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Molecular Mechanisms of Cell Cycle R...

Cai, Erica Pei-Shan.

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Molecular Mechanisms of Cell Cycle Regulation in Pancreatic alpha- and beta-cells that Control Glucose Homeostasis.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Molecular Mechanisms of Cell Cycle Regulation in Pancreatic alpha- and beta-cells that Control Glucose Homeostasis./
Author:	Cai, Erica Pei-Shan.
Published:	Ann Arbor : ProQuest Dissertations & Theses, : 2014,
Description:	198 p.
Notes:	Source: Dissertation Abstracts International, Volume: 77-04(E), Section: B.
Contained By:	Dissertation Abstracts International77-04B(E).
Subject:	Endocrinology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3735157
ISBN:	9781339239682

Molecular Mechanisms of Cell Cycle Regulation in Pancreatic alpha- and beta-cells that Control Glucose Homeostasis.
Cai, Erica Pei-Shan.

Molecular Mechanisms of Cell Cycle Regulation in Pancreatic alpha- and beta-cells that Control Glucose Homeostasis. - Ann Arbor : ProQuest Dissertations & Theses, 2014 - 198 p.

Source: Dissertation Abstracts International, Volume: 77-04(E), Section: B.

Thesis (Ph.D.)--University of Toronto (Canada), 2014.

Pancreatic islet cell mass is achieved through a rapid surge of neogenesis and proliferation during embryogenesis. However, this plasticity declines significantly in the postnatal period, resulting in the majority of mature islet cells, which permanently exit from cell cycle and are incapable of regenerating in adulthood. Understanding the molecular mechanisms that govern both neogenesis and proliferation in islet cells is paramount for treatment of both type 1 and type 2 diabetes. In this thesis, genetically modified mice were used to investigate molecular mechanisms of specific cell cycle regulators in alpha- and beta-cell homeostasis under physiological and experimentally-induced diabetes. Specifically, in Chapter IV, I describe the consequences of deleting the retinoblastoma protein (Rb) in proliferating islet progenitor cells. I show that loss of Rb increases alpha- to beta-cell ratio by regulating cell proliferation, differentiation and survival, leading to improved glucose homeostasis and protection against diabetes. In Chapter V, I demonstrate that a central role for Rb, but not its family member p107, in the dual effects of GLP-1 on alpha- and beta-cells in governing islet cell proliferation and survival. In Chapter VI, I show that the focal adhesion kinase (FAK) is critical for in vivo pancreatic beta-cell viability and function through regulation of insulin signalling, actin dynamics and granule trafficking. Thus, studies in this thesis define novel functions of cell cycle regulators, Rb, p107 and FAK in regulating pancreatic alpha- and beta-cell fate. Together, the results presented in the thesis provide novel mechanisms for enhancing islet mass and integrity, which may lead to new strategies to combat diabetes.

ISBN: 9781339239682Subjects--Topical Terms:

610914
Endocrinology.

Molecular Mechanisms of Cell Cycle Regulation in Pancreatic alpha- and beta-cells that Control Glucose Homeostasis.
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520 $a Pancreatic islet cell mass is achieved through a rapid surge of neogenesis and proliferation during embryogenesis. However, this plasticity declines significantly in the postnatal period, resulting in the majority of mature islet cells, which permanently exit from cell cycle and are incapable of regenerating in adulthood. Understanding the molecular mechanisms that govern both neogenesis and proliferation in islet cells is paramount for treatment of both type 1 and type 2 diabetes. In this thesis, genetically modified mice were used to investigate molecular mechanisms of specific cell cycle regulators in alpha- and beta-cell homeostasis under physiological and experimentally-induced diabetes. Specifically, in Chapter IV, I describe the consequences of deleting the retinoblastoma protein (Rb) in proliferating islet progenitor cells. I show that loss of Rb increases alpha- to beta-cell ratio by regulating cell proliferation, differentiation and survival, leading to improved glucose homeostasis and protection against diabetes. In Chapter V, I demonstrate that a central role for Rb, but not its family member p107, in the dual effects of GLP-1 on alpha- and beta-cells in governing islet cell proliferation and survival. In Chapter VI, I show that the focal adhesion kinase (FAK) is critical for in vivo pancreatic beta-cell viability and function through regulation of insulin signalling, actin dynamics and granule trafficking. Thus, studies in this thesis define novel functions of cell cycle regulators, Rb, p107 and FAK in regulating pancreatic alpha- and beta-cell fate. Together, the results presented in the thesis provide novel mechanisms for enhancing islet mass and integrity, which may lead to new strategies to combat diabetes.
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