New Brain Peptide Abolishes the “Munchies”
Wednesday, July 7, 2010
Readers may be well aware that the use of cannabis or “hashish” can induce the “munchies”, an acute craving for highly palatable foods.
Now Garron Dodd and colleagues from the University of Manchester, UK, have identified a new brain peptide called hemopressin that acts through cannabinoid receptors to reduce food intake in rats and mice. Their findings are published in the latest edition of the Journal of Neuroscience.
Hemopressin is a short, nine amino acid peptide found in the rat brain that behaves as an inverse agonist at the cannabinoid receptor CB(1), where it inhibits agonist-induced receptor internalization.
In their studies, Dodd and colleagues found that this peptide dose-dependently decreases night-time food intake in normal male rats and mice, as well as in obese ob/ob male mice, when administered centrally or systemically, without any obvious adverse side effects.
Hemopressin specifically blocks the hyperphagic response to CB(1) receptor agonists, while having no effect on eating behaviour in CB(1) receptor null mutant male mice.
Obviously, the discovery of this peptide not only increases our understanding of the complex neurobiology of ingestive behaviour but may also lead the way to new treatments for obesity.
It should however be noted that we have already had potent inhibitors of the CB(1) receptor for the treatment of obesity (readers will recall rimonabant), which were withdrawn from the market due to increased incidence of depression.
Nevertheless, it may well be that endogenous inhibitors of the endocannabinoid system (like hemopressin) may well be better tolerated previous inhibitors of this system.
Perhaps we have not seen the last of our attempts to decrease appetite by blocking the endocannabinoid system just yet.
AMS
Edmonton, Alberta
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Dodd GT, Mancini G, Lutz B, & Luckman SM (2010). The peptide hemopressin acts through CB1 cannabinoid receptors to reduce food intake in rats and mice. The Journal of neuroscience : the official journal of the Society for Neuroscience, 30 (21), 7369-76 PMID: 20505104
Wednesday, July 7, 2010
I subscribe to nature.com, the largest publisher of science in America. Even with all our great minds digging through synapses, neurons and genomes looking to find the keys to managing hunger, we still know very little. I have a small study within my obese patients focusing on “Intolerance of exercise”. I believe the cellular inflammation caused by long term obesity erodes muscular tissue and causes exercise intolerance. The longer a person has been obese (male or female) the greater the degree of discomfort for cardiovascular exercise. This activity intolerance could well be a meaningful change that occurs during the course of the disease, and could be a deterrent to a “behavior change” model.
Wednesday, July 7, 2010
Gee, Mavis, do you think that the inflammation that erodes muscular tissue could be preexisting and cause exercise intolerance, which leads to obesity? All you know about this is the correlation. You don’t know which came first, but it makes more sense to me that people who move less due to discomfort while exercising would be heavier, and people with more inflammation would move less than people with less inflammation. And that in turn would cause weight gain and then obesity.
Wednesday, July 7, 2010
Or, for that matter, that your obese patients might have exercise-induced asthma, never diagnosed? Or fibromyalgia? Or arthritis?