Caloric restriction in female reproduction: is it beneficial or detrimental?

Sun, Jiayi; Shen, Xin; Liu, Hui; Lu, Sen; Peng, Jing; Kuang, Haibin

doi:10.1186/s12958-020-00681-1

Cited by 34 publications

(12 citation statements)

References 97 publications

(97 reference statements)

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“…GDNF is the paracrine factor responsible for the maintenance and self-renewal of SSCs, and the differentiation of spermatogonia is inhibited by activating the zinc finger BTB domain containing 16 ( ZBTB16 ) and Lin-28 homolog B ( LIN28B ) [ 215 , 216 , 217 ]. In particular, FSH connects with the FSHR in the membrane of Sertoli cells that secrete GDNF, which, in turn, acts via RET tyrosine kinase, which requires a ligand-specific co-receptor GDNF family receptor alpha 1 (GFRα1), localized in the membrane of undifferentiated spermatogonia to promote self-renewal [ 216 , 217 , 218 , 219 , 220 ].…”

Section: Influence Of Fsh On Germ Cellsmentioning

confidence: 99%

Actions and Roles of FSH in Germinative Cells

Recchia

Jorge

Pessôa

et al. 2021

IJMS

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Follicle stimulating hormone (FSH) is produced by the pituitary gland in a coordinated hypothalamic–pituitary–gonadal (HPG) axis event, plays important roles in reproduction and germ cell development during different phases of reproductive development (fetal, neonatal, puberty, and adult life), and is consequently essential for fertility. FSH is a heterodimeric glycoprotein hormone of two dissociable subunits, α and β. The FSH β-subunit (FSHβ) function starts upon coupling to its specific receptor: follicle-stimulating hormone receptor (FSHR). FSHRs are localized mainly on the surface of target cells on the testis and ovary (granulosa and Sertoli cells) and have recently been found in testicular stem cells and extra-gonadal tissue. Several reproduction disorders are associated with absent or low FSH secretion, with mutation of the FSH β-subunit or the FSH receptor, and/or its signaling pathways. However, the influence of FSH on germ cells is still poorly understood; some studies have suggested that this hormone also plays a determinant role in the self-renewal of germinative cells and acts to increase undifferentiated spermatogonia proliferation. In addition, in vitro, together with other factors, it assists the process of differentiation of primordial germ cells (PGCLCs) into gametes (oocyte-like and SSCLCs). In this review, we describe relevant research on the influence of FSH on spermatogenesis and folliculogenesis, mainly in the germ cell of humans and other species. The possible roles of FSH in germ cell generation in vitro are also presented.

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Section: Influence Of Fsh On Germ Cellsmentioning

confidence: 99%

Actions and Roles of FSH in Germinative Cells

Recchia

Jorge

Pessôa

et al. 2021

IJMS

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“…At this time, we tentatively concluded that there is no strong correlation between body/ovarian weights and VO when maternal hypothyroidism model is employed. To confirm this idea, one should carefully compare the available data from several precocious and/ or delayed puberty of rat models ( Lee et al, 2009 ; Sun et al., 2021 ).…”

Section: Discussionmentioning

confidence: 99%

Effects of Maternal Hypothyroidism on the Pubertal Development in Female Rat Offspring

Park¹,

Lee²

2021

Dev. Reprod.

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The present study was performed to investigate the effect of maternal hypothyroidism and puberty onset in female rat pups. To do this, we employed propylthiouracil (PTU) to prepare a hypothyroid rat model. Pregnant rats were treated with PTU (0.025%) in drinking water from gestational day 14 to postnatal day 21 of offspring. Comparison of general indices such as body and tissue weights and puberty indices such as vaginal opening (VO) and tissue histology between control and PTU-treated rats were conducted. There was no significant difference in the date of VO between control and PTU group. The body weights of the PTU group were significantly lower, only 36.8% of the control group (p<0.001). Although the absolute thyroid weight was not changed by PTU treatment, the relative weight increased significantly about 2.8 times (p<0.001), indicating that hypothyroidism was successfully induced. On the other hand, the absolute weights of the ovary and uterus were markedly decreased by PTU administration (p<0.001), and the relative weight was not significantly changed. The ovarian histology of PTU group revealed the advanced state of differentiation (i.e., presence of corpora lutea). Inversely, the uterine histology of PTU group showed underdeveloped structures compared those in control group. Taken together, the present study demonstrates that our maternal hypothyroidism model resulted in minimal effect on pubertal development symbolized by VO despite of huge retardation in somatic growth. More sophisticatedly designed hypothyroidism model will be helpful to achieve a better understanding of pubertal development and related disorders.

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“…H&E staining and immunofluorescence assay were performed as previously described [ 24 , 25 ]. Histopathological assessment of spermatogenesis was performed by H&E staining.…”

Section: Methodsmentioning

confidence: 99%

Novel variants in helicase for meiosis 1 lead to male infertility due to non-obstructive azoospermia

Tang

Gao

et al. 2021

Reprod Biol Endocrinol

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Background Non-obstructive azoospermia (NOA) is the most severe form of male infertility; more than half of the NOA patients are idiopathic. Although many NOA risk genes have been detected, the genetic factors for NOA in majority of the patients are unknown. In addition, it is difficult to retrieve sperm from these patients despite using the microsurgical testicular sperm extraction (microTESE) method. Therefore, we conducted this genetic study to identify the potential genetic factors responsible for NOA and investigate the sperm retrieval rate of microTESE for genetically deficient NOA patients. Methods Semen analyses, sex hormone testing, and testicular biopsy were performed to categorize the patients with NOA. The chromosome karyotypes and Y chromosome microdeletion analyses were used to exclude general genetic factors. Whole exome sequencing and Sanger sequencing were performed to identify potential genetic variants in 51 patients with NOA. Hematoxylin and eosin staining (H&E) and anti-phosphorylated H2AX were used to assess the histopathology of spermatogenesis. Quantitative real time-polymerase chain reaction, western blotting, and immunofluorescence were performed to verify the effects of gene variation on expression. Results We performed whole exome sequencing in 51 NOA patients and identified homozygous helicase for meiosis 1(HFM1) variants (NM_001017975: c.3490C > T: p.Q1164X; c.3470G > A: p.C1157Y) in two patients (3.9%, 2/51). Histopathology of the testis showed that spermatogenesis was completely blocked at metaphase in these two patients carrying the HFM1 homozygous variants. In comparison with unaffected controls, we found a significant reduction in the levels of HFM1 mRNA and protein expression in the testicular tissues from these two patients. The patients were also subjected to microTESE treatment, but the sperms could not be retrieved. Conclusions This study identified novel homozygous variants of HFM1 that are responsible for spermatogenic failure and NOA, and microTESE did not aid in retrieving sperms from these patients.

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Caloric restriction in female reproduction: is it beneficial or detrimental?

Cited by 34 publications

References 97 publications

Actions and Roles of FSH in Germinative Cells

Actions and Roles of FSH in Germinative Cells

Effects of Maternal Hypothyroidism on the Pubertal Development in Female Rat Offspring

Novel variants in helicase for meiosis 1 lead to male infertility due to non-obstructive azoospermia

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