A Lancet Commission on 70 years of women's reproductive, maternal, newborn, child, and adolescent health in China.

The functions of Sertoli cells in spermatogenesis have attracted much more attention recently. Normal spermatogenesis depends on Sertoli cells, mainly due to their influence on nutrient supply, maintenance of cell junctions, and support for germ cells’ mitosis and meiosis. Accumulating evidence in the past decade has highlighted the dominant functions of the MAPK, AMPK, and TGF-β/Smad signaling pathways during spermatogenesis. Among these pathways, the MAPK signaling pathway regulates dynamics of tight junctions and adherens junctions, proliferation and meiosis of germ cells, proliferation and lactate production of Sertoli cells; the AMPK and the TGF-β/Smad signaling pathways both affect dynamics of tight junctions and adherens junctions, as well as the proliferation of Sertoli cells. The AMPK signaling pathway also regulates lactate supply. These signaling pathways combine to form a complex regulatory network for spermatogenesis. In testicular tumors or infertile patients, the activities of these signaling pathways in Sertoli cells are abnormal. Clarifying the mechanisms of signaling pathways in Sertoli cells on spermatogenesis provides new insights into the physiological functions of Sertoli cells in male reproduction, and also serves as a pre-requisite to identify potential therapeutic targets in abnormal spermatogenesis including testicular tumor and male infertility.

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Multiple signaling pathways in Sertoli cells: recent findings in spermatogenesis

Myo-inositol (MI) and D-chiro-inositol (DCI) are insulin second messengers, and MI is involved in follicular gonadotropin pathways which orchestrate ovulation. The tissue-specific MI/DCI ratio is modulated by insulin through aromatase and is altered in insulin resistance (IR), with reduced epimerization of MI to DCI in insulin-sensitive tissues. In ovaries, the MI/DCI ratio is 100:1, but is dramatically reduced by insulin-stimulated epimerase in hyperinsulinemic women with polycystic ovary syndrome (PCOS). Inositols have proved to be effective in PCOS, improving metabolic and hormonal state, and restoring spontaneous ovulation. In assisted reproductive technology, inositol improved ovarian stimulation parameters, although data concerning fertility outcomes are conflicting. Given their functions, inositols are an attractive treatment option for PCOS, although well-designed studies on spontaneous and non-spontaneous fertility are needed.

Inositol in Polycystic Ovary Syndrome: Restoring Fertility through a Pathophysiology-Based Approach

Infertility is defined as the inability of couples to have a baby after one year of regular unprotected intercourse, affecting 10 to 15% of couples. According to the latest WHO statistics, approximately 50-80 million people worldwide sufer from infertility, and male factors are responsible for approximately 20-30% of all infertility cases. The diagnosis of infertility in men is mainly based on semen analysis. The main parameters of semen include: concentration, appearance and motility of sperm. Causes of infertility in men include a variety of things including hormonal disorders, physical problems, lifestyle problems, psychological issues, sex problems, chromosomal abnormalities and single-gene defects. Despite numerous efforts by researchers to identify the underlying causes of male infertility, about 70% of cases remain unknown. These statistics show a lack of understanding of the mechanisms involved in male infertility. This article focuses on the histology of testicular tissue samples, the male reproductive structure, factors affecting male infertility, strategies available to find genes involved in infertility, existing therapeutic methods for male infertility, and sperm recovery in infertile men.

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Some of the Factors Involved in Male Infertility: A Prospective Review

Besides aging, a number of non-modifiable lifestyle-related factors, such as smoking, elevated consumption of caffeine and alcohol, stress, agonist sports, chronic exposure to environmental pollutants, and other nutritional habits exert a negative impact on a women's fertility. In particular, metabolic disorders including diabetes, obesity, and hyperlipidemia commonly associated to hypercaloric diets are suspected to affect a woman's fertility either by direct damage to oocyte health and differentiation, or by indirect interference with the pituitary-hypothalamic axis, resulting in dysfunctional oogenesis. Obese women show decreased insulin sensitivity determining persistent hyperinsulinemia, which may be involved in the pathogenesis of Polycystic Ovary Syndrome. Thus, the reduced insulin secretion induced by dietary adjustments is an attractive non-pharmacological treatment to prevent infertility, and a Mediterranean diet aimed at maintaining normal body mass may be effective in the preservation of ovarian health and physiology. Furthermore, in relation to the oxidative stress as a co-factor of defective oocyte maturation, an appropriate intake of proteins, antioxidants and methyl-donor supplements (1-Carbon Cycle) may decrease the bioavailability of toxic oxidants resulting in the protection of oocyte maturation.

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Mélodie Vander Borght

Papers

Fertility and infertility: Definition and epidemiology.