ASRN has learned of a breakthrough study involving brain function and hunger.  Researchers have identified the brain circuits which, as influenced by the hormone leptin, signal sensations of satiety and hunger. In clinical trials, leptin supplementation has produced moderate weight loss in some obese patients by inhibiting hunger and promoting feelings of satiety. The new findings suggest possible new therapeutic targets for obesity, an increasing problem in both adults and children.



Researchers at UCLA report that leptin reduces activation in regions of the brain linked to hunger while enhancing activation in regions linked to inhibition and feelings of being full. The researchers used functional magnetic resonance imaging (fMRI) to measure brain activity before and after leptin supplementation in three adults from a Turkish family who lack the leptin (ob) hormone due to a mutation. Such a mutation in the ob gene causes leptin deficiency and morbid obesity.  One drawback of the study is that it was based on findings of only three subjects, who were all from the same family.  This limitation was due to the fact that genetic deficiencies of leptin are extremely rare.

Indeed, research published in 2005 research based on the same three family members to show that when leptin replacement was provided, body weight and eating behavior were normalized. This earlier study also found that leptin produced sustained changes in the tissue composition of the cerebral cortex in the same individuals.

To determine the neural circuits through which leptin alters human feeding behavior, the researchers showed images of food to the family members while they underwent fMRI imaging, both before and after leptin treatment. After leptin replacement, feelings of hunger induced by the images and activity in certain brain regions associated with hunger — the insular, parietal and temporal cortices — were reduced, while brain activity increased in the prefrontal cortex, an area of the brain previously associated with feeling full or satisfied. 

The implications of this research are wide-reaching.  As care providers, clinicians, nurses, and nurse educators are well aware of the health risks imposed by our national obesity epidemic.  Moderation of lifestyle factors is essential in the management of obesity.  However, as this study demonstrates, genetic factors cannot be ignored.  Addressing only lifestyle issues in patients who are leptin deficient will likely be unsuccessful.

The research was supported in part by the National Institutes of Health and the UCLA General Clinical Research Center. During the course of this study, Amgen Inc. graciously provided leptin; Amylin Inc. now provides leptin to these patients. Neither Amgen nor Amylin contributed to the design, analysis or writing of this study.

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