Downloads and Tools

•  Article PDF
  4.66 MB PDF document

Supplemental Material

•  Supplemental File
  1.35 MB PDF document

This is an open access article.
Print this page Email this page

Recipient's Email:

---

Article Citation

RIS
MARC (XML)
FULL CITATION (TXT)

---

Share on Facebook

Authors: Uma Gunasekaran, Courtney W. Hudgens, Brian T. Wright, Matthew F. Maulis and Maureen Gannon

Uma Gunasekaran

Department of Medicine; Division of Diabetes, Endocrinology and Metabolism; Vanderbilt University Medical Center; Nashville, TN USA

Courtney W. Hudgens

Department of Medicine; Division of Diabetes, Endocrinology and Metabolism; Vanderbilt University Medical Center; Nashville, TN USA

Brian T. Wright

Department of Medicine; Division of Diabetes, Endocrinology and Metabolism; Vanderbilt University Medical Center; Nashville, TN USA

Matthew F. Maulis

Department of Medicine; Division of Diabetes, Endocrinology and Metabolism; Vanderbilt University Medical Center; Nashville, TN USA

Maureen Gannon

Corresponding author: maureen.gannon@vanderbilt.edu
Department of Medicine; Division of Diabetes, Endocrinology and Metabolism; Vanderbilt University Medical Center; Nashville, TN USA; Department of Molecular Physiology and Biophysics; Vanderbilt University Medical Center; Nashville, TN USA; Department of Cell and Developmental Biology; Vanderbilt University Medical Center; Nashville, TN USA; VA Medical Center; Nashville, TN USA

Abstract:
Diabetes results from an inadequate functional β cell mass, either due to autoimmune destruction (Type 1 diabetes) or insulin resistance combined with β cell failure (Type 2 diabetes). Strategies to enhance β cell regeneration or increase cell proliferation could improve outcomes for patients with diabetes. Research conducted over the past several years has revealed that factors regulating embryonic β cell mass expansion differ from those regulating replication of β cells post-weaning. This article aims to compare and contrast factors known to control embryonic and postnatal β cell replication. In addition, we explore the possibility that connective tissue growth factor (CTGF) could increase adult β cell replication. We have already shown that CTGF is required for embryonic β cell proliferation and is sufficient to induce replication of embryonic β cells. Here we examine whether adult β cell replication and expansion of β cell mass can be enhanced by increased CTGF expression in mature β cells.

Received: April 20, 2012; Accepted: April 28, 2012

Preview: