FP09-3 Effects of Dietary Glycemic Index On Brain Areas Associated With Addiction: A Randomized Controlled Feeding Study

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: FP09-Obesity: Physiologic Responses to Energy Balance Disruption
Bench to Bedside
Saturday, June 15, 2013: 11:00 AM-11:30 AM
Presentation Start Time: 11:10 AM
Room 307 (Moscone Center)

Poster Board SAT-698
Belinda S Lennerz*1, David C Alsop2, Laura M Holsen3, Emily Stern4, Rafael Rojas2, Cara B Ebbeling5, Jill M Goldstein3 and David S Ludwig6
1University of Ulm, Ulm, Germany, 2Beth Israel Deaconess Medical Center / Harvard Medical School, Boston, 3Brigham and Women's Hospital/Harvard Medical School, Boston, MA, 4Brigham and Womens Hospital / Harvard Medical School, Boston, 5New Balance Foundation Obesity Prevention Center / Harvard Medical School, Boston, 6Children's Hosp of Boston, Boston, MA
Context: Qualitative aspects of diet influence eating behavior and body weight, but the physiological mechanisms for these calorie-independent effects remain speculative. The postprandial rise in blood glucose as quantified by the glycemic index (GI) is of particular interest, as a high GI elicits hormonal and metabolic events that cause hunger and overeating. Thus, our aim was to examine the effects of GI on brain activity in the late postprandial period, after a typical inter-meal interval.

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

*Please take note of The Endocrine Society's News Embargo Policy at http://www.endo-society.org/endo2013/media.cfm

Sources of Research Support: This study was supported by grant K24DK082730 from the National336 Institute of Diabetes and Digestive and Kidney Diseases (NIDDK, Bethesda, MD), grant337 R01MH80729 from the National Institute of Mental Health (NIMH, Bethesda, MD),338 grant UL1 RR025758-01 from the National Center for Research Resources (NCRR,339 Bethesda, MA) to the Harvard Catalyst Clinical and Translational Science Center at340 Harvard University, a grant from the Pediatric Endocrine Society (McLean, VA), a grant341 from the Endocrine Fellows Foundation (Washington, DC), and a grant from the New342 Balance Foundation (Boston, MA).