Gonadal peptide hormone in the insulin–relaxin family
INSL3
INSL3 is an insulin–relaxin-family peptide hormone studied in gonadal development. Similarity of its name to insulin does not establish identity or allow insulin's metabolic findings to be transferred to it.
This is a research reference, not a product offered in the Asciende catalog. Published studies do not establish the identity, purity or availability of a commercial preparation.
Receptor, selectivity and context
Record the receptor panel actually measured. Absence of a result for another receptor does not establish absence of activity.
- Which receptor subtype and species were evaluated?
- Was affinity, functional potency or an integrated response measured?
- Does the comparison include the alternative receptors needed for a selectivity claim?
Mechanism described in the literature
In cells expressing LGR8, now called RXFP2, INSL3 stimulated cyclic AMP production in vitro, while it did not produce the same response through LGR7 in the cited comparison. The study also tested ligand–receptor interaction and cultured gubernacular cells.
Other names in the literature
- INSL-3
- Insulin-like peptide 3
- Relaxin-like factor
- RLF
A phenotype guided the receptor search
Investigators observed similarities between gonadal-development abnormalities associated with loss of the ligand and loss of the receptor in mice. This guided a hypothesis, but assigning INSL3 to LGR8 required cellular confirmation. A shared phenotype can guide a search without independently proving molecular contact.
Developmental components were separated experimentally
The 1999 work documented inadequate gubernacular development and abnormal testicular position in Insl3-deleted mice. Comparison with animals also deficient in the androgen receptor helped separate processes in ligament development. These findings concern a genetic model, not brief peptide exposure.
Deleting a gene is not the same as adding a hormone
A genetic experiment examines absence of a signal during development, whereas a culture examines responses under controlled conditions. Both inform INSL3 research but answer different questions. Loss of the ligand must also remain distinct from loss of its receptor: anatomical similarity was the starting point, not an identity between interventions.
Questions and answers
Is INSL3 an insulin variant?
No. It is a distinct hormone with its own receptor system within a related molecular family.
Does the genetic model show what adding INSL3 would do?
No. Absence during development and an experimental exposure are different interventions.
Sources
- INSL3/Leydig insulin-like peptide activates the LGR8 receptor important in testis descent. — J Biol Chem, 2002
- INSL3/Leydig insulin-like peptide activates the LGR8 receptor important in testis descent.
- Targeted disruption of the Insl3 gene causes bilateral cryptorchidism. — Mol Endocrinol, 1999
- Targeted disruption of the Insl3 gene causes bilateral cryptorchidism.