"We know that CRP binds to leptin, and this impairs its signaling, but we don't know how this is so. It may be that the coupling of the two makes crossing the blood-brain barrier difficult, or it may be that as a package it can't bind to leptin receptors in the brain," suggested Dr. Zhao.
Dr. Zhao and his collaborators sought to find factors normally circulating in blood that could inhibit leptin. CRP was the most potent of the five serum leptin-interacting proteins they identified.
In one set of studies, the researchers delivered human leptin continuously for six days into mice with receptors for leptin but without the ability to produce it. As expected, the plump mice ate less and lost weight, and their blood glucose levels normalized. Infusions containing both leptin and high doses of CRP blocked the action of leptin. The mice continued feasting, getting even fatter, and were no longer protected against
diabetes. Giving CRP alone affected neither food intake nor body weight.
In a different experiment, the researchers found that when exposed to leptin, human
liver cells increased their expression of CRP, suggesting that appetite may be regulated through a feedback loop that includes the liver in addition to the brain and fat cells that secrete leptin.
One of the many questions yet to be answered is whether too much fat increases CRP or if it's the high levels of CRP that make one fat. Dr. Zhao and his team are continuing their laboratory studies but they also plan to follow the outcomes of
obese patients who are being treated with statin
drugs, such as Lipitor and Zocor, for high cholesterol. Recent studies have found that statin drugs lower levels of CRP as well. Working with David E. Kelly, M.D., professor of medicine and director of the obesity and Nutrition research Center at the University of Pittsburgh and a co-author of the current paper, Dr. Zhao hopes to learn if such drugs.
The above information thankfully comes from the bio-medicine.org the following
link.
