Talk:Stress and appetite: Difference between revisions
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imported>Emelie Gustafson No edit summary |
imported>Gareth Leng No edit summary |
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The problem is that then the same topics will be covered. But if the course organise is okay with it, then I suppose it would be okay. But I doubt that there will be 7 different topics under this subject which will be big enough to write enough on. So they would end up pretty similar.[[User:Emelie Gustafson|Emelie Gustafson]] 13:36, 28 September 2010 (UTC) | The problem is that then the same topics will be covered. But if the course organise is okay with it, then I suppose it would be okay. But I doubt that there will be 7 different topics under this subject which will be big enough to write enough on. So they would end up pretty similar.[[User:Emelie Gustafson|Emelie Gustafson]] 13:36, 28 September 2010 (UTC) | ||
:This is potentially a very large topic; it will include peripheral actions of glucocorticoids, the role of the PVN as a target for appetite regulating circuits and as a controller of the HPA axis and the sympathetic nervous system, sympathetic regulation, "comfort" eating, effects of chronic severe stress (including cachexia), and should touch on POMC deficiency and clinical conditions (Cushings etc). | |||
:Stress has a bidirectional effect on appetite; mild intermittent stress generally stimulates appetite but chronic severe stress can lead to loss of appetite and severe weight loss. One natural separation might be to look separately at the mechanisms by which stress can lead to weight gain and mechanisms by which stress can lead to weight loss. One subtopic might be the actions of glucocorticoids and another the neural circuitry of interactions between the PVN and appetite regulating centres. [[User:Gareth Leng|Gareth Leng]] 09:50, 1 October 2010 (UTC) | |||
Revision as of 04:50, 1 October 2010
- Christina Lang 13:17, 28 September 2010 (UTC)
- Cyrus Dailami 12:42, 28 September 2010 (UTC)
- James Pattinson 13:08, 28 September 2010 (UTC)
- Emelie Gustafson 13:16, 28 September 2010 (UTC)
- Holly Clark 13:17, 28 September 2010 (UTC)
- Gillian McNeill 13:17, 28 September 2010 (UTC)
- Thomas C Horne 13:23, 28 September 2010 (UTC)
Testing! We are far too many on this topic. Max. 4. During the class last week it was decided that Holly, Gillian, Christina and I (Emelie) were doing this topic since we signed up to it. Just wondering what's going on, and how we are going to adress this.
I think the course organiser agreed that more than one group could carry out the same talk, is there any way we could split the talk? or maybe he wouldn't mind if two groups covered the same talk.
The problem is that then the same topics will be covered. But if the course organise is okay with it, then I suppose it would be okay. But I doubt that there will be 7 different topics under this subject which will be big enough to write enough on. So they would end up pretty similar.Emelie Gustafson 13:36, 28 September 2010 (UTC)
- This is potentially a very large topic; it will include peripheral actions of glucocorticoids, the role of the PVN as a target for appetite regulating circuits and as a controller of the HPA axis and the sympathetic nervous system, sympathetic regulation, "comfort" eating, effects of chronic severe stress (including cachexia), and should touch on POMC deficiency and clinical conditions (Cushings etc).
- Stress has a bidirectional effect on appetite; mild intermittent stress generally stimulates appetite but chronic severe stress can lead to loss of appetite and severe weight loss. One natural separation might be to look separately at the mechanisms by which stress can lead to weight gain and mechanisms by which stress can lead to weight loss. One subtopic might be the actions of glucocorticoids and another the neural circuitry of interactions between the PVN and appetite regulating centres. Gareth Leng 09:50, 1 October 2010 (UTC)