NCBI Summary:
The protein encoded by this gene contains a classical signature of the insulin superfamily and is highly similar to relaxin 3 (RLN3/INSL7). [provided by RefSeq, Jul 2008]
General function
Ligand, Hormone
Comment
Cellular localization
Secreted
Comment
Circulating insulin-like peptide 5 levels and its association with metabolic and hormonal parameters in women with polycystic ovary syndrome. Bicer M et al. (2018) Insulin-like peptide 5 (INSL5) is a gut peptide hormone that is a member of relaxin/insulin superfamily. Growing evidence implicates the crucial role of the peptide in some metabolisms including food intake, glucose homeostasis and reproductive system. Polycystic ovary syndrome (PCOS) is involved in both reproductive and metabolic issues. The aim of the study was determination of circulating levels of INSL5 alteration in women with PCOS and evaluation of the relationship between INSL5 and hormonal-metabolic parameters as well as carotid intima media thickness (cIMT). A total of 164 subjects were recruited in this cross-sectional study (82 women with PCOS and 82 age- and BMI-matched controls). Circulating INSL5 levels were assessed via ELISA method. High-resolution B-mode ultrasound was used to measure cIMT. The hormonal and metabolic parameters of the recruited subjects were determined. Circulating INSL5 levels were significantly elevated in women with PCOS compared to controls (27.63 ± 7.74 vs. 19.90 ± 5.85 ng/ml, P < 0.001). The mean values of INSL5 were significantly higher in overweight subjects compared to lean weight subjects in both groups. The women with PCOS having insulin resistance have increased INSL5 compared to those of PCOS subjects without insulin resistance. INSL5 is associated with insulin resistance, BMI, luteinizing hormone and free androgen index. Multivariate logistic regression analyses revealed that the odds ratio for having PCOS in the highest tertile of INSL5 was higher than in the lowest tertile. PCOS subjects exhibited an elevation in circulating INSL5 levels along with a link between INSL5 level induction and metabolic-hormonal parameters.//////////////////
Ovarian function
Comment
Expression regulated by
Comment
Ovarian localization
Comment
Hsu SY. 1999 reported the cloning of two novel mammalian paralogs of
relaxin/insulin family proteins and their expression in testis
and kidney. Izhar
Based on sequence homology to insulin and relaxin, the author isolated two
novel genes of the insulin superfamily from mouse tissues. Because these
proteins show a high similarity to relaxin and relaxin-like factor (RLF or Ley
I-L), they were named as RIF1 (relaxin/insulin-like factor 1) and RIF2
(relaxin/insulin-like factor 2). After RT-PCR, full-length cDNAs of RIF1 and
RIF2 were obtained from mouse testis and ovary, respectively. In addition, a
putative human ortholog of RIF1 was isolated from human testis. The
deduced coding regions of mRIF1, mRIF2, and hRIF1 were 191, 145, and
213 amino acids, respectively, and all three proteins contain a typical signal
sequence for secretion at their amino terminus. Sequence comparison
indicated that RIFs encode proteins consisting of B and A subunits connected
by a long C domain peptide, and the deduced mature proteins of these
putative ligands are most closely related to relaxin, RLF, and insulin from
different species.
Follicle stages
Comment
Phenotypes
PCO (polycystic ovarian syndrome)
Mutations
1 mutations
Species: mouse
Mutation name: None
type: null mutation fertility: subfertile Comment: INSL5-Deficient Mice Display an Alteration in Glucose Homeostasis and an Impaired Fertility. Burnicka-Turek O et al. Insulin-like factor 5 (INSL5), a member of the insulin superfamily, is expressed in the colorectum and hypothalamus. To facilitate studies into the role of INSL5, we generated Insl5(-/-) mice by gene targeting. Insl5(-/-) mice were born in the expected Mendelian ratio, reached normal body weight, but displayed impaired male and female fertility that are due to marked reduction in sperm motility and irregular length of the estrous cycle. Furthermore, Insl5(-/-) mice showed impairment in glucose homeostasis with characteristic elevation of serum glucose levels at an advanced age. Glucose and insulin tolerance tests revealed that the increased blood glucose in Insl5(-/-) mice was due to glucose intolerance resulting from reduced insulin secretion. Morphometric and immunohistological analyses revealed that the Insl5(-/-) mice had markedly reduced average islets area and -cell numbers. Furthermore, immunohistochemistry showed the expression of INSL5 in enteroendocrine cells in the colorectal epithelium and the presence of its putative receptor relaxin family peptide receptor 4 in pancreatic islet cells. These results suggest the potential role of INSL5 signaling in the regulation of insulin secretion and -cell homeostasis.