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Nesfatin-1

● Preclinical
Nucleobindin-2-Derived Satiety Peptide
Also known as: NUCB2 fragment, NES-1
Page last reviewed

Satiety Peptide Preclinical
Nesfatin-1 is an 82-amino acid peptide derived from the N-terminal cleavage of nucleobindin-2 (NUCB2), a calcium- and DNA-binding protein. Discovered in 2006 by Oh-I et al., nesfatin-1 acts as a potent anorexigenic (appetite-suppressing) signal in the hypothalamus. Unlike leptin/" class="wiki-internal-link">leptin, its effects are independent of leptin receptor signaling, making it a target of interest for obesity resistant to leptin-based therapies.
Storage Stability
Lyophilized
1–2 years (-20°C)
Reconstituted
~30 days (2–8°C)
Room temp
Avoid

Mechanism of Action

Hypothalamic Satiety Signaling

Nesfatin-1 is expressed in hypothalamic nuclei including the paraventricular nucleus (PVN), supraoptic nucleus (SON), and arcuate nucleus. It activates alpha-msh/" class="wiki-internal-link">melanocortin 3/4 receptors (MC3R/MC4R) via a leptin-independent pathway, reducing food intake and body weight. Central administration (ICV) potently suppresses feeding even in leptin-deficient ob/ob mice.

Peripheral Actions

Beyond the hypothalamus, nesfatin-1 is expressed in the stomach (X/A-like cells), pancreatic beta cells, heart, and testes. It inhibits gastric acid secretion, modulates insulin secretion, and exerts anti-inflammatory effects in peripheral tissues. Circulating nesfatin-1 levels are reduced in obesity and type 2 diabetes.


Research Summary

Obesity and Appetite

Preclinical

Rodent studies show that ICV or IP nesfatin-1 reduces food intake by 20-40% and promotes weight loss over days of administration. Chronic subcutaneous infusion in diet-induced obese mice reduces adiposity without inducing resistance, a key distinction from leptin.

Metabolic Effects

Preclinical

Nesfatin-1 improves glucose tolerance and insulin sensitivity in rodent models of type 2 diabetes. Pancreatic nesfatin-1 appears to potentiate glucose-stimulated insulin secretion. These dual central-peripheral metabolic actions suggest therapeutic potential for metabolic syndrome.

Stress and Anxiety

Preclinical

Nesfatin-1 neurons overlap substantially with stress-responsive circuits. Central administration activates the HPA axis and increases anxiety-like behavior in rodents. This stress-appetite coupling may be relevant to stress-induced anorexia.


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Research Protocols

GoalDoseFrequencyRoute
Appetite suppression (rodent)1-10 pmol/kg ICVSingle injectionIntracerebroventricular
Glucose tolerance (rodent)10-50 ug/kg IPDailyIntraperitoneal
Plasma level assessmentN/AN/ABlood draw (ELISA)

No human clinical trials. All protocols are rodent research contexts. Human therapeutic application is speculative.


Interactions

complementary
Leptin
Acts via parallel but distinct satiety pathways; additive appetite suppression
complementary
GLP-1 agonists
Different mechanisms converge on reduced food intake; potential synergy
antagonistic
ghrelin/" class="wiki-internal-link">Ghrelin
Ghrelin is orexigenic; nesfatin-1 counteracts its appetite-stimulating effects

Safety Profile

No human safety data exists. In rodent studies, ICV nesfatin-1 causes anxiety-like behavior at higher doses and activates the HPA stress axis. Peripheral administration appears better tolerated. No commercial human-grade product exists; nesfatin-1 is a research-only compound with no established human dosing framework.


References

  • [1]Oh-I S, et al. Identification of nesfatin-1 as a satiety molecule in the hypothalamus. Nature. 2006;443(7112):709-712.
  • [2]Shimizu H, et al. Nesfatin-1: an overview and future clinical application. Endocr J. 2009;56(4):537-543.
  • [3]Stengel A, Tache Y. Nesfatin-1, role as possible new potent regulator of food intake. Regul Pept. 2010;163(1-3):18-23.
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Verified Scientific Data Last audited:
Data Sources & External References
Source: peer-reviewed literature  ·  Domain: ascendpeptide.org

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