Type 2 diabetes is a complex disease. It results from a failure of the body to maintain energy homoeostasis. Multicellular organisms have evolved complex strategies to preserve a relatively stable internal nutrient environment, despite fluctuations in external nutrient availability. This complex strategy involves the co-ordinated responses of multiple organs to promote storage or mobilization of energy sources according to the availability of nutrients and cellular bioenergetics needs. The endocrine pancreas plays a central role in these processes by secreting insulin and glucagon. When this co-ordinated effort fails, hyperglycaemia and hyperlipidaemia develops, characterizing a state of metabolic imbalance and ultimately overt diabetes. Although diabetes is most likely a collection of diseases, scientists are starting to identify genetic components and environmental triggers. Genome-wide association studies revealed that by and large, gene variants associated with type 2 diabetes are implicated in pancreatic β-cell function, suggesting that the β-cell may be the weakest link in the chain of events that results in diabetes. Thus, it is critical to understand how environmental cues affect the β-cell. Phosphoinositides are important ‘decoders’ of environmental cues. As such, these lipids have been implicated in cellular responses to a wide range of growth factors, hormones, stress agents, nutrients and metabolites. Here we will review some of the well-established and potential new roles for phosphoinositides in β-cell function/dysfunction and discuss how our knowledge of phosphoinositide signalling could aid in the identification of potential strategies for treating or preventing type 2 diabetes.
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February 2016
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Cover Image
Scanning electron micrograph of a cell from the endosperm of a barley grain. The cell is tightly packed with large, disk-shaped (A-type) and much smaller, almost spherical (B-type) starch granules. The smooth areas in this image are the surface of the cell walls of neighbouring endosperm cells. For further details see pp. 157-163. Image kindly provided by Elaine Barclay and Vasilios Andriotis (John Innes Centre, Norwich). - PDF Icon PDF LinkTable of Contents
Review Article|
February 09 2016
Phosphoinositide signalling in type 2 diabetes: a β-cell perspective
Lucia E. Rameh;
Lucia E. Rameh
1
*Department of Medicine, Boston University School of Medicine, 650 Albany Street, Boston, MA 02118, U.S.A.
1To whom correspondence should be addressed (email rameh@bu.edu).
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Jude T. Deeney
Jude T. Deeney
*Department of Medicine, Boston University School of Medicine, 650 Albany Street, Boston, MA 02118, U.S.A.
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Publisher: Portland Press Ltd
Received:
November 30 2015
Online ISSN: 1470-8752
Print ISSN: 0300-5127
© 2016 Authors; published by Portland Press Limited
2016
Biochem Soc Trans (2016) 44 (1): 293–298.
Article history
Received:
November 30 2015
Citation
Lucia E. Rameh, Jude T. Deeney; Phosphoinositide signalling in type 2 diabetes: a β-cell perspective. Biochem Soc Trans 15 February 2016; 44 (1): 293–298. doi: https://doi.org/10.1042/BST20150229
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