OR09-3 Constitutional thinness: a bodyweight gain resistance human model with specific appetite, energetic and metabolomics responses to fat overfeeding

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: OR09-Obesity: Physiologic Responses to Energy Balance Disruption
Clinical
Saturday, June 15, 2013: 11:30 AM-1:00 PM
Presentation Start Time: 12:00 PM
Room 307 (Moscone Center)
Natacha Germain1, Bogdan Galusca1, Dominique Caron-Dorval1, Dominique Grouselle2, Estelle Pujos-Guillot3, Jean-Francois Martin3, Yves Boirie3, James S Minnion4, Stephen R Bloom4, Jacques P Epelbaum2 and Andre Bruno Estour*1
1University Hospital, Saint-Etienne, France, 2UMR894 INSERM, Paris, France, 3INRA, Clermont-Ferrand, France, 4Imperial College London, London, United Kingdom
Context:Constitutional thinness (CT) is a rare condition of natural low bodyweight in both genders, with preserved menstruation in females, no biological marker of undernutrition, a bodyweight gain desire and an anorexigenic hormonal profile. CT can be considered as the opposite of obesity, where some patients appear to resist bodyweight loss.

Objectives: We tested the hypothesis that CT would be resistant to bodyweight gain.

Design:A 4-week fat overfeeding (630 kcal excess), performed in an ambulatory position, compared 8 CT women (BMI<17.5kg/m²) and 8 female controls (BMI 18.5-25kg/m²): Bodyweight, food intake, urinary metabolomics profiles, body composition, energy expenditure (EE) and appetite regulatory hormones profile after test meal were monitored before and after dietary intervention.

Results: Four weeks of fat overfeeding failed to increase bodyweight in CTs (+0.225 kg ± 0.180; controls: +0.725 kg ± 0.268, p=0.26 and 0.03 vs. baseline respectively) despite a well-documented compliance with dietary intervention: dietary records, lipid assessment, fat oxidation and metabolomics. Appetite regulatory hormones exhibited an overall anorexigenic adaptive response in CTs with significant increase in post-meal Peptide YY and Glucagon like Peptide type 1, inefficient to counteract the supervised overfeeding but may partly explain CTs eating behavior and play a role in bodyweight gain resistance. Resting EE increased in CTs only with no increase in activity energy expenditure, explaining partially the bodyweight gain resistance. Over all, CTs displayed a paradoxical positive energy balance after overfeeding contrasting with the bodyweight gain resistance. This gap in energy balance could suggest specific EE in CTs.

Conclusion:This study proposes CT as a human model of bodyweight gain resistance in a fat overfeeding paradigm.

 This study is registered in Clinical Trial.gov, no. NCT01224561

Nothing to Disclose: NG, BG, DC, DG, EP, JFM, YB, JSM, SRB, JPE, ABE

*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 work was supported by regional innovation and research committee grant (PHRC no. 0701047). This study is registered in Clinical Trial.gov, no. NCT01224561.