Altered Brain Metabolism Linked to Overeating and Obesity

2012-02-09 20:19
PET image of brain

Regulation of glucose within the brain has an impact on behavior and plays an important role in many disease states including diabetes and dysfunctional memory and cognition. Researchers with the University of Turku and Aalto University have found that dysregulation with this system is linked to overeating leading to excessive energy intake and eventual obesity.

Adjunct Professor Lauri Nummenmaa from the University of Turku and colleagues studied the brain’s glucose metabolism in both morbidly obese individuals and in lean, healthy controls. Positron emission tomography was used to measure functioning brain circuits during conditions in which the body was satiated in terms of insulin signaling – meaning the subjects were not physically hungry. Brain responses were measured with functional magnetic resonance imaging when the subjects viewed pictures of food.

In those who were obese, brain glucose metabolism was significantly higher in the brain’s striatal regions, which are involved in the processing of rewards. These reward systems responded more vigorously to food pictures – particularly those high in fat and sugar, such as a cake - and responses in other brain regions involved in cognitive control were dampened.

"The results highlight the role of the brain in obesity and weight gaining. The results have major implications on the current models of obesity, but also on development of pharmacological and psychological treatments of obesity," Nummenmaa says.

The study isn’t the first to connect brain function with increased appetite. In 2009, scientists at Johns Hopkins released a study that suggests that the brain signal for appetite responded to certain sugars (fructose, high fructose corn syrup) which in turn leads to more eating.

Another team of researchers, this time at the Albert Einstein College of Medicine, noted that circulating levels of fatty acids in the body trigger an appetite stimulating brain signal that caused laboratory mice to eat more than they normally would have. While the theory hasn’t yet been tested in humans, the appetite signaling process could be a potential target for anti-obesity drugs.

Journal Reference:
Nummenmaa L , Hirvonen J , Hannukainen JC , Immonen H , Lindroos MM , et al. 2012 Dorsal Striatum and Its Limbic Connectivity Mediate Abnormal Anticipatory Reward Processing in Obesity. PLoS ONE 7(2): e31089. doi:10.1371/journal.pone.0031089

Photo Credit: PET Scan of Brain Wikimedia Commons

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