OHSU Research Reveals The Complexitites Of Obesity/Cortisol Interactions
02/02/06 Portland, Ore.
Research also helps explain the reasons why anti-obesity cortisol reducing supplements do not work.
Researchers at Oregon Health & Science University have revealed that the cortisol/obesity connection, touted by many weight-loss supplement marketers, may be even more tenuous than first thought. The research also highlights the complexities of the body's weight regulation system and is published in the current edition of The Journal of Clinical Investigation.
"We've all seen television ads for cortisol-reducing weight loss drugs," said Malcolm Low, M.D., Ph.D., a senior scientist and associate director in the OHSU Center for the Study of Weight Regulation and Associated Disorders. Low is also a professor of behavioral neuroscience in the OHSU School of Medicine, and a scientist in the Vollum Institute. "However, this research helps show that cortisol levels are not the sole, major factor involved in obesity and fat distribution. In reality, there are many other hormones involved in weight regulation and it's hard to say whether cortisol and corticosterone - both in a family of hormones called glucocorticoids - rise prior to weight gain or if their increases are impacts of the weight gain itself."
To conduct the research, scientists studied specially bred mice lacking the proopiomelanocortin (POMC) gene. Previous research has shown that mutations to the POMC gene in humans and mice cause obesity, but simultaneously decrease glucocorticoid levels. Because it was unknown whether the primary abnormality occurs in the brain or peripheral tissues, scientists attempted to repair the problem and counteract the obesity by manipulating POMC and glucocorticoid levels. The scientists did this using two methods. One method was to genetically restore POMC selectively in the pituitary, a gland at the base of the brain that regulates the secretion of cortisol from the adrenal glands, but not in the central portions of the brain. The second method was to directly replace glucocorticoids in POMC-lacking mice through their drinking water.
"In both cases, the mice lacking POMC in the brain did not show improvement in their metabolic state. The treatments actually led to an acceleration in weight gain and development of diabetes," explained Low. "Importantly, the identical treatments had no discernable effect in control mice with normal POMC levels in the brain. This research demonstrates the important function of the POMC gene in the central nervous system, independent of the pituitary and adrenal glands. It also demonstrates that cortisol alone is not the major culprit in weight gain. Glucocorticoids are merely part of a chain of hormonal and neuronal signals associated with obesity."
This research is being announced as the OHSU Center for the Study of Weight Regulation and Associated Disorders is moving into its permanent, new home: the state-of-the-art Biomedical Research Building on the OHSU Marquam Hill Campus. The new labs will allow basic researchers and physicians to work side by side in understanding the causes and in developing treatments and preventative measures for both obesity and cachexia and their secondary medical consequences.
For more information on the Center for the Study of Weight Regulation and Associated Disorders, visit http://www.ohsu.edu/weight