Detection of insulin-like growth factor receptor-1 in the human cremaster muscle and its role in the etiology of the undescended testis

Asian J Surg. 2019 Jan;42(1):290-296. doi: 10.1016/j.asjsur.2018.02.005. Epub 2018 Mar 31.

Abstract

Purpose: Previous studies of undescended testis (UT) has focused on insulin-like hormone 3 (INSL3), the genitofemoral nerve, and androgens in the testicular descent. Leydig cells, which are under the control of insulin-like growth factor-1 (IGF1), produce both androgens and INSL3. We aimed to investigate whether insulin-like growth factor receptor-1(IGFR1) exists in the cremaster muscle (CM) complex and is associated with normally descended testis as well as UT cases in humans.

Methods: We studied 30 CM from 15 patients who comprised the UT group (UTG), and 15 patients with unilateral testicular torsion (Control group; CG). Muscles, nerves, and vessels within the CM specimen were examined to determine the presence of IGFR1.

Results: The mean staining score (MSS) of IGFR1 in CM and its nerves were higher in the CG than in the UTG. These results were statistically significant (p = 0.01 and p = 0.02). Although the MSS of IGF1R was higher in the vessels of CM in the CG than the UTG, this was not statistically significant (p = 0.48).

Conclusions: IGFR1 with heterotetrameric receptor via IGF1, IGF2, insulin, and probably androgen, contribute to the remodeling and development of CM as well as the testis descent. In the current study, the presence of the IGFR1 in the CM was shown. Additionally, the IGFR1 density of the CM was lower in the UT cases than in the CG cases. Further evaluation of IGFR1 and other etiological factors can elucidate how they interact.

Keywords: Cremaster muscle; Insulin-like-growth factor receptor I; Undescended testis.

MeSH terms

  • Abdominal Muscles / metabolism*
  • Cryptorchidism / etiology*
  • Cryptorchidism / genetics
  • Gene Expression
  • Gene Expression Regulation, Developmental
  • Humans
  • Male
  • Receptor, IGF Type 1 / genetics
  • Receptor, IGF Type 1 / metabolism*
  • Receptor, IGF Type 1 / physiology*

Substances

  • Receptor, IGF Type 1