Effect of autologous platelet rich plasma on anti-mullerian hormone and antral follicle count in sub fertile women with poor ovarian reserve

Background: Ovarian aging may be reversible. Platelet rich plasma (PRP) has growth factors that promote cellular proliferation and folliculogenesis. Recently published studies and case reports suggest that ovarian rejuvenation can be done by PRP treatment. The objective of the study was to evaluate the effect of platelet rich plasma on ovarian reserve markers such as anti mullerian hormone (AMH) and antral follicle count (AFC) in sub fertile women with poor ovarian reserve (POR).Methods: The self-controlled quasi experimental study was carried out on 29 sub fertile women with poor ovarian reserve. They were selected for laparoscopic tubo-peritoneal evaluation as they could not afford in vitro fertilization. During laparoscopy, 5 ml of pre prepared autologous PRP was injected into each ovary. Post-PRP AMH and AFC were measured at every cycle for a period of at least three (3) months and compared with base line values.Results: Mean age of participants was 35.9±3.2 years. Baseline AMH was 0.31±0.17 ng/ml and baseline AFC was 3.41±0.73. AMH was raised on first, second and third cycle from base line values in 58.62%, 86.21% and 91.30% of the study population respectively. AMH changes in all three cycle were statistically significant. Pregnancy occurred in three (10.34%) women during the study period.Conclusions: The injection of autologous PRP into human ovaries is a safe procedure to improve ovarian reserve markers (AMH and AFC) in women with POR.

Age-associated changes in cumulus cells and follicular fluid: The local oocyte microenvironment as a determinant of gamete quality

The ovary is the first organ to age in humans with functional decline evident already in women in their early thirties. Reproductive aging is characterized by a decrease in oocyte quantity and quality which is associated with an increase in infertility, spontaneous abortions, and birth defects. Reproductive aging also has implications for overall health due to decreased endocrinological output. Understanding the mechanisms underlying reproductive aging has significant societal implications as women globally are delaying childbearing and medical interventions have greatly increased the interval between menopause and total lifespan. Age-related changes inherent to the female gamete are well-characterized and include defects in chromosome and mitochondria structure, function, and regulation. More recently, it has been appreciated that the extra-follicular ovarian environment may have important direct or indirect impacts on the developing gamete, and age-dependent changes include increased fibrosis, inflammation, stiffness, and oxidative damage. The cumulus cells and follicular fluid which directly surround the oocyte during its final growth phase within the antral follicle represent additional critical local microenvironments. Here we systematically review the literature and evaluate the studies that investigated the age-related changes in cumulus cells and follicular fluid. Our findings demonstrate unique genetic, epigenetic, transcriptomic, and proteomic changes with associated metabolomic alterations, redox status imbalance, and increased apoptosis in the local oocyte microenvironment. We propose a model of how these changes interact, which may explain the rapid decline in gamete quality with age. We also review the limitations of published studies and highlight future research frontiers.

Endocrine Disruption of the Follicle-Stimulating Hormone Receptor Signaling During the Human Antral Follicle Growth

An increasing number of pollutants with endocrine disrupting potential are accumulating in the environment, increasing the exposure risk for humans. Several of them are known or suspected to interfere with endocrine signals, impairing reproductive functions. Follicle-stimulating hormone (FSH) is a glycoprotein playing an essential role in supporting antral follicle maturation and may be a target of disrupting chemicals (EDs) likely impacting female fertility. EDs may interfere with FSH-mediated signals at different levels, since they may modulate the mRNA or protein levels of both the hormone and its receptor (FSHR), perturb the functioning of partner membrane molecules, modify intracellular signal transduction pathways and gene expression. In vitro studies and animal models provided results helpful to understand ED modes of action and suggest that they could effectively play a role as molecules interfering with the female reproductive system. However, most of these data are potentially subjected to experimental limitations and need to be confirmed by long-term observations in human.

Profile of Bile Acid Metabolomics in the Follicular Fluid of PCOS Patients

Polycystic ovary syndrome (PCOS) is a complex heterogeneous endocrine disease affected by genetic and environmental factors. In this manuscript, we aimed to describe the composition of bile acid metabolomics in the follicular fluid (FF) of PCOS. The FF was collected from 31 control patients and 35 PCOS patients diagnosed according to the Rotterdam diagnostic criteria. The Bile Acid Assay Kit and ultra-performance liquid chromatography/tandem mass spectrometry (UPLC-MS/MS) were used in this study to detect the total bile acid and 24 bile acid metabolites. Glycocholic acid (GC3A), taurocholic acid (TCA), glycochenodeoxycholic acid (GCDCA), and chenodeoxycholic acid-3-β-D-glucuronide (CDCA-3Gln) were elevated in the PCOS group. GCDCA was positively correlated with the serum follicle-stimulating hormone (FSH) (r = 0.3787, p = 0.0017) and luteinizing hormone (LH) (r = 0.2670, p = 0.0302). The level of CDCA-3Gln also rose with the increase in antral follicle counts (AFC) (r = 0.3247, p = 0.0078). Compared with the control group, the primary bile acids (p = 0.0207) and conjugated bile acids (p = 0.0283) were elevated in PCOS. For the first time, our study described the changes in bile acid metabolomics in the FF of PCOS patients, suggesting that bile acids may play an important role in the pathogenesis of PCOS.