Differential regulation of embryonic and adult β cell replication.
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.
Department of Medicine, Division of Diabetes, Endocrinology and Metabolism, Vanderbilt University Medical Center, Nashville, TN, USA.
Uma
U
Gunasekaran
Courtney W
CW
Hudgens
Brian T
BT
Wright
Matthew F
MF
Maulis
Maureen
M
Gannon
D000818:Animals; D049109:Cell Proliferation; D055513:Connective Tissue Growth Factor / Q000378:metabolism; D003922:Diabetes Mellitus, Type 1 / Q000378:metabolism / Q000473:pathology; D003924:Diabetes Mellitus, Type 2 / Q000378:metabolism / Q000473:pathology; D004622:Embryo, Mammalian; D047108:Embryonic Development; D006801:Humans; D007333:Insulin Resistance; D050417:Insulin-Secreting Cells / Q000166:cytology* / Q000378:metabolism
D055513:Connective Tissue Growth Factor