Thermogenesis challenges the adipostat hypothesis for body-weight control

Proc Nutr Soc. 2009 Nov;68(4):401-7. doi: 10.1017/S0029665109990255. Epub 2009 Sep 24.

Abstract

According to the adipostat hypothesis for body-weight control, alterations in body weight should always be compensated by adequate alterations in food intake and thermogenesis. Thus, increased thermogenesis should not be able to counteract obesity because food intake would be increased. However evidence is presented here that thermogenesis in different forms (through artificial uncouplers, exercise, cold exposure) may counteract obesity and is not always fully compensated by increased food intake. Correspondingly, a decreased capacity for metaboloregulatory thermogenesis (i.e. non-functional brown adipose tissue) may in itself lead to obesity. This is evident in mice and may be valid for human subjects, as a substantial proportion of adults possess brown adipose tissue, and those with less or without brown adipose tissue would seem to be more prone to obesity. Thus, increased thermogenesis may counteract obesity, without dietary intervention.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Adipose Tissue, Brown / pathology
  • Adipose Tissue, Brown / physiopathology*
  • Animals
  • Body Weight / physiology*
  • Energy Intake / physiology*
  • Humans
  • Mice
  • Obesity / etiology*
  • Thermogenesis / physiology*