What REALLY happens when you infuse insulin in to the cerebro spinal fluid of a mouse? You know, the satiety hormone... Just in to the brain, nothing systemic, no hypoglycaemia.
Insulin = big fat adipocytes. Big fat mice. Lovely micrographs.
http://www.jci.org/articles/view/31073/figure/5 will give you the legend.
http://www.jci.org/articles/view/31073 will give you the full text. Might discuss the paper better in a few months time!
But main conclusion:
The brain fine tunes the storage of lipid under the influence of insulin (by increasing fat storage via lipoprotein lipase and also by DNL from glucose). It uses the sympathetic nervous system outflow from the ventromedial hypothalamus to do this. Interpret with caution as these are C57BL/6, mice who may well have some very specific weakness in their ventromedial hypothalamus.
OMG did I laugh when I found this one.
Wanna loose some weight, go eat some potatoes. LMFAO!
Sorry for the crudity. Been on call too long this weekend!
Peter
12 comments:
And yet in the discussion the authors state "where it (insulin)modulates a variety of functions, including the regulation of food intake..."
And ref #28 http://www.ncbi.nlm.nih.gov/pubmed/12021765?dopt=Abstract
Decreasing hypothalamic insulin receptors causes hyperphagia and insulin resistance in rats.
There you go, satiety hormone ;-)
@O Numnos: "where it (insulin)modulates a variety of functions, including the regulation of food intake..."
So are we to assume that "regulation" of food intake has only one action... that of inhibiting it?
I think the bottom line is that insulin's anabolic affect is substantially greater than its affect to promote satiety.
Besides the complication of needing to consider what receptor insulin binds to ( which is really what matters ), if insulin was any good suppressing appetite then injecting insulin should reduce food intake and reverse obesity.
But we all know what injecting insulin really does..............
It's offtopic, I seem to have taeniasis possibly acquired after a few days in Thailand.
What drugs would you recommend?
It used to be that there were a few bad papers published - it is getting to the point where there are more bad papers (where the experiment is flawed, the conclusions defy logic, application of matlab without understanding the underlying statistics or just plain fraud) than good. Instead of advancing science they are muddying the water.
I do remember that insulin has been used to stimulate appetite in treating anorexia. Has this been forgotten?
I think there are a number of papers that are intended to simply keep the grant money flowing - carefully designed as to not challenge the accepted theory. The effort should be to establish the arrow of causation of correlations - apply the null hypothesis - yet there are so many experiments that no matter what the results were - at the end we have learned nothing.
Yaya sleep stupid peter.
I remember once I investigated S. Guyenet's references and discovered he completely misrepresented them. Like, entirely and utterly , overt fraud. It was apparent when he copy + pasta'd he didn't G.A.F. what the link contained, just as long as he could put a number next to his writing and make it look all serious.
Scary to think they are all this bad. Or worse.
PS this was funny. Here he's pretending to be an objective impartial servant of science, blindly going where the evidence leads him. HAHA! This from the same man who just a few weeks ago was behaving like a SNL superfan regarding his hypothesis. According to Stephan Guyenet, if the food reward hypothesis were matched against god + insulin hypothesis in football the score would be 338439 to 1.
karl,
The writing style itself is so different. Whereas the tone used to seem inquisitive, papers are now written as close-minded persuasions.
As Woo sort of implies, Whole Health Source made a similar transition, but it took only a couple years.
O Numnos, no no no. You are not following the process through. Central insulin promotes DNL in adipocytes using the sympathetic nervous system. DNL generates palmitoleate which increases whole body insulin sensitivity, normally in association with increased adipocyte storage of the de novo lipids, ie it makes you fat, as per the micrographs (did you look at them?). This is obvious, you would expect that high insulin indicates an need for running metabolism on glucose and a need to divert fat to storage. Blocking this action by knocking down selected hypothalmic insulin receptors should leads to whole body insulin resistance (reduced palmitoleate from adipocytes) and a need to increase insulin to maintain normoglycaemia if you are on a high carbohydrate diet, with a subsequent storage of fat in adipocytes secondary to this hyperinsulinaemia, obviously once the hyperinsulinaemia is sufficient to overcome the lack of palmitoleate generation in adipocytes.
You're sounding like an obesity researcher, sorry for the gross insult.
These might help you:
http://www.ncbi.nlm.nih.gov/pubmed/21284985
http://www.ncbi.nlm.nih.gov/pubmed/18805087
@Unknown, see a pharmacist!
@Its, we all know you're crazy as well as very perceptive, but how the hell do you STILL mamange to read WHS? That is pathological! Are you stealing ondansetron from work????
Peter
I try to avoid it only to cave and read a few days after he posts an entry like some kind of weak willed junk sick addict. The crazy cancels out the response to nausea, sort of how haloperidol or metoclopramide does.
@Unknown
Caffeine, nicotine, and alcohol are my favorites, but I'm limited to those drugs that won't show up in a urinalysis.
@Peter
Er, I was being sarcastic....as it was a shits 'n' giggles piece
O Numnos., Oh sh*t. Too tired!
Post a Comment