Nesfatin-1 as a New Potent Regulator in Reproductive System

Abstract

Nesfatin-1 is a recently discovered anorexigenic peptide which is distributed in several brain areas implicated in the feeding and metabolic regulation. Recently, it has been reported that nesfatin-1 is expressed not only in brain, but also in peripheral organs such as digestive organs, adipose tissues, heart, and reproductive organs. Nesfatin-1 is markedly expressed in the pancreas, stomach and duodenum. Eventually, the nesfatin-1 expression in the digestive organs may be regulated by nutritional status, which suggests a regulatory role of peripheral nesfatin-1 in energy homeostasis. Nesfatin-1 is also detected in the adipose tissues of humans and rodents, indicating that nesfatin-1 expression in the fat may regulate food intake independently, rather than relying on leptin. In addition, nesfatin-1 is expressed in the heart as a cardiac peptide. It suggests that nesfatin-1 may regulate cardiac function and encourage clinical potential in the presence of nutrition-dependent physio-pathologic cardiovascular diseases. Currently, only a few studies demonstrate that nesfatin-1 is expressed in the reproductive system. However, it is not clear yet what function of nesfatin-1 is in the reproductive organs. Here, we summarize the expression of nesfatin-1 and its roles in brain and peripheral organs and discuss the possible roles of nesfatin-1 expressed in reproductive organs, including testis, epididymis, ovary, and uterus. We come to the conclusion that nesfatin-1 as a local regulator in male and female reproductive organs may regulate the steroidogenesis in the testis and ovary and the physiological activity in epididymis and uterus.

Nucleobindin 2 (NUCB2) in human endometrial carcinoma: a potent prognostic factor associated with cell proliferation and migration

“…Previously, we identified NUCB2 as an estrogen responsive gene in breast carcinoma cells. Moreover, Kim and Yang have pointed out the possibility that NUCB2 expression in mouse uterus is under the control of estrogens [26], and recently Chung et al reported that NUCB2 expression in mouse pituitary gland was under the control of estrogen and progesterone [36]. However, in the present study, significant correlation was not detected between NUCB2 and ER or PR status.…”

“…We first showed that NUCB2 immunoreactivity was detected in 22% of endometrial carcinomas examined, and was increased compared to non-neoplastic endometrial glands. It has been reported that NUCB2 protein and its binding sites are expressed in mouse uterus, and play pivotal roles in the collapse and recovery of endometrium [26]. Honda et al also found out that NUCB2 expression was differentially detected in endometriosis by Serial Analysis of Gene Expression (SAGE) methods [27].…”

Th 17 Cells and Nesfatin-1 are associated with Spontaneous Abortion in the CBA/j × DBA/2 Mouse Model

“…Moreover, it has been reported that the number of decidual IL-17+ cells was positively correlated with the number of neutrophils in spontaneous abortion cases ( Nakashima et al, 2010a ). Given these results, the finding that nesfatin-1 binding sites were localized on the neutrophils suggests that the uterine function may be regulated by nesfatin-1 to attract neutrophils from the blood into the endometrium ( Kim & Yang, 2012 ).…”

“…Our previous studies have also demonstrated that the nesfatin-1 protein was localized on the epithelial cells of the endometrium and uterine glands. Nesfatin-1 binding sites were detected in the epithelial cells of the uterine gland and the neutrophils in the endometrium ( Kim & Yang, 2012 ). Neutrophils are known to play an important role in the collapse and recovery of the endometrium ( Kaitu'u-Lino et al, 2007 ).…”

Contingent role of phoenixin and nesfatin‐1 on secretions of the male reproductive hormones

“…Multiple previous reports have revealed that nesfatin‐1 could play a remarkable role in HPGA regulation. Kim and Yang () have reported that GnRH treatment enhanced NUCB2/nesfatin‐1 expression rate in testis and epididymis of male mice. Nesfatin‐1 provoked a rise in LH levels in both sexes in rats, when injected ICV (Garcia‐Galiano et al, , ).…”