Gut Microbiome Reveals Molecular Origins of Eating Disorders

[leela]

http://www.neomatica.com/2014/10/08/molecular-origins-eating-disorders-found-gut-microbe/

 

[Simon]

Molecular Origins Of Eating Disorders Found In Gut Microbe | Neomatica

Researchers...have found strong evidence that a protein made by intestinal bacteria are a causative agent for the disorders. Specifically, antibodies made by the host against this protein cross-react with a mammalian satiety hormone.

The severity of symptoms in [Eating Disorder] patients was also found to correlate with levels of the neutralizing antibodies. The researchers believe that this understanding will ultimately lead to a chemical therapeutic strategies to correct eating disorders.

Few comments from me

This is about 'molecular mimicry': the idea is that a gut microbiome bacteria, E coli K12, by sheer bad luck produces a protein (ClpB) that looks very much like alpha-MSH, a human protein that helps regulate our feeding and energy levels.The anit-ClpB antibodies aimed against the bacteria take out the human alpha-MSH protein as collateral damage. And in this study, patients with more severe eating disorders have higher levels of this damaging antibody (reacting against both the bacterial ClpB protein and the human alpha-MSH one).

So far, so good. Some of the findings, however, are not so clear cut.

Some of the research was done on mice, and giving mice alpha-MSH causes anorexia (weight loss/reduced eating) as expected. Mice given the E. coli strain that makes ClpB produce antibodies against ClpB and alpha-MSH, again as expected. And these mice are immune to the effect of alpha-MSH therapy - presumably because their anti-ClpB antibodies take out the injected alpha-MSH, blocking its biological effect.

So the model is that the E coli strain plays a role in eating disorders by inadvertently taking out natural alpha-MSH, which normally leads to feeling full/ induces anorexia.

BUT, when the researchers gave mice the E coli bacteria, the mice initally lost weight (as you'd predict) but then surprisingly (at least to me) gained weight, by 5%. This suggests something more complicated is going on:

Next, the researchers checked how a host responds to dosages of ClpB. Mice which were dosed with ClpB indeed lost weight briefly but a month later increased their weight by 5%. These mice remarkably also became immune to α-MSH, which usually induces anorexic-like effects. In summary, these results show that ClpB provokes a feeding or energy usage reaction in the host that at early times looks like weight loss but at later times weight gain.

I'd be interested in @Jonathan Edwards take on this, as I think he is sceptical of the evidence for molecular mimicry.

 

[IreneF]

Haven't read the article, but my understanding is that people suffering from anorexia nervosa are actually hungry all the time and obsessed by food. (At least some of them.)