Talk:Energostatic hypothesis: Difference between revisions

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imported>Amanda Jayne Swan
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imported>Gareth Leng
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[[User:Gaia Wu|Gaia Wu]] 10:01, 21 September 2011 (UTC)
[[User:Gaia Wu|Gaia Wu]] 10:01, 21 September 2011 (UTC)
[[User:Lydia Ntari|Lydia Ntari]] 08:50, 22 September 2011 (UTC)
[[User:Lydia Ntari|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.[[User:Gareth Leng|Gareth Leng]] 12:53, 10 October 2011 (UTC)

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 Definition:  The theory that appetite is regulated by the availability of energy for the brain. [d] [e]
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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.Gareth Leng 12:53, 10 October 2011 (UTC)

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