Title page for ETD etd-05142008-162857


Type of Document Master's Thesis
Author Yuskavage, Julia Kathryn
Author's Email Address yuskava@vt.edu
URN etd-05142008-162857
Title Epigallocatechin Gallate in the Regulation of Insulin Secretion
Degree Master of Science
Department Human Nutrition, Foods, and Exercise
Advisory Committee
Advisor Name Title
Liu, Dongmin Committee Chair
Barbeau, William E. Committee Member
Gwazdauskas, Francis C. Committee Member
Keywords
  • insulin
  • catechin
  • diabetes
  • green tea
  • EGCG
  • islets
  • pancreatic β-cell
Date of Defense 2008-04-30
Availability unrestricted
Abstract
In both Type 1 diabetes (T1D) and Type 2 diabetes (T2D), inadequate beta-cell mass and beta-cell dysfunction lead to impaired insulin secretion, and ultimately worsen glycemic control. Green tea has drawn wide attention due to its possible health-promoting properties, including enhancement of beta-cell function. We assessed the acute and relative long-term effects of epigallocatechin gallate (EGCG) on insulin secretion and synthesis from clonal beta-cells (INS1E cells), rat islets, and human islets, using 0.1, 1, or 5 µM. We determined if EGCG decreased blood glucose in healthy rats acutely, using 50 or 150 mg/kg body weight (BW), and after 12 days of supplementation in drinking water, using 0.1% and 0.5%. In the in vitro studies, EGCG significantly potentiated glucose-stimulated insulin secretion (GSIS) in rat islets (at 0.1, 1, and 5 µM) and human islets (at 1 µM), and elevated insulin content within INS1E cells (at 0.1, 1, and 5 µM) and human islets (at 1 µM), (P<0.05). Nutritional supplementation of EGCG (0.5% in drinking water) for 12 days in healthy rats significantly increased insulin synthesis, compared to that of controls, from 0.2 ± 0.02 to 1.4 ± 0.2 ng/mg protein, without alteration of insulin secretion in isolated islets (P<0.05). These findings demonstrate that EGCG may play a role in the regulation of pancreatic beta-cell function, thereby contributing to an anti-diabetic effect of this agent.
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