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admin | Multivitamin Benefits | 28.12.2014
Growth hormone (GH), also known as somatotropin, is an anabolic hormone made and secreted by the pituitary gland. These growth factors create the cascade of events typically associated with higher GH concentrations. Interestingly, as GH limits the storage of fats and mobilizes them for energy, blood sugar levels concurrently increase. The effects of GH on fat mobilization can begin at 20 minutes after release and last up to 3 hours.
You may wonder why intense exercise is so effective at helping you lose fat, even though it doesn’t seem like a few sets of heavy squats would burn that many calories.
When someone is GH deficient, GH replacement seems to be safe and may even promote health – at least with long-term monitoring by a physician.
Increases in GH secretion are related to increases in acids, by-products of high intensity exercise. GH slowly rises during an intense workout, but it actually peaks only when the workout is over. After exercise, neutrophil concentrations increase for several hours, most likely in response to delayed GH surge; this may enhance immune function. Menstrual cycle has little effect on the secretion of GH during exercise; however, higher levels of GH may be noticed while at rest. Excessive secretion of GH throughout the “growth years” results in an irregular pace of skeletal growth.
GH is structurally similar to the placental hormone human chorionic somatomammotropin (AKA human placental lactogen). Carbohydrate and protein intake before and after exercise sessions can enhance GH response. To learn more about making important improvements to your nutrition and exercise program, check out the following 5-day video courses. They’re probably better than 90% of the seminars we’ve ever attended on the subjects of exercise and nutrition (and probably better than a few we’ve given ourselves, too).
The testes secrete four hormones (anti-Müllerian hormone, insulin-like peptide 3, Inhibin B and testosterone) from two endocrine cell types. Effects of prenatal leydig cell function on the ratio of the second to fourth digit lengths in school-aged children. Prenatal sex hormones can induce abnormalities in the reproductive system and adversely impact on genital development. An investigation of the endocrine-disruptive effects of bisphenol a in human and rat fetal testes. Few studies have been undertaken to assess the possible effects of bisphenol A (BPA) on the reproductive hormone balance in animals or humans with often contradictory results.
STUDY QUESTION: How does insulin-like factor 3 (INSL3) concentration in blood vary across the menstrual cycle in women?
LIMITATIONS, REASONS FOR CAUTION: These were retrospective studies and the results were obtained from natural cycles only, with their inherent variability.
Insulin-like factor 3 (INSL3) is a small peptide hormone made and secreted uniquely by mature Leydig cells in the testes of all mammals. OBJECTIVES: Testicular function declines with obesity as a result of central and peripheral mechanisms, including a primary dysfunction of the Leydig cells. PURPOSE OF REVIEW: Biomarkers of prepubertal testicular function have become widely available only in recent years.
RECENT FINDINGS: Sertoli cells are the most representative cells of the prepubertal testis. SUMMARY: The widespread use of these biomarkers has enhanced our knowledge on the pathophysiology and diagnosis of prepubertal male hypogonadism.


Neohormone systems are defined as evolutionarily new endocrine or paracrine adaptations that supplement basic physiologic functions and define mammalian success.
Testicular descent is a unique physiological adaptation found in therian mammals allowing optimal spermatogenesis below core body temperature. The relaxin peptides are a family of hormones that share a structural fold characterized by two chains, A and B, that are cross-braced by three disulfide bonds. Serum samples for immunoreactive INSL3 concentration analysis were assayed in duplicate by using a commercial RIA (Phoenix Pharmaceutical, Belmont, CA). The administration of testosterone plus a progestogen functions as a male contraceptive by inhibiting the release of pituitary gonadotropins. Serum insulin-like factor 3 at the end of treatment by study and combined in subjects with azoospermia (A shaded) compared with those with nonazoospermia (A top) and in those with severe oligospermia (SO shaded) compared with those with nonsevere oligospermia (B bottom) by study and combined. Serum INSL3 was measured by a radioimmunoassay (RIA) (Phoenix Pharmaceuticals Inc, Belmont, Calif).
Ablation of LGR7-activation activity of AncRFLC and restoration of lost LGR7-activation activity in human INSL3 by point mutation. Median and 95% confidence intervals of the median of measurements of age, INSL3, testosterone, LH, FSH, and mean testicular volume at each stage of puberty. Tips: See More Research Abstracts, Antibody Stainings, Immunoassay Kits Curves and Sequences by clicking the tabs on the top.
GH is released in response to growth hormone releasing hormone (GHRH) produced by the hypothalamus.
In this way, GH “spares” carbohydrates from breakdown, and the level of sugar in the blood increases.
Many researchers credit the concomitant appearance of high concentrations of plasma fatty acids and GH that follow intense training.
Sleep deprivation in young individuals reduces GH secretion and may contribute to premature development of the metabolic syndrome. Data indicate that cutting calorie intake by 25% doesn’t significantly reduce GH levels, and people who exercise with the right type of training may actually see GH increase.
One of the reasons females mobilize more fatty acids during exercise is due to greater blood concentrations of GH. The effect of caloric restriction interventions on growth hormone secretion in non-obese men and women. Prior endurance exercise attenuates growth hormone response to subsequent resistance exercise. It is unknown whether anti-Müllerian hormone and insulin-like peptide 3 levels have a diurnal variation, and if so, whether they covary during the day with testosterone and InhB.
While the understanding of its effects is growing, very little is known about the structural and functional properties of native INSL3.
First, 18 healthy women of reproductive age were followed longitudinally for one and a half cycles, with blood sampling and hormone measurement every 2-3 days. Importantly, this expression and secretion appears to be constitutive and therefore reflects the differentiation status and number of the Leydig cells present, differing thereby from testosterone, which is acutely and homeostatically regulated by the hormones of the hypothalamic-pituitary-gonadal axis. The levels of insulin-like factor 3 (INSL3), a sensitive marker of Leydig cell impairment, have never been evaluated in obese men. The aim of this review is to update the knowledge on key biomarkers used to assess hypogonadism in boys. Anti-Müllerian hormone and inhibin B are essential biomarkers of Sertoli cell function.
Beyond their well known germ-cell toxicity, oncologic treatments may also affect Sertoli cell function. Recent studies show that INSL3, produced by Leydig cells, and its receptor LGR8 (RXFP2) are essential for mediating the transabdominal phase of testicular descent during early development.


Relaxins signal through two different classes of G-protein-coupled receptors (GPCRs), leucine-rich repeat-containing GPCRs LGR7 and LGR8 together with GPCR135 and GPCR142, now referred to as the relaxin family peptide (RXFP) receptors 1-4, respectively.
The assay is based on a polyclonal rabbit antiserum raised against full-length human INSL3 and on 125I-labeled INSL3 as the tracer. Sleep associated GH secretion has also been linked to the nocturnal rise in fatty acid release.
Of the 514 children who participated in a prospective cohort study on birth in Sapporo between 2002 and 2005, the following sex hormone levels were measured in 294 stored cord blood samples (135 boys and 159 girls); testosterone (T), estradiol (E), progesterone, LH, FSH, inhibin B, and insulin-like factor 3 (INSL3). A second cohort comprised a cross-sectional study of 909 women attending an infertility clinic, with a single blood sample taken at entry, together with other clinical and hormonal parameters.
Pathophysiology is not the same in all aneuploidies leading to infertility: while hypogonadism is not evident until mid-puberty in Klinefelter syndrome, it is established in early infancy in Down syndrome. The assay performance was checked before analysis by verifying specificity, sensitivity, precision, and accuracy. However, 10% to 20% of men have persistent sperm production despite profound gonadotropin suppression. P for the comparisons between groups is included above the line above the box and whiskers plot. A total of 350 children, who were of school age and could be contacted for this survey, were then requested via mail to send black-and-white photocopies of the palms of both the left and right hands. In Noonan syndrome, the occurrence of primary hypogonadism depends on the existence of cryptorchidism, and Prader-Willi syndrome may present with either primary or combined forms of hypogonadism. To detect the specificity, a cross-reactivity test was conducted via a binding assay with decreasing concentrations of human insulin, INSL4, INSL5, INSL6, and INSL7. Since insulin-like factor 3 (INSL3) has been shown to prevent germ cell apoptosis in mice, we hypothesized that INSL3 might be higher in men with persistent spermatogenesis during treatment with male hormonal contraceptives. BPA at 10(-7)-10(-5)M for 72 h suppressed the levels of fetal rat Leydig cell insulin-like factor 3 (INSL3). Current evidence points to autocrine, paracrine, and endocrine roles, acting through the G-protein-coupled receptor called RXFP2, although more research is required to characterize these functions in detail. In a retrospective analysis, we measured serum INSL3 in 107 men from 3 recent male hormonal contraceptive studies and determined the relationship between suppression of spermatogenesis and serum INSL3.
The precision was checked by using replicates of a serum pool control to measure intraassay and interassay variability.
At the end of treatment 63 men (59%) were azoospermic and 44 men (41%) had detectable sperm in their ejaculates. For the lowest doses, the effects observed occurred only when no gonadotrophin was added to the culture media and were associated with a poorly preserved testicular morphology. Finally, to detect the accuracy of the method, linearity of dilution was determined by serially diluting serum pool control, and recovery was evaluated by measuring pooled serum samples spiked with increasing standard human INSL3 concentrations before analysis in the RIA. Cross-reactivity with human insulin, INSL4, INSL5, INSL6, and INSL7, used to evaluate the specificity of the INSL3 assay, was 0%. After 6 months of treatment with a hormonal male contraceptive regimen, higher serum INSL3 concentrations were associated with persistent sperm production. Suitability of the assay to measure INSL3 accurately was demonstrated by results of linearity and recovery (slope of 1; mean of recovery of 104%), which demonstrated the absence of bias. INSL3 may play a role in preventing complete suppression of spermatogenesis in some men on hormonal contraceptive regimens. This finding suggests that INSL3 may be a potential target for male contraceptive development.



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