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Plasticity of skeletal muscle metabolism via insulin and IGF receptor-mediated AKT activation

Reference	BBS/E/B/0000L166
Principal Investigator / Supervisor	Dr Jennifer Pell
Co-Investigators / Co-Supervisors
Institution	Babraham Institute
Department	Babraham Institute Department
Funding type	Research
Value (£)	120,849
Status	Completed
Type	Institute Project
Start date	28/11/2005
End date	27/11/2008
Duration	36 months

Abstract

Cell behaviour (should they grow, take up nutrients, do nothing or they die?) is often controlled by molecules called hormones. The aim of this project is to look at two hormones: 1) insulin that tells cells when to absorb nutrients, mostly glucose and 2) a hormone that is related to insulin, called insulin-like growth factor (called IGF) which tells cells to grow (divide or get bigger). The actions of insulin and IGFs were first discovered by injecting the hormones into animals and seeing what happened.There are now much better new ways of looking at hormone action. Insulin and IGF are both proteins and therefore each is derived from a gene. It is now possible to either remove a gene (and therefore its protein) from an animal, called a knock-out. Conversely, we can give the animal extra copies of the gene, called an overexpressor. Scientists have now knocked-out insulin and IGF with surprising results. In certain conditions, insulin can do the job of IGF, in other words tell cells to grow. Also IGF can sometimes behave like insulin telling cells to take up nutrient. This probably happens more than we had assumed before.Insulin and IGF bind to special molecules on the outside of the cell, called receptors, and the insulin receptor and IGF receptor are very similar indeed. The receptor tells the cell that the hormone has arrived by making a whole series of proteins active inside the cell. This usually occurs by changing the charge of the protein, thus changing its shape, which means it can activate the next protein in the sequence. These are called signalling pathways.The aim of this project is to answer the question: 'How can insulin do the job of IGF, and how can IGF do the job of insulin?', which will shed light on the events leading to the development of human diseases like type 2 diabetes, caused by insufficient activity of both insulin and IGF.

Summary

unavailable

Committee	Closed Committee - Animal Sciences (AS)
Research Topics	X – not assigned to a current Research Topic
Research Priority	X – Research Priority information not available
Research Initiative	X - not in an Initiative
Funding Scheme	X – not Funded via a specific Funding Scheme

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