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Investigating the Effects of Stearoyl-CoA Desaturase on Diet-Induced Adiposity and the Regulation of Insulin-Like Growth Factor-Binding Protein 1- [electronic resource]
Investigating the Effects of Stearoyl-CoA Desaturase on Diet-Induced Adiposity and the Regulation of Insulin-Like Growth Factor-Binding Protein 1- [electronic resource]
상세정보
- 자료유형
- 학위논문
- Control Number
- 0016930946
- International Standard Book Number
- 9798379695392
- Dewey Decimal Classification Number
- 574
- Main Entry-Personal Name
- O'Neill, Lucas M. .
- Publication, Distribution, etc. (Imprint
- [S.l.] : The University of Wisconsin - Madison., 2021
- Publication, Distribution, etc. (Imprint
- Ann Arbor : ProQuest Dissertations & Theses, 2021
- Physical Description
- 1 online resource(189 p.)
- General Note
- Source: Dissertations Abstracts International, Volume: 84-12, Section: B.
- General Note
- Advisor: Ntambi, James.
- Dissertation Note
- Thesis (Ph.D.)--The University of Wisconsin - Madison, 2021.
- Restrictions on Access Note
- This item must not be sold to any third party vendors.
- Restrictions on Access Note
- This item must not be added to any third party search indexes.
- Summary, Etc.
- 요약Currently, obesity remains a worldwide epidemic and increases the risk of comorbidities such as type 2 diabetes, non-alcoholic fatty liver disease, cardiovascular disease, and cancer. Therefore, comprehensive investigations into the biochemical pathways that promote obesity continue to be warranted. One biochemical pathway of interest is the de novo biosynthesis of monounsaturated fatty acids, which is catalyzed by the stearoyl-CoA desaturase family of enzymes. There are four SCD isoforms in mice (SCD1-4) and two in humans (hSCD1 & hSCD5). In mice, global deletion of Scd1 (GKO) conveys protection against both high-fat diet (HFD) and high-carbohydrate diet (HCD) -induced obesity. Furthermore, deletion of Scd1 in the skin (SKO) and liver (LKO) recapitulated protection against HFD and HCD, respectively. GKO and SKO mice are protected against HFD because they are hypermetabolic due to a defective skin barrier that leads to a breakdown in adaptive thermoregulation. The mechanism of HCD protection in LKO mice is currently unclear but evidence suggests it involves multiple hepatokines. One hepatokine of interest is insulin-like growth factor-binding protein-1 (IGFBP1). IGFBP1 is one of the most differentially expressed genes between GKO and wild-type mice and enhanced IGFBP1 expression has been reported to promote glucose uptake and insulin sensitivity. To date, the relationship between Scd1 deficiency and up-regulation of IGFBP1 has not been established and it is unknown if global deletion of other SCD isoforms will yield similar protection against diet-induced adiposity. In this dissertation, I examine the metabolic effects of the SCD2 isoform under HFD and HCD diet feeding conditions, the role of SCD2 in preadipocyte differentiation in vivo and in vitro, and the relationship between hepatic SCD1 and IGFBP1. Specifically, I show that: 1. Global deletion of Scd2 conveys protection against diet-induced adiposity and improves glucose and insulin tolerance; 2. SCD2 is not required for preadipocyte differentiation in vivo despite being required in vitro; and 3. Hepatic oleic acid levels regulate insulin-like growth factor-binding protein 1 partially through the mTOR-FGF21 axis during high-carbohydrate feeding.
- Subject Added Entry-Topical Term
- Biochemistry.
- Subject Added Entry-Topical Term
- Public health.
- Subject Added Entry-Topical Term
- Epidemiology.
- Index Term-Uncontrolled
- Obesity
- Index Term-Uncontrolled
- Fatty acids
- Index Term-Uncontrolled
- Biochemical pathway
- Index Term-Uncontrolled
- Hepatic oleic acid
- Index Term-Uncontrolled
- Liver disease
- Index Term-Uncontrolled
- Cancer
- Added Entry-Corporate Name
- The University of Wisconsin - Madison Biochemistry-ALS
- Host Item Entry
- Dissertations Abstracts International. 84-12B.
- Host Item Entry
- Dissertation Abstract International
- Electronic Location and Access
- 로그인을 한후 보실 수 있는 자료입니다.
- Control Number
- joongbu:639272
MARC
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■020 ▼a9798379695392
■035 ▼a(MiAaPQ)AAI28496796
■040 ▼aMiAaPQ▼cMiAaPQ
■0820 ▼a574
■1001 ▼aO'Neill, Lucas M. .
■24510▼aInvestigating the Effects of Stearoyl-CoA Desaturase on Diet-Induced Adiposity and the Regulation of Insulin-Like Growth Factor-Binding Protein 1▼h[electronic resource]
■260 ▼a[S.l.]▼bThe University of Wisconsin - Madison. ▼c2021
■260 1▼aAnn Arbor▼bProQuest Dissertations & Theses▼c2021
■300 ▼a1 online resource(189 p.)
■500 ▼aSource: Dissertations Abstracts International, Volume: 84-12, Section: B.
■500 ▼aAdvisor: Ntambi, James.
■5021 ▼aThesis (Ph.D.)--The University of Wisconsin - Madison, 2021.
■506 ▼aThis item must not be sold to any third party vendors.
■506 ▼aThis item must not be added to any third party search indexes.
■520 ▼aCurrently, obesity remains a worldwide epidemic and increases the risk of comorbidities such as type 2 diabetes, non-alcoholic fatty liver disease, cardiovascular disease, and cancer. Therefore, comprehensive investigations into the biochemical pathways that promote obesity continue to be warranted. One biochemical pathway of interest is the de novo biosynthesis of monounsaturated fatty acids, which is catalyzed by the stearoyl-CoA desaturase family of enzymes. There are four SCD isoforms in mice (SCD1-4) and two in humans (hSCD1 & hSCD5). In mice, global deletion of Scd1 (GKO) conveys protection against both high-fat diet (HFD) and high-carbohydrate diet (HCD) -induced obesity. Furthermore, deletion of Scd1 in the skin (SKO) and liver (LKO) recapitulated protection against HFD and HCD, respectively. GKO and SKO mice are protected against HFD because they are hypermetabolic due to a defective skin barrier that leads to a breakdown in adaptive thermoregulation. The mechanism of HCD protection in LKO mice is currently unclear but evidence suggests it involves multiple hepatokines. One hepatokine of interest is insulin-like growth factor-binding protein-1 (IGFBP1). IGFBP1 is one of the most differentially expressed genes between GKO and wild-type mice and enhanced IGFBP1 expression has been reported to promote glucose uptake and insulin sensitivity. To date, the relationship between Scd1 deficiency and up-regulation of IGFBP1 has not been established and it is unknown if global deletion of other SCD isoforms will yield similar protection against diet-induced adiposity. In this dissertation, I examine the metabolic effects of the SCD2 isoform under HFD and HCD diet feeding conditions, the role of SCD2 in preadipocyte differentiation in vivo and in vitro, and the relationship between hepatic SCD1 and IGFBP1. Specifically, I show that: 1. Global deletion of Scd2 conveys protection against diet-induced adiposity and improves glucose and insulin tolerance; 2. SCD2 is not required for preadipocyte differentiation in vivo despite being required in vitro; and 3. Hepatic oleic acid levels regulate insulin-like growth factor-binding protein 1 partially through the mTOR-FGF21 axis during high-carbohydrate feeding.
■590 ▼aSchool code: 0262.
■650 4▼aBiochemistry.
■650 4▼aPublic health.
■650 4▼aEpidemiology.
■653 ▼aObesity
■653 ▼aFatty acids
■653 ▼aBiochemical pathway
■653 ▼aHepatic oleic acid
■653 ▼aLiver disease
■653 ▼aCancer
■690 ▼a0487
■690 ▼a0766
■690 ▼a0573
■71020▼aThe University of Wisconsin - Madison▼bBiochemistry-ALS.
■7730 ▼tDissertations Abstracts International▼g84-12B.
■773 ▼tDissertation Abstract International
■790 ▼a0262
■791 ▼aPh.D.
■792 ▼a2021
■793 ▼aEnglish
■85640▼uhttp://www.riss.kr/pdu/ddodLink.do?id=T16930946▼nKERIS▼z이 자료의 원문은 한국교육학술정보원에서 제공합니다.
■980 ▼a202402▼f2024
