Research

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 Note: Rimonabant was withdrawn from the market due to safety concerns; this mechanism highlights the potential of targeting energy expenditure pathways.

GoodSupportsHIGH confidence
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.
Omar Jbilo et al. · The FASEB Journal · 2005

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

mechanism_onlyCited 345×
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DOI resolved against Crossref · corpus check 2026-06-10

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