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Am J Physiol Endocrinol Metab 296: E1-E10, 2009. First published September 23, 2008; doi:10.1152/ajpendo.90538.2008
0193-1849/09 $8.00
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REVIEW

Emerging roles for the ubiquitin-proteasome system and autophagy in pancreatic β-cells

Taila Hartley,1,2 John Brumell,3,4,6 and Allen Volchuk1,2,5

1Division of Cell and Molecular Biology, Toronto General Research Institute, University Health Network, Toronto; Departments of 2Biochemistry, 3Molecular Genetics, 4Institute of Medical Science, and 5Physiology, University of Toronto; and 6Cell Biology Program, The Hospital for Sick Children, Toronto, Ontario, Canada

Submitted 24 June 2008 ; accepted in final form 12 September 2008

ABSTRACT

Protein degradation in eukaryotic cells is mediated primarily by the ubiquitin-proteasome system and autophagy. Turnover of protein aggregates and other cytoplasmic components, including organelles, is another function attributed to autophagy. The ubiquitin-proteasome system and autophagy are essential for normal cell function but under certain pathological conditions can be overwhelmed, which can lead to adverse effects in cells. In this review we will focus primarily on the insulin-producing pancreatic β-cell. Pancreatic β-cells respond to glucose levels by both producing and secreting insulin. The inability of β-cells to secrete sufficient insulin is a major contributory factor in the development of type 2 diabetes. The aim of this review is to examine some of the crucial roles of the ubiquitin-proteasome system and autophagy in normal pancreatic β-cell function and how these pathways may become dysfunctional under pathological conditions associated with metabolic syndromes.

autophagy; insulin secretion; ubiquitin proteasome; endoplasmic reticulum stress


Address for reprint requests and other correspondence: A. Volchuk, Toronto General Research Institute, 101 College St., TMDT 10-707, Toronto, ON, M5G 1L7 Canada (e-mail: avolchuk{at}uhnres.utoronto.ca)






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