Where it comes from
- Made in
- The paraventricular and arcuate nuclei, the brainstem, and outside the brain the stomach’s ghrelin cells, islets and fat
- Sent out by
- Fasting lowers its production in brain and stomach and refeeding raises it again; blood levels are less consistent
- Acts on
- Hypothalamic feeding circuits
- Brainstem
- Islets (insulin)
- Heart and vessels
What it does
- Reduces food intake and weight when given into the brain, even in leptin-resistant animals 1
- Raises blood pressure and slows gastric emptying
- Takes part in anxiety and stress responses
In medicine
- No medicine copies it or blocks it. Blood nesfatin-1 is a research marker, and the findings in obesity and diabetes do not agree 2
- Pooled studies show the disagreement plainly: across type 2 diabetes cohorts the direction of the difference varies with the assay and the population, and the same is true in polycystic ovary syndrome 23
Beyond the body’s own use
- Nothing containing nesfatin-1 is in trials, approved or obtainable outside the laboratory
- What makes it worth following is that it works without leptin: given into the brain of a leptin-resistant animal it still reduces food intake and weight, which no leptin-based approach does 1
- What is unknown is what it binds. No receptor has been identified in twenty years, its effects are traced through melanocortin and oxytocin circuits instead, and without a receptor there is nothing for a medicine to aim at 1
Sources
- Oh-I et al., Identification of nesfatin-1 as a satiety molecule in the hypothalamus, Nature 2006
- Zhai et al., Circulating nesfatin-1 levels and type 2 diabetes, a systematic review and meta-analysis, Journal of Diabetes Research 2017
- Bahreiny et al., Circulating nesfatin-1 in polycystic ovary syndrome, a systematic review and meta-analysis, International Journal of Reproductive Biomedicine 2023
This card describes what a medicine is for and what the evidence says; it recommends nothing. Talk to your clinician about anything you read here.