How your fat cells signal your brain about long-term energy stores.
What the evidence says
- Produced by adipocytes (fat cells) in proportion to fat mass[1],[2]
- Signals to hypothalamus about long-term energy stores[1],[2]
- On the lipostat account, leptin reduces appetite and increases energy expenditure when stores are full[1]
- The lipostat is a model, not a settled description — `cls04` is Friedman’s perspective piece, and Friedman discovered leptin, so this is the model’s clearest articulation by its own champion. `kls04` states the corpus position: neither the set-point nor the settling-point model is adequate[1]
- Short-term carbohydrate overfeeding increases plasma leptin by ~28% and 24-hour energy expenditure by 7%; fat overfeeding does neither[3]
- The leptin increase from carbohydrate overfeeding does not correlate with the energy expenditure increase, suggesting independent mechanisms[3]