Energy balance
Long-term administration of the CB1 receptor antagonist rimonabant (SR141716) reverses diet-induced obesity in mice by enhancing lipolysis and increasing energy expenditure through futile cycling, rather than solely through reduced food intake.
This research suggests that sustained fat loss can be driven by increasing the body's energy expenditure and fat burning (lipolysis) rather than just eating less. The drug rimonabant achieved this by activating metabolic pathways in fat tissue. Note: Rimonabant was withdrawn from the market due to safety concerns; this mechanism highlights the potential of targeting energy expenditure pathways.
Our data clearly indicated that SR141716 reversed the phenotype of obese adipocytes at both macroscopic and genomic levels... the reduction of adipose mass by the molecule resulted from an enhanced lipolysis through the induction of enzymes of the β-oxidation and TCA cycle, increased energy expenditure, mainly through futile cycling (calcium and substrate), and a tight regulation of glucose homeostasis.
Why this rating
High-quality controlled animal study with molecular validation (microarrays, immunohistochemistry) and clear phenotypic outcomes.
Source
The CB1 receptor antagonist rimonabant reverses the diet‐induced obesity phenotype through the regulation of lipolysis and energy balance
Omar Jbilo et al. · The FASEB Journal · 2005
DOI 10.1096/fj.04-3177fje
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