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Cited by 142Regulation of Appetite and ObesityEating Disorders and BehaviorsAdipokines, Inflammation, and Metabolic Diseases

Energy intake in weight-reduced humans

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Rosenbaum, Michael, Kissileff, Harry R., Mayer, Laurel E.S., Hirsch, Joy, Leibel, Rudolph L.·2010·Brain Research
DOI 10.1016/j.brainres.2010.05.062PMC PMC2926239
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Abstract

Almost anyone who has ever lost weight can attest that it is harder to sustain weight loss than to lose weight. Maintenance of a 10% or greater reduced body weight is accompanied by decreases in energy expenditure to levels significantly below what is predicted solely on the basis of weight and body composition changes. This disproportionate decline in energy expenditure would not be sufficient to account for the over 80% recidivism rate to pre-weight loss levels of body fatness after otherwise successful weight reduction if there were a corresponding reduction in energy intake. In fact, reduced body weight maintenance is accompanied by increased energy intake above that required to maintain reduced weight. The failure to reduce energy intake in response to decreased energy output reflects decreased satiation and perception of how much food is eaten and multiple changes in neuronal signaling in response to food which conspire with the decline in energy output to keep body energy stores (fat) above a CNS-defined minimum (threshold). Much of this biological opposition to sustained weight loss is mediated by the adipocyte-derived hormone "leptin."

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  • This state of positive energy balance maintained over a prolonged period-or energy burden-drives adipocyte hypertrophy and, to a lesser extent, hyperplasia, as well as weight gain.

    “This state of positive energy balance maintained over a prolonged period—or energy burden—drives adipocyte hypertrophy and, to a lesser extent, hyperplasia, as well as weight gain.85,86”

    From Definition and diagnostic criteria of clinical obesity (2025) · cites this paper as [86]

    The Introduction reports weight gain during overfeeding and explains that a small energy surplus can produce substantial weight gain over time. It does not say that prolonged positive energy balance causes adipocyte hypertrophy or hyperplasia, or that hypertrophy occurs to a greater extent. (LLM, conf=0.86)

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Authors
Rosenbaum, M., Kissileff, H. R., Mayer, L. E. S., Hirsch, J., & Leibel, R. L.
Affiliations
  • Columbia University Irving Medical Center (US)
  • St. Luke's-Roosevelt Hospital Center (US)
  • New York State Psychiatric Institute (US)
  • Columbia University (US)
Corresponding author
Rosenbaum, Michael
ORCID
Venue
Brain Research
Publisher
Elsevier BV
Published
2010-09
Volume
1350
Pages
95-102
ISSN
0006-8993 (ISSN-L)
DOI
10.1016/j.brainres.2010.05.062
PMC
PMC2926239
OpenAlex
W2027116377
Cited by
142
References
85
Citations by year
2026: 6 · 2025: 7 · 2024: 1 · 2023: 2 · 2022: 6 · 2021: 11 · 2020: 8 · 2019: 6 · 2018: 9 · 2017: 10 · 2016: 9 · 2015: 19 · 2014: 11 · 2013: 13 · 2012: 10
FWCI
1.18
Type
journal article
Language
en
Open access
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Brain Research (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
NIH (DK30583, DK26687, DK37948, DK64773, DKP30 26687, RR00102, RR00645, and RR024156)
Topics
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
  • Social Sciences › Psychology › Clinical Psychology › Eating Disorders and Behaviors
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
Keywords
energy intake, weight loss maintenance, energy expenditure, satiation, leptin, adipocytes, food intake regulation, fat mass, weight regain, neuronal signaling, energy homeostasis
MeSH terms
Body Weight, Eating, Energy Metabolism, Feeding Behavior, Humans, Obesity, Weight Loss

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