📚 Wiki Hormonal & Reproductive Insulin-Like Peptide 3

Insulin-Like Peptide 3

● Preclinical/Biomarker
Relaxin/Insulin-Like Factor 3 (INSL3)
Also known as: INSL3, Leydig insulin-like peptide, relaxin-like factor (RLF)
Page last reviewed

Quick Summary

Insulin-like peptide 3 (INSL3) is a member of the relaxin peptide family produced constitutively by testicular Leydig cells in males and theca cells in females. It is the primary hormonal signal driving gubernacular development and testicular descent during fetal development.

Reproductive Hormone Preclinical
Insulin-like peptide 3 (INSL3) is a member of the relaxin peptide family produced constitutively by testicular Leydig cells in males and theca cells in females. It is the primary hormonal signal driving gubernacular development and testicular descent during fetal development. In adult males, circulating INSL3 is a Leydig cell biomarker and modulates bone metabolism and reproductive axis signaling. Its receptor, RXFP2 (relaxin family peptide receptor 2), mediates its endocrine and paracrine actions.
Storage Stability
Lyophilized
1–2 years (-20°C)
Reconstituted
~30 days (2–8°C)
Room temp
Avoid

Mechanism of Action

RXFP2 Receptor Signaling

INSL3 binds RXFP2 with high affinity and activates adenylyl cyclase via Gs proteins, elevating cAMP. In gubernacular cells during fetal development, this drives tissue remodeling and testicular descent. In adult bone, RXFP2 signaling stimulates osteoblast differentiation and bone formation. In the testis, INSL3 modulates germ cell development and testicular blood flow via RXFP2 on peritubular myoid cells.

Fetal Development Role

INSL3 knockout mice exhibit bilateral cryptorchidism (retained testes) due to failed gubernacular development, establishing INSL3 as the critical signal for the first transabdominal phase of testicular descent. Human RXFP2 mutations cause cryptorchidism in boys. This developmental function is distinct from the adult endocrine roles.


Research Summary

Male Reproductive Health Biomarker

Clinical Evidence

Adult serum INSL3 levels are a direct quantitative marker of functional Leydig cell mass, more sensitive than testosterone for detecting Leydig cell dysfunction. Low INSL3 with normal testosterone indicates Leydig cell reserve depletion. It is reduced in varicocele, aging, chemotherapy-exposed men, and Klinefelter syndrome. INSL3 measurement is gaining clinical utility for male reproductive assessment.

Bone Metabolism

Preclinical

INSL3 via RXFP2 promotes osteoblast activity and bone formation in vitro and in vivo. INSL3 knockout mice show reduced bone mass. In human osteoporosis cohorts, low serum INSL3 associates with reduced bone mineral density in men, suggesting INSL3 may contribute to the androgen-independent bone protective effects of the male gonadal axis.


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Research Protocols

GoalDoseFrequencyRoute
Leydig cell function assessmentN/AMorning serum drawBlood draw (ELISA)
Bone formation (rodent)1-10 ug/kg SCDaily x 28 daysSubcutaneous
Cryptorchidism rescue (neonatal rodent)Continuous SC infusionPostnatal days 1-7Subcutaneous

Human therapeutic use is speculative. INSL3 is primarily a research and biomarker tool. No clinical trials for exogenous INSL3 administration in humans.


Interactions

upstream regulator
LH (luteinizing hormone)
LH stimulates INSL3 production acutely; INSL3 is constitutively produced at low levels independent of acute LH pulses
parallel
Testosterone
Both are Leydig cell products; INSL3 measures Leydig cell mass, testosterone measures acute function
family member
Both relaxin family peptides; different receptors (RXFP2 vs RXFP3) and physiological roles

Safety Profile

No human administration safety data for exogenous INSL3. As an endogenous peptide with constitutive Leydig cell production, physiological INSL3 appears well tolerated. Theoretical concerns for supraphysiological dosing include RXFP2 desensitization and effects on osteoblast/gonadal axis. No commercial therapeutic INSL3 product exists.


References

  • [1]Ivell R, Anand-Ivell R. Biological role and clinical significance of insulin-like peptide 3. Curr Opin Endocrinol Diabetes Obes. 2009;16(3):210-214.
  • [2]Nef S, Parada LF. Cryptorchidism in mice mutant for Insl3. Nat Genet. 1999;22(3):295-299.
  • [3]Bay K, et al. Insulin-like factor 3 levels in cord blood and serum from children: effects of age, gestational age, and weight. J Clin Endocrinol Metab. 2007;92(12):4636-4641.
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Data Sources & External References
Source: peer-reviewed literature  ·  Domain: ascendpeptide.org

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