Thermogenesis challenges the adipostat hypothesis for body-weight control.
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.
The Wenner-Gren Institute, The Arrhenius Laboratories F3, Stockholm University, SE-106 91 Stockholm, Sweden. barbara.cannon@wgi.su.se
Barbara
B
Cannon
Jan
J
Nedergaard
D002001:Adipose Tissue, Brown / Q000473:pathology / Q000503:physiopathology*; D000818:Animals; D001835:Body Weight / Q000502:physiology*; D002149:Energy Intake / Q000502:physiology*; D006801:Humans; D051379:Mice; D009765:Obesity / Q000209:etiology*; D022722:Thermogenesis / Q000502:physiology*