Talk:Energostatic hypothesis: Difference between revisions
imported>Gareth Leng No edit summary |
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: Excellent progress - you're writing fluently - what you say is very clearly and logically expressed and you're illustrating it well with very lucid summaries of key contemporary evidence. Well done![[User:Gareth Leng|Gareth Leng]] 10:23, 2 November 2011 (UTC) | : Excellent progress - you're writing fluently - what you say is very clearly and logically expressed and you're illustrating it well with very lucid summaries of key contemporary evidence. Well done![[User:Gareth Leng|Gareth Leng]] 10:23, 2 November 2011 (UTC) | ||
::Good work in making a difficult and complex topic clear.[[User:Gareth Leng|Gareth Leng]] 18:10, 30 November 2011 (UTC) |
Latest revision as of 09:30, 1 December 2013
Amanda Jayne Swan 15:14, 3 October 2011 (UTC)Amanda Jayne Swan 16:13, 20 September 2011 (UTC)
Gaia Wu 10:01, 21 September 2011 (UTC) Lydia Ntari 08:50, 22 September 2011 (UTC)
Hi guys.
The basic idea underlying this hypothesis is that appetite is triggered when receptor cells in the brain recognise a shortage of energy for their own needs - i.e. these are cells that drive an increased energy intake when they sense an energy deficit. A decrease in fatty acid oxidation or a decrease in glucose utilisation increases the intracellular AMP/ATP ratio and activates the cellular enery sensor AMP kinase (AMPK). So to see where this theory is going look for papers on AMPK in the hypothalamus and its role in appetite. It's an interesting and very fast moving area. See hereGareth Leng 12:53, 10 October 2011 (UTC)
Hi Amanda, good work for the references.
Nancy Sabatier 12:36, 11 October 2011 (UTC)
- Excellent progress - you're writing fluently - what you say is very clearly and logically expressed and you're illustrating it well with very lucid summaries of key contemporary evidence. Well done!Gareth Leng 10:23, 2 November 2011 (UTC)
- Good work in making a difficult and complex topic clear.Gareth Leng 18:10, 30 November 2011 (UTC)
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