Fenugreek (Methika)
Dilip Ghosh, Prasad Thakurdesai in Fenugreek, 2022
An open-label, one-arm, non-randomized, post-marketing surveillance study in 50 premenopausal women (18–45 years, BMI < 42) diagnosed with PCOS using a novel Trigonella foenum-graecum seed extract (fenugreek seed extract, Furocyst, 2 capsules of 500 mg/day) enriched in approximately 40% furostanolicsaponins, over a period of 90 consecutive days was done. Approximately 46% of study population showed reduction in cyst size, while 36% of subjects showed complete dissolution of cyst. Further 71% of subjects reported the return of a regular menstrual cycle on completion of the treatment and 12% of subjects subsequently became pregnant. Overall, 94% of patients benefitted from the regimen. Significant increases in luteinizing hormone (LH) and follicular stimulating hormone (FSH) levels were observed compared to the baseline values. Extensive blood chemistry, haematological and biochemical assays demonstrated the broad-spectrum safety. Furocyst caused significant decrease in both ovarian volume and the number of ovarian cysts. Serum ALT, BUN, and CK were assessed to demonstrate the broad-spectrum safety of Furocyst. No significant adverse effects were observed. In summary, Furocyst was efficacious in ameliorating the symptoms of PCOS.30
Anatomy and physiology
Suzanne Everett in Handbook of Contraception and Sexual Health, 2020
There are four main hormones which are the principal regulators of the female reproductive system. Follicle-stimulating hormone (FSH) stimulates follicle development and oestrogen production.Luteinizing hormone (LH) stimulates the release of the ovum.Oestrogen prepares the body and uterus for ovulation and pregnancy. Responsible for growth of body, sex organs, secondary sex characteristics, prepares the endometrium for pregnancy, makes cervical mucus thinner and more alkaline.Progesterone prepares the body for pregnancy by maintaining the endometrium when pregnancy occurs. It stimulates the development of lobules and alveoli in the mammary glands. Premenstrual water retention is attributed to progesterone, and it causes a slight rise in basal body temperature during luteal phase following ovulation.
Azoospermia
Botros Rizk, Ashok Agarwal, Edmund S. Sabanegh in Male Infertility in Reproductive Medicine, 2019
The hypothalamic-pituitary-gonadal (HPG) axis controls spermatogenesis, which requires the presence of normal level of follicle-stimulating hormone (FSH) and testosterone in high concentrations in the testicles. Normal hormonal profiles are detected in men with pure OA, and many men (about 25%–35%) with NOA have high FSH levels caused by the lack of feedback inhibition from the dysfunctional seminiferous tubules. It must be emphasized that FSH level has only a moderate diagnostic value as an independent predictor for sperm retrieval in patients with NOA. Luteinizing hormone (LH) levels are usually elevated or within normal upper limits in these men. Hypogonadism, as indicated by low testosterone levels, is seen in approximately half the patients with NOA and generally reflects Leydig cell insufficiency, so the term “hypogonadotropic hypogonadism” can be given to such patients [18].
What must be considered when prescribing hormonal pharmacotherapy for male infertility?
Published in Expert Opinion on Pharmacotherapy, 2022
Olivia Holtermann Entwistle, Aditi Sharma, Channa N. Jayasena
Exogenous gonadotropin administration to men with hypogonadotropic hypogonadism (HH) is highly effective for restoring spermatogenesis. The rationale for providing hormonal stimulation for patients with NOA secondary to testicular failure has been extrapolated from this. Spermatogenesis occurs in the seminiferous tubules of the testes and is dependent on the HPT axis (Figure 1). In the testes, follicle stimulating hormone (FSH) stimulates Sertoli cells, which supports germ cell development, and luteinizing hormone (LH) stimulates Leydig cells to produce testosterone. Intra-testicular testosterone (ITT) is essential for spermatogenesis to progress beyond meiosis, although the exact molecular mechanisms by which testosterone supports spermatogenesis are still incompletely understood [8]. In hypogonadal men with NOA, hormonal stimulation is proposed as a means of increasing ITT levels in order to stimulate spermatogenesis and increase the chances of successful TESE [9]. However, the majority of men with primary testicular failure will be hypergonadotropic [1]. It has been suggested that Sertoli cells may undergo desensitization as a result of persistently high FSH levels and therefore that further exogenous hormonal stimulation may overcome this desensitization, although the evidence for this remains equivocal [8,9].
CYP17 gene polymorphic sequence variation is associated with hyperandrogenism in Kashmiri women with polycystic ovarian syndrome
Published in Gynecological Endocrinology, 2021
Sairish Ashraf, Shayaq Ul Abeer Rasool, Mudasar Nabi, Mohd Ashraf Ganie, Farhat Jabeen, Fouzia Rashid, Shajrul Amin
The blood sample required for hormonal and biochemical investigations was collected in clot activated vials whereas for DNA extraction, the blood sample was collected in anti-coagulative Na2EDTA vials from participants after an overnight fast on 2nd – 3rd day of their menstrual cycle. The biochemical parameters assessed include oral glucose tolerance test, cholesterol, triglyceride, High Density Lipoprotein cholesterol levels, Low-Density Lipoprotein cholesterol levels, Urea, Creatinine, Alanine aminotransferase, Aspartate aminotransferase. All the parameters were estimated using Erba bioassay diagnostic kits on semi-automatic analyzer (Erba Chemtouch 7, Biochemistry Analyzer, Wiesbaden, Germany). The hormonal profile included Luteinizing hormone, Follicle stimulating hormone and Testosterone. All the measurements were done by Radioimmunoassay (RIA) on Beckman coulter UniCelDxl 800(Access Immunoassay system) using RIA kits (Immunotech s.r.o, Prague, Czech Republic).
Aluminum reproductive toxicity: a summary and interpretation of scientific reports
Published in Critical Reviews in Toxicology, 2020
The development of an oocyte begins as a primordial germ cell. Early in embryonic development these cells migrate into the future site of the ovaries, undergo meiotic cell division, and multiply, resulting in primary oocytes (primordial follicle) within the ovary. Their development is arrested until puberty, when follicle stimulating hormone (FSH) produced by the pituitary gland stimulates some to begin to mature, developing through follicle stages (primary, secondary, and if fertilized tertiary (Graafian) follicles), in the process of folliculogenesis. Most die (atresia) during these stages. During the resumption of cell division, the oocyte’s nucleus (germinal vesicle) breaks down and the first polar body (that forms concomitantly during oocyte division) is extruded. Follicle cells secrete and release estrogen that feeds back to the pituitary gland to decrease FSH release and increase luteinizing hormone (LH) release. This causes the follicle to rupture, resulting in release of the egg (ovulation), that migrates into the fallopian tubes where it can be fertilized by sperm. The ruptured follicle forms a corpus luteum, a transitory endocrine organ that secretes estrogen and progesterone. The latter feeds back to the pituitary gland to decrease LH release. The fertilized oocyte forms a mature egg cell (ovum). When the oocyte and sperm chromosomes combine, it becomes a zygote, which divides as it migrates into the uterus, creating the pregnant (gravid) state.
Related Knowledge Centers
- Anterior Pituitary
- Leydig Cell
- Ovulation
- Protein Dimer
- Testosterone
- Corpus Luteum
- Hormone
- Gonadotropic Cell
- Gonadotropin-Releasing Hormone
- Follicle-Stimulating Hormone