Kristie L O'Connor1, Jenna L Scisco1, Tracey J Smith1, Andrew J Young1, Scott J Montain1, Lori Lyn Price2, Harris R Lieberman1, J Philip Karl3. 1. US Army Research Institute of Environmental Medicine, Military Nutrition Division, Natick, MA; and. 2. Institute for Clinical Research and Health Policy Studies, Tufts Medical Center and Tufts Clinical and Translational Science Institute, Tufts University, Boston, MA. 3. US Army Research Institute of Environmental Medicine, Military Nutrition Division, Natick, MA; and james.p.karl.civ@mail.mil.
Abstract
BACKGROUND: Adaptive responses of appetite-mediating hormones to negative energy balance are thought to contribute to a counterregulatory response that drives weight regain, but they have not been studied while controlling for reduced diet volume. OBJECTIVE: In this secondary analysis, we aimed to determine the effects of short-term, severe energy deprivation (ED) on appetite and appetite-mediating hormone concentrations. METHODS:Twenty-one adults with a mean ±SD age of 21 ± 3 y and body mass index of 25 ± 3 kg/m(2) consumed isovolumetric diets provided over separate 48-h periods while increasing habitual energy expenditure by 1683 ± 329 kcal/d through light- and moderate-intensity exercise. Energy intake was matched to energy expenditure to maintain energy balance (EB) (-44 ± 92 kcal/d) or was <10% of energy expenditure to generate a -3696 ± 742-kcal/d energy deficit. Postprandial appetite, glucose, insulin, acyl ghrelin, peptide YY, pancreatic polypeptide (PP), and glucagon-like peptide-1 (GLP-1) responses and ad libitum energy intake were measured as secondary outcomes after both experimental periods. RESULTS:Fasting insulin (-56% ± 42%) and acyl ghrelin (-60% ± 17%) concentrations decreased during ED but not during EB (condition-by-time interaction; P-interaction ≤ 0.01), whereas fasting leptin concentrations decreased more during ED compared with during EB (-47% ± 27% compared with -20% ± 27%; P-interaction = 0.05). Postprandial insulin (57% ± 63%; P < 0.001), GLP-1 (14% ± 28%; P = 0.04), and PP (54% ± 52%; P < 0.001) areas under the curve (AUCs) were higher, whereas the acyl ghrelin AUC was lower (-56% ± 13%; P < 0.001) after ED compared with after EB. After ED, self-rated appetite was greater, and ad libitum energy intake was 811 kcal/36 h (95% CI: 184, 1439 kcal/36 h) higher relative to after EB (P = 0.01). CONCLUSIONS: Short-term, severe ED suppressed acyl ghrelin concentrations and increased postprandial anorexigenic hormone concentrations. These effects preceded compensatory overeating, suggesting that in adults without obesity, altered sensitivity to appetite-mediating hormones may contribute to an adaptive counterregulatory response during the initial stages of negative EB. This trial was registered at clinicaltrials.gov as NCT01603550.
RCT Entities:
BACKGROUND: Adaptive responses of appetite-mediating hormones to negative energy balance are thought to contribute to a counterregulatory response that drives weight regain, but they have not been studied while controlling for reduced diet volume. OBJECTIVE: In this secondary analysis, we aimed to determine the effects of short-term, severe energy deprivation (ED) on appetite and appetite-mediating hormone concentrations. METHODS: Twenty-one adults with a mean ± SD age of 21 ± 3 y and body mass index of 25 ± 3 kg/m(2) consumed isovolumetric diets provided over separate 48-h periods while increasing habitual energy expenditure by 1683 ± 329 kcal/d through light- and moderate-intensity exercise. Energy intake was matched to energy expenditure to maintain energy balance (EB) (-44 ± 92 kcal/d) or was <10% of energy expenditure to generate a -3696 ± 742-kcal/d energy deficit. Postprandial appetite, glucose, insulin, acyl ghrelin, peptide YY, pancreatic polypeptide (PP), and glucagon-like peptide-1 (GLP-1) responses and ad libitum energy intake were measured as secondary outcomes after both experimental periods. RESULTS: Fasting insulin (-56% ± 42%) and acyl ghrelin (-60% ± 17%) concentrations decreased during ED but not during EB (condition-by-time interaction; P-interaction ≤ 0.01), whereas fasting leptin concentrations decreased more during ED compared with during EB (-47% ± 27% compared with -20% ± 27%; P-interaction = 0.05). Postprandial insulin (57% ± 63%; P < 0.001), GLP-1 (14% ± 28%; P = 0.04), and PP (54% ± 52%; P < 0.001) areas under the curve (AUCs) were higher, whereas the acyl ghrelin AUC was lower (-56% ± 13%; P < 0.001) after ED compared with after EB. After ED, self-rated appetite was greater, and ad libitum energy intake was 811 kcal/36 h (95% CI: 184, 1439 kcal/36 h) higher relative to after EB (P = 0.01). CONCLUSIONS: Short-term, severe ED suppressed acyl ghrelin concentrations and increased postprandial anorexigenic hormone concentrations. These effects preceded compensatory overeating, suggesting that in adults without obesity, altered sensitivity to appetite-mediating hormones may contribute to an adaptive counterregulatory response during the initial stages of negative EB. This trial was registered at clinicaltrials.gov as NCT01603550.
Authors: Amrendra Mishra; Hamed Mirzaei; Novella Guidi; Manlio Vinciguerra; Alice Mouton; Marina Linardic; Francesca Rappa; Rosario Barone; Gerardo Navarrete; Min Wei; Sebastian Brandhorst; Stefano Di Biase; Todd E Morgan; S Ram Kumar; Peter S Conti; Matteo Pellegrini; Michel Bernier; Rafael de Cabo; Valter D Longo Journal: Nat Metab Date: 2021-10-14
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