Advanced search options

Advanced Search Options 🞨

Browse by author name (“Author name starts with…”).

Find ETDs with:

in
/  
in
/  
in
/  
in

Written in Published in Earliest date Latest date

Sorted by

Results per page:

Sorted by: relevance · author · university · dateNew search

You searched for +publisher:"Vanderbilt University" +contributor:("John M. Stafford, M.D., Ph.D."). Showing records 1 – 2 of 2 total matches.

Search Limiters

Last 2 Years | English Only

No search limiters apply to these results.

▼ Search Limiters


Vanderbilt University

1. Trefts, Elijah. Integrin Linked Kinase is Critical for Hepatic Cellular Organization, Metabolism, and Glucoregulation.

Degree: PhD, Molecular Physiology and Biophysics, 2019, Vanderbilt University

The current obesity public health crisis is linked directly with liver health through a parallel epidemic of non-alcoholic fatty liver disease (NAFLD). NAFLD has direct effects on liver health while acting as an independent risk factor for type II diabetes, chronic heart disease, and chronic kidney disease. NAFLD is rooted in the metabolic consequences of overnutrition. As such, understanding hepatic metabolism and its many control systems serves to better define the origin of these diseases while leading to novel therapies. Alterations to extracellular matrix (ECM) composition and integrin signaling systems have now been implicated in the progression of metabolic pathologies including hepatic insulin resistance and NAFLD. This work focuses on newly appreciated metabolic regulation by the ECM-integrin signaling system as a means to understand metabolic disease of the liver. This body of work expands the current understanding of integrin involvement in metabolic processes in vivo through the lens of integrin-linked kinase (ILK). Results of this work demonstrate pathologic contributions of this protein during obesity and the spectrum of benefits that occur when this protein is removed from hepatocytes. This work also establishes the underlying mechanisms whereby removal of ILK from hepatocytes elicits these benefits. To conclude, this work establishes the hepatic metabolic functions mediated by ILK in order to expand understanding of novel pathways and targets in the progression of pathologic understanding and treatment. Advisors/Committee Members: John M. Stafford, M.D., Ph.D. (chair), Alan D. Cherrington, Ph.D. (committee member), Roy Zent, M.D., Ph.D. (committee member), Ambra Pozzi, Ph.D. (committee member).

Subjects/Keywords: Liver; Metabolism; Integrin-linked kinase; Glucose; Physiology

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Trefts, E. (2019). Integrin Linked Kinase is Critical for Hepatic Cellular Organization, Metabolism, and Glucoregulation. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://etd.library.vanderbilt.edu/available/etd-04172019-122919/ ;

Chicago Manual of Style (16th Edition):

Trefts, Elijah. “Integrin Linked Kinase is Critical for Hepatic Cellular Organization, Metabolism, and Glucoregulation.” 2019. Doctoral Dissertation, Vanderbilt University. Accessed September 17, 2019. http://etd.library.vanderbilt.edu/available/etd-04172019-122919/ ;.

MLA Handbook (7th Edition):

Trefts, Elijah. “Integrin Linked Kinase is Critical for Hepatic Cellular Organization, Metabolism, and Glucoregulation.” 2019. Web. 17 Sep 2019.

Vancouver:

Trefts E. Integrin Linked Kinase is Critical for Hepatic Cellular Organization, Metabolism, and Glucoregulation. [Internet] [Doctoral dissertation]. Vanderbilt University; 2019. [cited 2019 Sep 17]. Available from: http://etd.library.vanderbilt.edu/available/etd-04172019-122919/ ;.

Council of Science Editors:

Trefts E. Integrin Linked Kinase is Critical for Hepatic Cellular Organization, Metabolism, and Glucoregulation. [Doctoral Dissertation]. Vanderbilt University; 2019. Available from: http://etd.library.vanderbilt.edu/available/etd-04172019-122919/ ;

2. Barnes, Tammy Michelle. Interleukin-6 Enhances Glucagon Secretion: Amplification via the Pancreas and Brain.

Degree: PhD, Molecular Physiology and Biophysics, 2015, Vanderbilt University

Inappropriate glucagon secretion contributes to hyperglycemia in inflammatory disease. Previous work implicates the pro-inflammatory cytokine, interleukin-6 (IL-6), in glucagon secretion. IL-6 knock-out mice have a blunted glucagon response to lipopolysaccharide (LPS) that is restored by intravenous replacement of IL-6. Given that IL-6 has previously been demonstrated to have a transcriptional (i.e. slow) effect on glucagon secretion from islets, I hypothesized that the rapid increase in glucagon following LPS occurred by a faster mechanism such as by action within the brain. Using chronically catheterized, conscious mice, it was found that central IL-6 stimulates glucagon secretion uniquely in the presence of an accompanying stressor (hypoglycemia or LPS). Contrary to the original hypothesis, however, IL-6 was found to amplify glucagon secretion in two ways: IL-6 not only stimulates glucagon secretion via the brain but also by direct action on islets. Interestingly, IL-6 augments glucagon secretion from both sites only in the presence of an accompanying stressor (such as epinephrine). Given that both adrenergic tone and plasma IL-6 are elevated in multiple inflammatory diseases, the interactions of the IL-6 and catecholaminergic signaling pathways in regulating GCG secretion may contribute to our present understanding of these diseases. Advisors/Committee Members: David H. Wasserman, Ph.D. (chair), David A. Jacobson, Ph.D. (committee member), Danny G. Winder, Ph.D. (committee member), John M. Stafford, M.D., Ph.D. (committee member), David Robertson, M.D. (committee member).

Subjects/Keywords: lipopolysaccharide; Interleukin-6; glucagon secretion; glucagon; autonomic; hypoglycemia

Record DetailsSimilar RecordsGoogle PlusoneFacebookTwitterCiteULikeMendeleyreddit

APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Barnes, T. M. (2015). Interleukin-6 Enhances Glucagon Secretion: Amplification via the Pancreas and Brain. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://etd.library.vanderbilt.edu/available/etd-12312014-082201/ ;

Chicago Manual of Style (16th Edition):

Barnes, Tammy Michelle. “Interleukin-6 Enhances Glucagon Secretion: Amplification via the Pancreas and Brain.” 2015. Doctoral Dissertation, Vanderbilt University. Accessed September 17, 2019. http://etd.library.vanderbilt.edu/available/etd-12312014-082201/ ;.

MLA Handbook (7th Edition):

Barnes, Tammy Michelle. “Interleukin-6 Enhances Glucagon Secretion: Amplification via the Pancreas and Brain.” 2015. Web. 17 Sep 2019.

Vancouver:

Barnes TM. Interleukin-6 Enhances Glucagon Secretion: Amplification via the Pancreas and Brain. [Internet] [Doctoral dissertation]. Vanderbilt University; 2015. [cited 2019 Sep 17]. Available from: http://etd.library.vanderbilt.edu/available/etd-12312014-082201/ ;.

Council of Science Editors:

Barnes TM. Interleukin-6 Enhances Glucagon Secretion: Amplification via the Pancreas and Brain. [Doctoral Dissertation]. Vanderbilt University; 2015. Available from: http://etd.library.vanderbilt.edu/available/etd-12312014-082201/ ;

.