Dr. Suraj Unniappan, along with Drs. Gonzalez,Perry, Ceddia, Reingold, Gao, Gaidhu, and Tsushima from York University (Canada) have been expanding their research on nefstatin-1, a brain protein. This protein was first described in Nature (2006) by Dr. Mori (along with 14 other researchers from Japan), where it was found to interact with receptors in the nucleus and hypothalamus.
Injection of the protein into the brain (and not its metabolites or precurors) decreased food intake in a dose-dependent manner. Moreover, the injection of an antibody that neutralizes nefstatin-1 stimulated the appetite. This anorexigen may be of use in helping of use in controlling the obesity epidemic.
Dr. Unniappan’s group found that when rats are administered the protein, they ate less, they consumed stored fat, their activity increased, and insulin secretion from the pancreas (from the islets of Langerhans) was increased. This last fact is not totally surprising, since the gut and brain are both involved in hunger regulation (via neural and endocrine signals).
The first publication, in the Journal of Endocrinology, was an in vitro study, using β-cells (min-6) and islets (of Langerhans) isolated from mice. The administration of Nesfatin-1 stimulated insulin release from the mouse islets and cells in a dose-dependent fashion (meaning a larger response as more was added). However, if the blood glucose levels were too low, there was no such stimulation.
The second paper, published in Endocrinology, proved that the anorexigen was involved in the regulation of insulin secretion, whole body energy balance, and glucose homeostasis in rats, as opposed to in vitro. The results were the same as for the in vitro studies.
Given this information, one hopes the studies progress to include humans. Assuming the results demonstrate similar results, the anorexigen should be able to control obesity and maintain blood sugar levels.
That sure is good news, Roy! Although, it could be terrifying if the anorexigen has to be placed directly into the brain and not through precursors. Is it a strong molecule not to be metabolized in by the liver -like alcohol in big dozes- or you have to use syringes for that matter? I don’t care too much about needles in my head.
Gustavo| Frugal Science recently posted..When In Doubt, Meditate.
Gustavo:
I am not sure anyone plans to inject this anywhere. But, it certainly would be useful to know if we are producing the compound- or employing its pathways. If we aren’t, then there’s a metabolic problem than needs correction. But, I am willing to bet the cost for this chemical would be far more expensive than the average couch potato would be willing to pay!
Thanks for the thoughts- and I promise- I won’t drill any needles into your head 🙂
Roy
So many theories on obesity. If we went back to hunting and foraging and only ate what was available locally, we would find a distinct decrease in obesity. But then what would happen to the economy – so many young people who work in the fast food industry and where would they go if we stopped eating there?
Roberta recently posted..Get out of stuck by changing your Language
This is not really a theory of obesity, Roberta. It’s the determination of what chemical affects our ability to determine we are full. It is not much different than learning that insulin regulates the glucose levels in our body.
No one is looking to have couch potatoes continue to ferment in place. Because even if we can stimulate the body to digest more food, there is the issue of muscle tonality, brain function (other chemicals are produced from exercise that augment or elevate our general moods, etc.).
But, what if someone has the inability to process this compound, which leads to lower insulin production or diminished feelings of satiety?
Thanks for the comment.
Roy
Or we could emphasize exercise again and again! 🙂
Hajra recently posted..Vampires and Being Yourself
Oh, exercise is absolutely critical, Hajra.
But, what if this is the reason why some folks who eat less and exercise just don’t seem to be losing the weight one would expect? If we could correct an improper pathway, that would be fantastic.
Roy