Repletion of TNFα or leptin in calorically restricted mice suppresses post-restriction hyperphagia

Catherine Hambly, Jacqueline S Duncan, Zoë A Archer, Kim M Moar, Julian G Mercer, John R Speakman

Research output: Contribution to journalArticlepeer-review

22 Citations (Scopus)
6 Downloads (Pure)


The causes of post-restriction hyperphagia (PRH) represent a target for drug-based therapies to prevent obesity. However, the factors causing PRH are poorly understood. We show that, in mice, the extent of PRH was independent of the time under restriction, but depended on its severity, suggesting that PRH was driven by signals from altered body composition. Signals related to fat mass were important drivers. Circulating levels of leptin and TNFa were significantly depleted following caloric restriction (CR). We experimentally repleted their levels to match those of controls, and found that in both treatment groups the level of PRH was significantly blunted. These data establish a role for TNFa and leptin in the non-pathological regulation of energy homeostasis. Signals from adipose tissue, including but not limited to leptin and TNFa, regulate PRH and might be targets for therapies that support people engaged in CR to reduce obesity.
Original languageEnglish
Pages (from-to)83-94
Number of pages12
JournalDisease Models & Mechanisms
Issue number1
Early online date27 Sep 2011
Publication statusPublished - Jan 2012


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