Journal
MOLECULAR ENDOCRINOLOGY
Volume 28, Issue 8, Pages 1211-1220Publisher
OXFORD UNIV PRESS INC
DOI: 10.1210/me.2014-1095
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Funding
- National Institutes of Health [R01DK-078752]
- American Diabetes Association [7-12-BS-167]
- Juvenile Diabetes Research Foundation
- JNJSI [40-2011-1]
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Pancreatic beta-cells are responsible for insulin production, and loss of functional beta-cell mass is now recognized as a critical step in the pathogenesis of both type 1 and type 2 diabetes. However, the factors controlling the life and death of the pancreatic beta-cell have only started to be elucidated. Discovered as the top glucose-induced gene in a human islet microarray study 12 years ago, thioredoxin-interacting protein (TXNIP) has now emerged as such a key player in pancreatic beta-cell biology. Since then, beta-cell expression of TXNIP has been found to be tightly regulated by multiple factors and to be dramatically increased in diabetic islets. Elevated TXNIP levels induce beta-cell apoptosis, whereas TXNIP deficiency protects against type 1 and type 2 diabetes by promoting beta-cell survival. TXNIP interacts with and inhibits thioredoxin and thereby controls the cellular redox state, but it also belongs to the beta-arrestin family of proteins and regulates a variety of metabolic processes. Most recently, TXNIP has been discovered to control beta-cell microRNA expression, beta-cell function, and insulin production. In this review, the current state of knowledge regarding regulation and function of TXNIP in the pancreatic beta-cell and the implications for drug development are discussed.
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