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Thermogenesis challenges the adipostat hypothesis for body-weight control
Barbara Cannon1, Jan Nedergaard
1The Wenner-Gren Institute, The Arrhenius Laboratories F3, Stockholm University, SE-106 91 Stockholm, Sweden. barbara.cannon@wgi.su.se
The Proceedings of the Nutrition Society
|September 25, 2009
Summary
Increased thermogenesis, including from brown adipose tissue, can counteract obesity. Reduced thermogenesis capacity may lead to obesity, even without dietary changes.
Area of Science:
- Physiology
- Metabolism
- Obesity Research
Background:
- The adipostat hypothesis suggests body weight is tightly regulated by food intake and thermogenesis.
- This hypothesis implies increased thermogenesis cannot overcome obesity due to compensatory increases in food intake.
Purpose of the Study:
- To investigate whether thermogenesis can counteract obesity independently of dietary intake.
- To explore the role of metaboloregulatory thermogenesis, particularly brown adipose tissue, in obesity development.
Main Methods:
- Examined the effects of various thermogenesis-inducing methods (uncouplers, exercise, cold exposure) on body weight.
- Assessed the link between brown adipose tissue function and obesity in mouse models.
- Considered the implications for human subjects based on brown adipose tissue prevalence.
Main Results:
- Evidence indicates that enhanced thermogenesis can counteract obesity without compensatory increases in food intake.
- Decreased capacity for metaboloregulatory thermogenesis, such as non-functional brown adipose tissue, is linked to obesity.
- Mice studies suggest a causal relationship, with potential relevance to human obesity.
Conclusions:
- Thermogenesis, particularly via brown adipose tissue, plays a crucial role in preventing obesity.
- Reduced brown adipose tissue function may predispose individuals to obesity.
- Targeting thermogenesis offers a potential strategy for obesity management without dietary intervention.
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