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Diabetes, Vol 49, Issue 5 838-846, Copyright © 2000 by American Diabetes Association
Differential brain responses to satiation in obese and lean men
JF Gautier, K Chen, AD Salbe, D Bandy, RE Pratley, M Heiman, E Ravussin, EM Reiman and PA Tataranni
Clinical Diabetes and Nutrition Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Phoenix 85016, USA.
Knowledge of how the brain contributes to the regulation of food intake in
humans is limited. We used positron emission tomography and measures of
regional cerebral blood flow (rCBF) (a marker of neuronal activity) to
describe the functional anatomy of satiation (i.e., the response to a
liquid meal) in the context of extreme hunger (36-h fast) in 11 obese (BMI
> or =35 kg/m2, age 27+/-5 years, weight 115+/-11 kg, 38+/-7% body fat;
mean +/- SD) and 11 lean (BMI < or =25 kg/m2, age 35+/-8 years, weight
73+/-9 kg, 19+/-6% body fat) men. As in lean men, satiation in obese men
produced significant increases in rCBF in the vicinity of the ventromedial
and dorsolateral prefrontal cortex and significant decreases in rCBF in the
vicinity of the limbic/paralimbic areas (i.e., hippocampal formation,
temporal pole), striatum (i.e., caudate, putamen), precuneus, and
cerebellum. However, rCBF increases in the prefrontal cortex were
significantly greater in obese men than in lean men (P < 0.005). rCBF
decreases in limbic/paralimbic areas, temporal and occipital cortex, and
cerebellum were also significantly greater in obese men than in lean men (P
< 0.005), whereas rCBF decreases in the hypothalamus and thalamus were
attenuated in obese men compared with lean men (P < 0.05). This study
raises the possibility that the brain responses to a meal in the prefrontal
areas (which may be involved in the inhibition of inappropriate response
tendencies) and limbic/paralimbic areas (commonly associated with the
regulation of emotion) may be different in obese and lean men. Additional
studies are required to investigate how these differential responses are
related to the pathophysiology of obesity.

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Copyright © 2000 by the American Diabetes Association.
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