolic activity
Identifier
ETD_1559
Identifier
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http://hdl.rutgers.edu/1782.2/rucore10001600001.ETD.000051350
Language
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eng
Genre
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theses
Subject
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Topic
Plant Biology
Subject
(ID = SBJ-1);
(authority = ETD-LCSH)
Topic
Ecdysteroids
Subject
(ID = SBJ-1);
(authority = ETD-LCSH)
Topic
Plants
Subject
(ID = SBJ-1);
(authority = ETD-LCSH)
Topic
Pharmacognosy
Abstract
Phytoecdysteroids, polyhydroxylated ketosteroids, are the plant analogues of insect growth hormones. Although their role in insect molting is well characterized, their function in plants is less clear. Lacking the properties of classic plant hormones, phytoecdysteroids may be involved in plant growth and defense. One of the main benefits of phytoecdysteroids may be their therapeutic effects on mammals, including humans. Their claimed medicinal properties include anabolic, adaptogenic, hepatoprotective, and hypoglycemic activity. Although ethnobotanical use has been supported by some evidence, the research is quite limited, lacking the scientific rigor necessary to be convincing.
Two ecdysteroid containing plants, Ajuga turkestanica, and Spinacia olearaceae (Spinach), were selected as beneficial sources of phytoecdysteroids. Cultivation, analysis of ecdysteroid content, and characterization of anabolic activity were performed to support future medicinal use.
Phytoecdysteroids' anabolic activity, one of their most interesting properties due to the claimed lack of androgenic effect, was studied. Anabolic activity was confirmed in animal studies and a cellular model of skeletal muscle. The cellular model was used to characterize ecdysteroids' effect on protein incorporation and to elucidate the signal transduction pathway involved. Ecdysteroid's lack of androgenic activity was confirmed in vivo and in vitro, with ecdysteroids showing no specific binding to the androgen receptor.
Identification of mammalian nuclear receptors homologous with the insect nuclear ecdysone receptor led to binding and activation assays of potential receptors using ecdysteroids. The discovery of a lesser known membrane bound G Protein Coupled Receptor (GPCR) insect ecdysone receptor, DoEcR, suggested the existence of a hypothetical mammalian membrane bound GPCR ecdysone receptor.
Use of specific inhibitors supported the involvement of G protein signaling, Phospholipase C (PLC), Inositol Phosphate 3 Receptor (IP3R), and Akt. Ecdysteroid stimulated activation of Akt confirmed its role in the anabolic effect. Ecdysteroid generated increases in intracellular calcium were also characterized, with the rapid flux in Ca2+ linked with Akt activation and anabolic activity. The evidence produced suggests the involvement of a putative mammalian GPCR ecdysteroid receptor mediating the anabolic effect through the rapid activation of the PLC/IP3R pathway, generating Ca2+ flux which leads to activation of the Phosphoinositide 3 Kinase/Akt pathway, eventually causing increases in protein incorporation.
Two ecdysteroid containing plants, Ajuga turkestanica, and Spinacia olearaceae (Spinach), were selected as beneficial sources of phytoecdysteroids. Cultivation, analysis of ecdysteroid content, and characterization of anabolic activity were performed to support future medicinal use.
Phytoecdysteroids' anabolic activity, one of their most interesting properties due to the claimed lack of androgenic effect, was studied. Anabolic activity was confirmed in animal studies and a cellular model of skeletal muscle. The cellular model was used to characterize ecdysteroids' effect on protein incorporation and to elucidate the signal transduction pathway involved. Ecdysteroid's lack of androgenic activity was confirmed in vivo and in vitro, with ecdysteroids showing no specific binding to the androgen receptor.
Identification of mammalian nuclear receptors homologous with the insect nuclear ecdysone receptor led to binding and activation assays of potential receptors using ecdysteroids. The discovery of a lesser known membrane bound G Protein Coupled Receptor (GPCR) insect ecdysone receptor, DoEcR, suggested the existence of a hypothetical mammalian membrane bound GPCR ecdysone receptor.
Use of specific inhibitors supported the involvement of G protein signaling, Phospholipase C (PLC), Inositol Phosphate 3 Receptor (IP3R), and Akt. Ecdysteroid stimulated activation of Akt confirmed its role in the anabolic effect. Ecdysteroid generated increases in intracellular calcium were also characterized, with the rapid flux in Ca2+ linked with Akt activation and anabolic activity. The evidence produced suggests the involvement of a putative mammalian GPCR ecdysteroid receptor mediating the anabolic effect through the rapid activation of the PLC/IP3R pathway, generating Ca2+ flux which leads to activation of the Phosphoinositide 3 Kinase/Akt pathway, eventually causing increases in protein incorporation.
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electronic resource
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viii, 143 p. : ill.
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Note
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Ph.D.
Note
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Includes bibliographical references (p. 131-142)
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by Jonathan Isaac Gorelick-Feldman
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Gorelick-Feldman
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Jonathan Isaac
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Jonathan Isaac Gorelick-Feldman
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Raskin
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Ilya
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chair
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Ilya Raskin
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Simon
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James
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internal member
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James Simon
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Giafagna
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Tom
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Tom Giafagna
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Cohick
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Wendie
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Advisory Committee
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Wendie Cohick
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Rutgers University
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Graduate School - New Brunswick
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OriginInfo
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2009
DateOther
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2009-05
Place
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xx
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Rutgers University Electronic Theses and Dissertations
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ETD
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Graduate School - New Brunswick Electronic Theses and Dissertations
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rucore19991600001
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NjNbRU
Identifier
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doi:10.7282/T3WQ041H
Genre
(authority = ExL-Esploro)
ETD doctoral
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Rights
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The author owns the copyright to this work.
Copyright
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Copyright protected
Availability
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Open
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Permission or license
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Non-exclusive ETD license
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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.
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Technical
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application/pdf
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application/x-tar
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2099200
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