Session: FP09-Obesity: Physiologic Responses to Energy Balance Disruption
Bench to Bedside
Room 307 (Moscone Center)
Poster Board SAT-698
Methods: Using a randomized, blinded, crossover design, 12 overweight or obese men age 18-35 years consumed high and low GI meals controlled for calorie content, macronutrient composition and palatability on two occasions. Frequent hunger ratings and blood samples were obtained. Functional neuroimaging was performed 4 hours after the test meals. Main outcome measures were cerebral blood flow as a measure of resting brain activity, assessed by arterial spin labelling MRI (the primary outcome), plasma glucose and insulin levels, and reported palatability and hunger. We hypothesized that brain activity would be greater after the high vs. low GI meal in areas involved in the regulation of eating behavior, reward and addiction, including the striatum, hypothalamus, amygdala, hippocampus, cingulate, orbitofrontal cortex and insular cortex.
Results: Incremental plasma glucose (2hr area under the curve) was 2.4 fold greater after the high vs. low GI meal (P=0.0001). Plasma glucose was lower (83.9 mg/dL vs. 95.6 mg/dL, P=0.005) and reported hunger was greater (P=0.04) four hours after the high GI meal. At this time, the high GI meal elicited greater brain activity centered in the right nucleus accumbens (P<0.0001), spreading to other areas of the right striatum (caudate, putamen and globus pallidus) and to the olfactory area.
Conclusion: Compared to an isocaloric low GI meal, a high GI meal decreased plasma glucose, increased hunger and selectively stimulated brain areas associated with addiction in the late postprandial period, a time with special significance to eating behavior at the next meal. These findings provide a possible mechanism for the previously described excess food intake after high GI meals, and a target for therapeutic interventions.
Disclosure: DCA: Research Funding, GE Healthcare. Nothing to Disclose: BSL, LMH, ES, RR, CBE, JMG, DSL
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