Talk:Aminostatic hypothesis

Gianna Maurer 10:12, 24 September 2011 (UTC) Ashleigh Fraser 12:25, 25 September 2011 (UTC) Gianna Maurer 14:38, 11 October 2011 (UTC) Gianna Maurer 14:07, 16 October 2011 (UTC)

Hi Gianna, good work with the references, it would have been even better with a small summary for each article.

Lisa, I moved the references you added into the Bibliography page.

Nancy Sabatier 15:13, 12 October 2011 (UTC)

Yes, good selection - but now you need to add a summary of the key points from each - that will make writing the article much simpler.Gareth Leng 19:57, 12 October 2011 (UTC)

Signatures

Normal practice on this and other wikis is to sign talk page comments with ~~~~ but not to sign article contributions. It is possible to tell who contributed what by looking at the article history, and sigs tend to clutter the article.

This article has many sigs. I removed some, almost as a reflex action, but stopped when I realised you seem to be using them to keep comments straight during article development. Certainly they should all go eventually, but I'm not certain if they should be removed immediately or left as long as you need them. Sandy Harris 06:45, 26 October 2011 (UTC)

Thanks Sandy; I'll clean up in due course, but for now don't want to get in the way of enthusiasm.Gareth Leng 10:04, 26 October 2011 (UTC)

Progress

Well done on the figures - clear and thoughtful schematics. Remember to proofread!!! - brainstem not brainstorm (Freudian slip? :-)) Gareth Leng 10:41, 26 October 2011 (UTC)

I see some problems here "Peptide YY acts in two different ways through targets in the hypothalamic arcuate nucleus. It activates the mammalian target of rapamycin to increase α-MSH which increases anorexigenic effects at the same time as suppressing AMPK phosphorylation to decrease neuropeptide Y and agouti related peptide and cause a decrease in orexigenic effects"

NPY is an orexigenic peptide that acts via specific receptors, named Y1...Y5. The Y2 receptor is an inhibitory autoreceptor, i.e. it is expressed by the NPY/AcRP cells and mediates direct negative feedback. PYY is an agonist at the Y2 receptor, so PYY directly inhibits the NPY/AgRP cells. Because NPY cells inhibit the POMC cells, PYY indirectly stimulates the POMC cells to cause an increase in a-MSH release. AMPK is a widely expressed enzyme associated with cellular metabolism - as an "energy sensing" pathway. In the arcuate nucleus, AMPK is thought to play an important role in energy sensing in the regulation of appetite, and PYY may well affect this pathway. I don't know where rapamycin fits - you need a reference and explanation if you include this.

At Honours level, we look for understanding that is backed up by evidence ('facts') - but understanding is paramount, so it's very important that you convey understanding in everything you write - this is the real value of clear writing. Expand what you've written to fill in the logical gaps, and then edit down again if needed but keeping the logical flow.

For example 'to decrease neuropeptide Y and agouti related peptide' - what exactly do you mean here - reduce content, expression or release - what exactly is the evidence? Do we know how it decreases these? What is the evidence?Gareth Leng 12:52, 1 November 2011 (UTC)

- Good - AMPK IS NOT A PEPTIDE. Check out exactly what GLP-1 is and the evidence behind its importance.||||