INsL3
- Known as:
- INsL3
- Catalog number:
- PA1044
- Product Quantity:
- 100μg
- Category:
- -
- Supplier:
- SDlabs
- Gene target:
- INsL3
Related genes to: INsL3
- Gene:
- INSL3 NIH gene
- Name:
- insulin like 3
- Previous symbol:
- RLNL
- Synonyms:
- RLF, MGC119818, MGC119819
- Chromosome:
- 19p13.11
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-02
- Date modifiied:
- 2018-03-22
Related products to: INsL3
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- We investigated circulating insulin-like peptide 3 (INSL3) in boys with constitutional delay of growth and puberty treated with exogenous testosterone (T) or oral letrozole (Lz). Twenty-eight boys were randomized to Lz (2.5 mg/day; = 15) or intramuscular T (1 mg/kg every 4 weeks; = 13) for 6 months and followed up to 12 months. Blood samples were collected at baseline and at 3, 6, and 12 months to measure INSL3 and other pubertal hormones (ClinicalTrials.gov NCT01797718). At baseline, INSL3 levels were similar between groups (T: 1.4 ng/mL [0.8], Lz: 1.9 ng/mL [1.8], = .39). T suppressed luteinising hormone (LH), follicle-stimulating hormone (FSH), and INSL3 between 0 and 3 months ( < .01), and changes in INSL3 correlated with changes in LH ( = 0.61, < .001) and FSH ( = 0.67, < .001). Between 3 and 6 months, INSL3 and gonadotropins rose in the T group, while both increased from 0 to 6 months with Lz ( < .001). At 12 months, INSL3 levels did not differ between groups. Exogenous testosterone thus transiently suppresses INSL3 via gonadotropin inhibition in early puberty. - Source: PubMed
Publication date: 2026/05/30
Raivio TaneliTanner MilaVaaralahti KirsiHero MattiMiettinen Päivi JVarimo Tero - Cryptorchidism is one of the most frequently diagnosed developmental disorders of the male canine reproductive system, defined as the failure of one or both testes to descend into the scrotum. Physiologically, testicular descent is typically completed by six to eight weeks of age, although some authors extend this period to sixteen weeks. Failure of testicular descent beyond this timeframe is considered pathological. The condition has multiple causes and affects between 1% and 10% of the canine population. Genetics is the most significant factor, indicating the hereditary basis of cryptorchidism. In addition, increasing attention has been directed toward the potential impact of environmental and epigenetic factors on the incidence of cryptorchidism, suggesting that the condition may result from complex interactions between genetic predisposition and external influences. The effect of hormones (such as INSL3 and testosterone), mechanical factors (including narrowing of the inguinal canal, abnormalities of the gubernaculum, and shortening of the spermatic cord), and environmental factors (for example, exposure to external estrogens and maternal stress during pregnancy) all contribute to the development of this disorder. Recent results have emphasized the role of the orexin system, particularly the OX2R receptor, in regulating endocrine and reproductive functions in cryptorchid testes. Computed tomography is increasingly utilized in complex cases due to its high precision in localizing retained testes. Clinically, cryptorchidism may present unilaterally or bilaterally. Unilateral cryptorchidism may preserve partial fertility, whereas bilateral cryptorchidism results in complete infertility. Undescended testes may be located in the abdominal cavity or inguinal canal. Major complications include an increased risk of testicular cancer (Sertoli cell tumors and seminomas) and endocrine disorders leading to feminization. Diagnosis is based on clinical examination and imaging modalities such as ultrasound. Orchiectomy, involving the removal of both the retained and normally descended testicles, is thought to be the gold standard for treatment. This method helps avoid complications and the transmission of the defect to offspring. According to Fédération Cynologique Internationale (FCI) standards, affected individuals should not be used for breeding or shows. Early detection, surgical intervention, and consistent exclusion from breeding programs are the primary strategies for reducing the incidence of this disorder in the canine population. - Source: PubMed
Publication date: 2026/05/15
Agata RafalskaAnna Domosławska - Cadmium (Cd) is a well-documented environmental pollutant associated with male reproductive disorders, necessitating the urgent development of effective therapeutic agents. Nano-selenium (Nano-Se) represents an advanced selenium supplement with robust antioxidant properties, which can mitigate various forms of heavy metal toxicity. However, the role of Nano-Se in alleviating Cd-induced testis damage remains unclear. Family with sequence similarity 134 member B (FAM134B) is the first identified Endoplasmic reticulophagy (ER-phagy) receptor, and the ER-phagy it mediates plays a crucial role in the reproductive system. In this study, Hy-line White roosters were randomly divided into four groups and subjected to a 90-day observation period. Serum samples and testicular tissue samples from roosters were collected for subsequent detection. Hematoxylin-eosin (H&E) staining, periodic acid-Schiff (PAS) staining, ELISA kit detection, Western blotting (WB), immunofluorescence (IF), cellular thermal shift assay (CETSA) and molecular docking techniques were employed to explore the effects of Cd on the reproductive system and the alleviating effect of Nano-Se. In vivo assays revealed that Nano-Se efficiently mitigated testicular atrophy and histological damage triggered by Cd exposure. Nano-Se reversed the Cd-mediated inhibition of steroidogenesis-related proteins, and elevated the expression of Leydig cell markers including 3β-HSD and INSL3, thereby ameliorating Cd-evoked Leydig cell dysfunction. Consistent with in vivo outcomes, in vitro tests using primary rooster Leydig cells demonstrated that Nano-Se notably restrained Cd-activated ER-phagy and excessive lysosomal acidification. Mechanistically, such protective effects were achieved by blocking TFEB nuclear translocation and preventing the downregulation of FAM134B. This present study provides a foundation for preclinical research for its usefulness as a potential therapeutic for reproductive toxicity induced by environmental heavy metal pollutants. - Source: PubMed
Publication date: 2026/05/08
Liang Yun-ShuangDu Jia-YingCai Wen-NaGuo KaiMeng Wei-JingLi Jin-LongLi Xue-Nan - [This retracts the article DOI: 10.1155/2019/1041760.]. - Source: PubMed
Publication date: 2026/04/28
Endocrinology International Journal Of - The RXFP2 gene is a key regulator of horn morphology in sheep (Ovis aries Linnaeus), with a 1.78-kb insertion in its 3'-untranslated region (UTR) previously linked to the polled phenotype. However, horned individuals homozygous for this insertion (1.78 kb/) have been observed in typically polled breeds such as Hu sheep, suggesting additional regulatory mechanisms. In this study, a significant horn-associated quantitative trait locus (QTL) on chromosome 10 was identified through genome-wide association analysis which was consistent with a previous study. We found that the 1.78-kb insertion in the 3'-UTR of RXFP2 is associated with horn status across sheep breeds, and that elevated RXFP2 expression correlates with horn development even in 1.78 kb/ individuals, as revealed by expression analyses in multiple breeds. RNA-seq and hormonal profiling further demonstrated that the INSL3/RXFP2 signaling axis, particularly its interactions with hormones such as testosterone, plays a central role in horn morphogenesis. These results indicate that horn development is modulated not only by structural variations in RXFP2, but also through its transcriptional and hormonal regulation, providing new insights into the polygenic basis of horn formation and informing breeding strategies for polled sheep. - Source: PubMed
Wang HaitaoLi TingtingChen JieranWang LiminLi XiaZhang YutingZhang NaZhang ZhichaoMa RunlinWang DaxiangHuang XunLiu Qiuyue