Normal pubertal development and the menstrual cycle as a vital sign *
Joseph S. Sanfilippo, Eduardo Lara-Torre, Veronica Gomez-Lobo in Sanfilippo's Textbook of Pediatric and Adolescent GynecologySecond Edition, 2019
Puberty is initiated and controlled by a complex relationship of multiple hormones. The regulatory steps to initiation of puberty are still unknown. The hypothalamus secretes gonadotropin-releasing hormone (GnRH), which signals the gonadotrophs in the pituitary to release gonadotrophins: luteinizing hormone (LH) and follicle-stimulating hormone (FSH). Luteinizing hormone acts on the theca cells in the ovary to produce androgens, and FSH acts on ovarian follicles to produce estradiol, inhibin, and gametes. The interplay is called the hypothalamic-pituitary-gonadal (HPG) axis (Figure 1.1).3 During the first 3 months of life, under the influence of maternal estrogen exposure in utero, LH and FSH levels are high. By age 6 months, LH levels are almost undetectable. While FSH levels decrease after the first 6 months, they can remain elevated until age 3–4 years.3 At this point, the HPG axis remains quiescent until activation initiates puberty. The LH level is generally the most useful marker for assessing onset of puberty with elevated levels in childhood indicating central nervous system activity related to onset of puberty.3 Levels of FSH may be found elevated with thelarche (which can be an isolated event), so they are not a reliable indicator of pubertal onset.4 Estradiol and testosterone levels are low in prepubertal girls and rise with onset of puberty and should be consistent with laboratory reference levels for age. Leptin does not have a direct role in puberty initiation but likely influences GnRH secretion.3
Diet and Exercise Approaches for Reversal of Exercise-Associated Menstrual Dysfunction
Henry C. Lukaski in Body Composition, 2017
Low EA has been associated with malfunction of the HPG axis provoking decreased estrogen release and menstrual dysfunction (Stafford 2005; Mountjoy et al. 2014; Melin et al. 2015; Thomas et al. 2016). In healthy women, hypothalamic gonadotropin releasing hormone (GnRH) stimulates the pituitary release of luteinizing hormone (LH), which triggers the production of estrogen and progesterone (Stafford 2005). In low EA, GnRH pulsatility is disrupted and thus results in decreased estrogen release from the ovaries (Stafford 2005; Mountjoy et al. 2014). Leptin is thought to play an important role in the regulation of the GnRH pulse generator (Stafford 2005). Several direct and indirect pathways have been proposed for leptin (Stafford 2005; Vazquez et al. 2015). Currently, leptin appears to regulate the release of kisspeptins from the Kiss1 neurons in the hypothalamus, which in turn regulate the GnRH pulse generator (Vazquez et al. 2015). As noted previously, low leptin levels are not consistently observed in individuals with low EA and menstrual dysfunction (Cialdella-Kam et al. 2014; Melin et al. 2015). Thus, other hormonal disruptions such as high cortisol and high ghrelin among others may contribute to low estrogen levels and menstrual disturbances (Stafford 2005; Pauli and Berga 2010; Maggi et al. 2016). The control of GnRH pulse generator appears to be modulated by several neuropeptides and hormones (Maggi et al. 2016; Vazquez et al. 2015); thus, further research is needed to elucidate the pathway related to menstrual dysfunction and low EA.
Testosterone in Sport
Datta Sourya, Debasis Bagchi in Extreme and Rare Sports, 2019
Whilst the MacConnie study did not show any significant differences between the basal testosterone levels of high-mileage runners and sedentary controls, it did reveal that runners displayed a significantly (p < 0.05) reduced frequency of LH pulses (2.2 ± 0.48 vs. 3.6 ± 0.24) as well as a significantly (p < 0.02) reduced amplitude of the LH pulse (0.9 ± 0.24 mIU/ml vs. 1.6 ± 0.15 mIU/ml). A pulse of LH results as a direct consequence from a pulse of gonadotropin releasing hormone, and downstream, LH acts on the Leydig cells of the testes, stimulating them to produce testosterone (Rowe et al. 1975, 17–26). Although the basal levels of testosterone levels measured were not reduced compared to controls, the changes in LH pulse frequency and amplitude do indicate that the runners may less strongly stimulate the release of testosterone.
Male subclinical hypogonadism and late-onset hypergonadotrophic hypogonadism: mechanisms, endothelial function, and interplay between reproductive hormones, undercarboxylated osteocalcin, and endothelial dysfunction
Published in The Aging Male, 2022
Ragaa Abedelshaheed Matta, Hazem Mohamed-Ali Farrag, Ahmed Abdelfadel Saedii, Mohamed Mamdouh Abdelrahman
According to the European Male Aging Study (EMAS), late-onset hypogonadism (LOH) is a clinical and biochemical syndrome characterized by a gradual decrease in serum testosterone (T) levels as an aspect of age-related reproductive and sexual decay across a life span. Its diagnosis depends on the presence of at least three sexual symptoms and either repeated (at least twice) total T levels <8 nmol/l or serum total T levels of 8–11 nmol/l and free T levels <220 pmol/l. Subclinical hypogonadism (SCH), or compensated hypogonadism, has been recognized as a clinical entity that affecting 9.5% of men. Similar to other subclinical endocrine disorders, its diagnosis depends on normal T and elevated luteinizing hormone (LH) levels [1]. The hypothalamic–pituitary–testicular (HPT) axis is highly regulated. The gonadotropin-releasing hormone pulse generator controls gonadotropin release, namely LH and follicle stimulating hormone (FSH) from the anterior pituitary gland. They bind to testicular receptors on Leydig cells for T production and Sertoli cells for spermatogenesis, respectively. Aromatase enzymes convert T to estradiol (E) in the gonads and extra-gonadal target tissues. Both T and E mediate negative feedback on the HPT axis by binding to their receptors and regulating the HPT set point for LH [2]. Impaired Leydig cell function, altered androgen receptor sensitivity, and aromatization capacity can all affect the LH set point. They can be estimated using the LH/T ratio, androgen sensitivity index (ASI), and E/T ratio [3–5].
Inter-organ regulation by the brain in Drosophila development and physiology
Published in Journal of Neurogenetics, 2023
Sunggyu Yoon, Mingyu Shin, Jiwon Shim
Recent studies have extended the significance of brain functions to animal physiology and homeostasis (Castillo-Armengol et al., 2019; Roh et al., 2016). One example of such control is the endocrine system involving the pituitary gland, hypothalamus, or pineal gland in humans, where various hormones are released into blood vessels to modulate the function of other organs. The mechanism underlying the human menstrual cycle is modified by follicle-stimulating hormone (FSH) and luteinizing hormone (LH) generated by gonadotropic cells of the anterior pituitary gland. The release of FSH and LH is activated by gonadotropin-releasing hormone (GnRH), controlled by negative estrogen feedback produced by the ovary (Mihm et al., 2011). In addition to endocrine pathways transmitted via representative hormones, unconventional signaling molecules, including neurotransmitters and metabolic byproducts, also serve as signaling messengers (Gancheva et al., 2018; Marina et al., 2018; Newsholme et al., 2003), which together facilitate inter-organ interaction. However, owing to the sophisticated nature of such interactions, it is challenging to delineate the mechanistic details underlying inter-organ communication in vivo, especially in higher vertebrates.
A Proprietary Herbal Blend Containing Extracts of Punica granatum Fruit Rind and Theobroma cocoa Seeds Increases Serum Testosterone Level in Healthy Young Males: A Randomized, Double-Blind Placebo-Controlled Study
Published in Journal of Dietary Supplements, 2023
Poorna Gopal Azad Sreeramaneni, Amulya Yalamanchi, Manikyeswara Rao Konda, Sree Harsha Varma Cherukuri, Joseph C. Maroon
The most notable observation from the present study is that the LN18178 supplemented participants increased free and total testosterone levels. In parallel, the participants also improved the hand grip strength and mid-upper arm diameter compared with the placebo. Testosterone is an anabolic hormone. It increases muscle mass, strength, and stamina, hence, enhances physical performance (24). The present findings suggest a potential application of LN18178 as a natural ergogenic supplement for males. The use of dietary ergogenic supplements to boost testosterone levels is commonly practiced in young males to improve their sports performances. Another important observation from the present study is that the herbal blend concomitantly increased serum LH in the study participants. The gonadotropin-releasing hormone (GnRH) from the hypothalamus regulates testosterone biosynthesis via stimulating the release of LH from the pituitary. LH increases cAMP signaling and activates the steroidogenic acute regulatory (StAR) protein in the Leydig cells to increase testosterone synthesis (25, 26). In the present study, we did not estimate the serum GnRH level in the participants. However, our results suggest a possibility that LN18178 might have regulated the pituitary-gonadal cross-talk and increased the testosterone level.
Related Knowledge Centers
- Anterior Pituitary
- Luteinizing Hormone
- Peptide Hormone
- Tropic Hormone
- Hypothalamus
- Releasing & Inhibiting Hormones
- Follicle-Stimulating Hormone
- Gnrh Neuron
- Gonadotropin-Releasing Hormone Family
- Hypothalamic–Pituitary–Gonadal Axis