Leptin — Fullness Signal from Fat Tissue
The hormone that tells your brain, “We’re well stocked — it’s safe to ease off the hunger pedal.”
Leptin is a hormone secreted by fat cells in proportion to how much energy they’re storing. More fat → more leptin in the blood. In a healthy system, leptin travels to the hypothalamus and essentially files a status report: “Energy reserves are high, you can dial down appetite and turn up energy expenditure.”
When leptin is working, it acts like a long‑term fullness gauge. If your fat stores drop (after prolonged dieting), leptin levels fall, the brain interprets “famine risk”, and it ramps up hunger while quietly lowering metabolic rate. That’s one mechanism behind post‑diet weight regain: your hormones are trying to push you back to your previous set point.
In obesity, the paradox is that leptin levels are often high, but the brain responds as if they’re low — a state called leptin resistance. Inflammation, genetics, and chronic nutrient surplus seem to blunt the signal. The hypothalamus then behaves as though you’re under‑stored, defending a higher weight with stubborn hunger and reduced spontaneous activity.
GLP‑1‑based therapies and lifestyle changes don’t “fix” leptin directly, but by reducing food intake and improving insulin-resistance, they can slowly improve the environment that made leptin resistance worse. Long term, the goal is not zero leptin but a brain that can hear the message again.
Why It Matters
Once you understand leptin, weight regain after dieting stops looking like personal failure and starts looking like a predictable hormonal response to perceived scarcity.
Closing Line
Leptin is your fat tissue’s PR agent — if the brain stops taking its calls, the message “we’re safe” never lands, and appetite keeps fighting for lost ground.