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Related Experiment Video

Updated: Jun 18, 2026

Characterization of Adipocyte-Derived Extracellular Vesicle Secretion Using a CD63-GFP Reporter Mouse Model In Vivo and In Vitro
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Published on: December 5, 2025

Do leptin and insulin signal adiposity?

Jacquelien J G Hillebrand, Nori Geary

    Forum of Nutrition
    |December 4, 2009
    PubMed
    Summary

    The brain uses endocrine signals like insulin and leptin to regulate body fat. Current evidence is insufficient to confirm if these hormones effectively signal adipose tissue mass to the brain.

    Area of Science:

    • Physiology
    • Neuroendocrinology
    • Energy Homeostasis

    Background:

    • Adiposity regulation relies on endocrine signals informing the brain about adipose tissue (AT) mass.
    • Insulin and leptin are established adiposity signals, with amylin, ghrelin, and peptide YY also hypothesized.
    • Evidence supporting these signals includes hormone-adiposity correlations, receptor presence, and effects of mutations.

    Purpose of the Study:

    • To evaluate if circulating insulin and leptin levels encode necessary information to function as adiposity signals.
    • To distinguish between regulation of AT mass in steady versus dynamic states.
    • To assess the strength of evidence supporting insulin and leptin as adiposity signals.

    Main Methods:

    • Focus on evidence from associations between basal hormone levels and adiposity levels.

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  • Emphasis on the distinction between steady and dynamic states of AT mass regulation.
  • Analysis of experimental designs, particularly those involving perturbations causing changes in adiposity.

    • Main Results:

    • Limited studies exist that investigate adiposity signals during dynamic changes in AT mass.
    • Available evidence does not strongly support the hypothesis that insulin and leptin function as adiposity signals.
    • The focus on steady-state associations may not fully capture the regulatory role of adiposity signals.

    Conclusions:

    • The question of how adiposity is signaled to the brain remains largely unresolved.
    • Current evidence is insufficient to confirm the role of insulin and leptin as effective adiposity signals.
    • Further research using dynamic state experimental designs is needed to elucidate adiposity signaling pathways.