http://www.jci.org/articles/view/57873Circulating glucose levels modulate neural control of desire for high-calorie foods in humans
Kathleen A. Page1,2, Dongju Seo3, Renata Belfort-DeAguiar1, Cheryl Lacadie4, James Dzuira5, Sarita Naik1, Suma Amarnath1, R. Todd Constable4, Robert S. Sherwin1 and Rajita Sinha3
1Section of Endocrinology, Yale University School of Medicine, New Haven, Connecticut, USA.
2Division of Endocrinology, University of Southern California Keck School of Medicine, Los Angeles, California, USA.
3Department of Psychiatry,
4Department of Radiology, and
5Yale Center for Clinical Investigation, Yale University School of Medicine, New Haven, Connecticut, USA.
Address correspondence to: Robert S. Sherwin, C.N.H. Long Professor of Medicine, Director, Yale Center for Clinical Investigation, Yale School of Medicine, The Anlyan Center S141, PO Box 208020 New Haven, Connecticut 06520-8020, USA. Phone: 203.785.4183; Fax: 203.737.5558; E-mail: firstname.lastname@example.org.
Authorship note: Kathleen A. Page and Dongju Seo contributed equally to this work and serve as joint first authors. Rajita Sinha and Robert S. Sherwin contributed equally and serve as joint senior authors.
First published September 19, 2011
Submitted: March 4, 2011; Accepted: July 27, 2011.
Obesity is a worldwide epidemic resulting in part from the ubiquity of high-calorie foods and food images. Whether obese and nonobese individuals regulate their desire to consume high-calorie foods differently is not clear. We set out to investigate the hypothesis that circulating levels of glucose, the primary fuel source for the brain, influence brain regions that regulate the motivation to consume high-calorie foods. Using functional MRI (fMRI) combined with a stepped hyperinsulinemic euglycemic-hypoglycemic clamp and behavioral measures of interest in food, we have shown here that mild hypoglycemia preferentially activates limbic-striatal brain regions in response to food cues to produce a greater desire for high-calorie foods. In contrast, euglycemia preferentially activated the medial prefrontal cortex and resulted in less interest in food stimuli. Indeed, higher circulating glucose levels predicted greater medial prefrontal cortex activation, and this response was absent in obese subjects. These findings demonstrate that circulating glucose modulates neural stimulatory and inhibitory control over food motivation and suggest that this glucose-linked restraining influence is lost in obesity. Strategies that temper postprandial reductions in glucose levels might reduce the risk of overeating, particularly in environments inundated with visual cues of high-calorie foods.
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