Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2010 Oct;34 Suppl 1(0 1):S47-55.
doi: 10.1038/ijo.2010.184.

Adaptive thermogenesis in humans

M Rosenbaum  1 , R L Leibel
Affiliations
Review

Adaptive thermogenesis in humans

M Rosenbaum et al. Int J Obes (Lond). 2010 Oct.

Abstract

The increasing prevalence of obesity and its comorbidities reflects the interaction of genes that favor the storage of excess energy as fat with an environment that provides ad libitum availability of energy-dense foods and encourages an increasingly sedentary lifestyle. Although weight reduction is difficult in and of itself, anyone who has ever lost weight will confirm that it is much harder to keep the weight off once it has been lost. The over 80% recidivism rate to preweight loss levels of body fatness after otherwise successful weight loss is due to the coordinate actions of metabolic, behavioral, neuroendocrine and autonomic responses designed to maintain body energy stores (fat) at a central nervous system-defined 'ideal'. This 'adaptive thermogenesis' creates the ideal situation for weight regain and is operant in both lean and obese individuals attempting to sustain reduced body weights. Much of this opposition to sustained weight loss is mediated by the adipocyte-derived hormone 'leptin'. The multiple systems regulating energy stores and opposing the maintenance of a reduced body weight illustrate that body energy stores in general and obesity in particular are actively 'defended' by interlocking bioenergetic and neurobiological physiologies. Important inferences can be drawn for therapeutic strategies by recognizing obesity as a disease in which the human body actively opposes the 'cure' over long periods of time beyond the initial resolution of symptomatology.

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Leibel R, Chua S, Rosenbaum M. Chapter 157. Obesity. In: Scriver C, Beaudet A, Sly W, Valle D, editors. The metabolic and molecular bases of inherited disease. 8. III. New York: McGraw-Hill; 2001. pp. 3965–4028.
    1. West DB, Boozer CN, Moody DL, Atkinson RL. Dietary obesity in nine inbred mouse strains. Am J Physiol. 1992;262:R1025–R32. - PubMed
    1. Bouchard C, Tremblay A. Genetic influences on the response of body fat and fat distribution to positive and negative energy balances in human identical twins. J Nutr. 1997;127:943S–47S. - PubMed
    1. Bouchard C, Tremblay A, Despres JP, Nadeau A, Lupien PJ, Theriault G, et al. The response to long-term overfeeding in identical twins. N Engl J Med. 1990;322:1477–82. - PubMed
    1. Rosenbaum M. Epidemiology of pediatric obesity. Ped Annals. 2007;36:89–95. - PubMed