Teneurin C-terminal Associated Peptide (TCAP)-1 is postulated to play a critical role in cellular defense mechanisms as it is highly neuroprotective against alkalotic and hypoxic stress. Optimization of metabolic pathways is recognized as an essential survival tactic by alleviating energy deficits and meeting the demands to cope with the stressors. The aim of this research was to delineate the mechanism through which TCAP-1 confers protection. My findings show that TCAP-1 increases the overall expression of GLUT1 and enhances overall expression and membrane localization of GLUT3. With respect to metabolic parameters, chronic TCAP-1 application led to increased intracellular [ATP] with decreased intracellular [lactate], both in a dose-dependent manner, but did not alter tumourgenic glycolytic enzyme expression or mitochondrially associated apoptotic protein expression. Contrastingly, acute TCAP-1 led to decreased intracellular [ATP]. Indicative of increased cellular ATP production and physiological energy expenditure, TCAP-1 reduced serum insulin levels and subcutaneous adipocyte size in vivo.
| Identifer | oai:union.ndltd.org:TORONTO/oai:tspace.library.utoronto.ca:1807/33592 |
| Date | 27 November 2012 |
| Creators | Xu, Mei |
| Contributors | Lovejoy, David A. |
| Source Sets | University of Toronto |
| Language | en_ca |
| Detected Language | English |
| Type | Thesis |
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