Corrigendum: High Circulating Follicle-Stimulating Hormone Level Is a Potential Risk Factor for Renal Dysfunction in Post-Menopausal Women.
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SUBMITTER: Li Q
PROVIDER: S-EPMC8439174 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:ObjectiveMenopause contributes to renal dysfunction in women, which is generally attributed to estrogen withdrawal. In addition to decreased estrogen level, serum follicle-stimulating hormone (FSH) level increases after menopause. This study investigated the association between high circulating FSH level and renal function in post-menopausal women.MethodsThis observational cross-sectional study included 624 pre-menopausal, 121 peri-menopausal, and 2540 post-menopausal women. The levels of female sex hormones were examined by chemiluminescence and indices of renal function were measured using a clinical chemistry analyzer. The post-menopausal women were grouped into quartiles according to serum FSH levels.ResultsRenal function progressively declined from pre-menopause to peri-menopause to post-menopause, which was accompanied by increasing serum FSH level. In post-menopausal women, serum creatinine level increased with increasing FSH quartile, which was accompanied by a decrease in estimated glomerular filtration rate (eGFR) (p for trend <0.001); moreover, the prevalence of declined eGFR (<90 ml/min/1.73 m2) and chronic kidney disease (CKD; eGFR <60 ml/min/1.73 m2) increased (p for trend <0.001). Even after adjusting for confounders, the odds ratios (ORs) of declined eGFR and CKD increased with increasing FSH quartiles in post-menopausal women. The ORs of declined eGFR (OR=2.19, 95% confidence interval [CI]: 1.63-2.92) and CKD (OR=10.09, 95% CI: 2.28-44.65) in the highest FSH quartile were approximately 2- and 10-fold higher, respectively, than in the lowest FSH quartile (p<0.05). After stratifying post-menopausal women by median age (61 years), the OR for declined eGFR for each FSH quartile in the older group was higher than that for the corresponding FSH quartile in the younger group.ConclusionsA high circulating FSH level is an independent risk factor for renal dysfunction in women after menopause. Additionally, aging may aggravate the association of high FSH levels with reduced renal function in post-menopausal women.
| S-EPMC8047631 | biostudies-literature
Project description:: Menopause compounds many cardiometabolic risk factors through endogenous estrogen withdrawal. This study aimed to find the association between serum follicle-stimulating hormone (FSH) levels and cardiometabolic risk factors in post-menopausal Korean women. A total of 608 post-menopausal women from eight randomized double-blind, placebo-controlled clinical trials on menopause during the year 2012-2019 were analyzed. Cardiometabolic risk factors such as body mass index, waist circumference, systolic blood pressure, fasting glucose, triglycerides (TG), high density lipoprotein-cholesterol (HDL-C), and TG/HDL-C ratio were significantly improved as the FSH quartiles increased. Metabolic syndrome (MetS) and the number of components of MetS decreased as FSH quartiles increased. In regression analysis, FSH level was negatively associated with cardiometabolic risk factors including body mass index, body weight, waist circumference, fasting glucose and TG, while it was positively associated with HDL-C. The odds ratio of MetS in the first quartile of FSH was 2.682 compared with that in the fourth quartile of FSH in a logistic regression model. Serum FSH levels had a negative correlation with cardiometabolic risk factors in post-menopausal Korean women, suggesting that a low FSH can be a predictor for cardiovascular disease in post-menopausal women.
| S-EPMC7230188 | biostudies-literature
Project description:FSH glycosylation varies in two functionally important aspects: microheterogeneity, resulting from oligosaccharide structure variation, and macroheterogeneity, arising from partial FSHβ subunit glycosylation. Although advances in mass spectrometry permit extensive characterization of FSH glycan populations, microheterogeneity remains difficult to illustrate, and comparisons between different studies are challenging because no standard format exists for rendering oligosaccharide structures. FSH microheterogeneity is illustrated using a consistent glycan diagram format to illustrate the large array of structures associated with one hormone. This is extended to commercially available recombinant FSH preparations, which exhibit greatly reduced microheterogeneity at three of four glycosylation sites. Macroheterogeneity is demonstrated by electrophoretic mobility shifts due to the absence of FSHβ glycans that can be assessed by Western blotting of immunopurified FSH. Initially, macroheterogeneity was hoped to matter more than microheterogeneity. However, it now appears that both forms of carbohydrate heterogeneity have to be taken into consideration. FSH glycosylation can reduce its apparent affinity for its cognate receptor by delaying initial interaction with the receptor and limiting access to all of the available binding sites. This is followed by impaired cellular signaling responses that may be related to reduced receptor occupancy or biased signaling. To resolve these alternatives, well-characterized FSH glycoform preparations are necessary.
| S-EPMC6534497 | biostudies-literature
Project description:Purpose of reviewTo review the current knowledge of genetic variants in the two genes affecting the individual responsiveness to follicle-stimulating hormone (FSH) action-the FSH beta-subunit (FSHB) and the FSH receptor (FSHR), as well as the pharmacogenetic ramifications of the findings.Recent findingsFour common variants in the FSHB and the FSHR genes were shown to exhibit significant effect on FSH action: linked FSHR variants Thr307Ala and Asn680Ser determining common receptor isoforms, and gene expression affecting polymorphisms FSHR -29G/A and FSHB -211G/T. In women, the FSHR Thr307Ala/Asn680Ser polymorphisms show consistent predictive value for estimating the most optimal recombinant FSH dosage in controlled ovarian hyperstimulation (COH). The same variants exhibit a potential for the pharmacogenetic assessment of the treatment of polycystic ovarian syndrome. The FSHR -29G/A variant was also shown to contribute to ovarian response to COH. Pilot studies have suggested the FSHB -211 TT homozygous oligozoospermic men with genetically determined low concentration of FSH, as potentially the best responders to FSH treatment; furthermore, modulation of this response by FSHR polymorphisms is possible.SummaryGenetic variants in FSHB and FSHR exhibit a potential for pharmacogenetic applications in selecting appropriate treatment options (timing and dosage) in male and female conditions requiring or benefiting from FSH therapy.
| S-EPMC3348539 | biostudies-literature
Project description:Background and aimThe follicle-stimulating hormone (FSH) gene is an essential regulator of fertility in livestock. This study aims to provide information on the genetic makeup of Madrasin cattle experiencing hypofunction by the FSH profile and FSH receptors (FSHR) polymorphism.Materials and methodsBlood samples were collected from the Bangkalan regency in Indonesia. DNA was isolated and purified following the extraction protocol of polymerase chain reaction (PCR) and PCR-restriction fragment length polymorphism.ResultsOur results showed that the FSH gene had a band length of 310 bp and produce two alleles (A and B) with restriction enzymes at 250 bp, 230 bp, and 145 bp. Furthermore, the FSHR gene had a band length of 303 bp and produced two homozygous genotypes: GG at bp 239 and CC at bp 188.ConclusionBased on these differences, there was no change in allele frequency and genotype between Madura and Madrasin cattle due to crossbreeding with Limousin cattle. Thus, further detailed investigations of Madrasin cattle are required to elucidate the profile of the LH and LHR genes.
| S-EPMC7311873 | biostudies-literature
Project description:Background The increased risk of metabolic syndrome (MetS) during the menopausal transition might partly attribute to the changes in follicle-stimulating hormone (FSH) and luteinizing hormone (LH). However, few studies were conducted to examine the associations of FSH and LH concentrations with MetS at the full range of reproductive aging, especially in the US population. The aim of this study is to examine the associations of FSH, LH, and LH/FSH ratio with the risk of MetS and severity score in the US women. Methods Data were derived from the National Health and Nutrition Examination Survey. Women aged from 35 to 60 years were eligible. MetS was defined as having at least 3 of the following: a waist circumference ≥ 88 cm, a triglycerides level ≥ 150 mg/dL, a high density lipoprotein < 50 mg/dL, a systolic blood pressure ≥ 130 mm Hg or a diastolic blood pressure ≥ 85 mm Hg or taking hypertension medications, or a fasting plasma glucose level ≥100 mg/dL or taking diabetes medications. The MetS severity score was calculated according to race/ethnicity- specific equation. Results There were 3,831 women included in this study. Increases in serum FSH and LH levels per 1 SD were separately linked to a 22.6% (OR: 0.774; 95% CI: 0.646, 0.929; and P= 0.006) and 18.5% (OR: 0.815; 95% CI: 0.690, 0.962; and P= 0.006) lower risk of MetS only in postmenopausal women. Meanwhile, increases in serum FSH and LH levels per 1SD were associated with a decrease of -0.157 (95% CI :-2.967, -2.034) and -0.078 (95% CI: -2.688, -1.806) MetS severity score in perimenopausal women and -0.195 (95% CI: -2.192, -1.023) and -0.098 (95% CI:-1.884, -0.733) in postmenopausal women. However, LH/FSH ratio had no connections with the risk of MetS and MetS severity score across the menopausal transition. Conclusions Elevated serum FSH and LH levels, but not LH/FSH ratio, were associated with a lower risk of MetS and MetS severity score, especially in postmenopausal women. Therefore, serum FSH and LH levels might be efficient predictors for screening and identifying women at risk of MetS across the menopausal transition.
| S-EPMC9947143 | biostudies-literature
Project description:Thyroid-stimulating hormone (TSH) and follicle-stimulating hormone (FSH) have both been recently implicated in bone remodelling. Clinical evidence, as well as data from TSH receptor and thyroid hormone receptor knockout mice, suggest that TSH has a direct effect on skeletal homeostasis, although some data are conflicting. Recently, the exogenous administration of TSH has been shown to positively impact bone in oophrectomised rats. These data, along with their potential implications for the treatment of severe osteoporosis, are discussed.
| S-EPMC2266660 | biostudies-other
Project description:Follicle-stimulating hormone (FSH), a pituitary glycoprotein hormone, is an integral component of the endocrine axis that regulates gonadal function and fertility. To transmit its signal, FSH must bind to its receptor (FSHR) located on Sertoli cells of the testis and granulosa cells of the ovary. Thus, both the magnitude and the target of hormone response are controlled by mechanisms that determine FSHR levels and cell-specific expression, which are supported by transcription of its gene. The present review examines the status of FSHR/Fshr gene regulation, emphasizing the importance of distal sequences in FSHR/Fshr transcription, new insights gained from the influx of genomics data and bioinformatics, and emerging trends that offer direction in deciphering the FSHR/Fshr regulatory landscape.
| S-EPMC4480823 | biostudies-literature
Project description:BackgroundFollicle stimulating hormone (FSH) is an important hormone responsible for growth, maturation and function of the human reproductive system. FSH regulates the synthesis of steroid hormones such as estrogen and progesterone, proliferation and maturation of follicles in the ovary and spermatogenesis in the testes. FSH is a glycoprotein heterodimer that binds and acts through the FSH receptor, a G-protein coupled receptor. Although online pathway repositories provide information about G-protein coupled receptor mediated signal transduction, the signaling events initiated specifically by FSH are not cataloged in any public database in a detailed fashion.FindingsWe performed comprehensive curation of the published literature to identify the components of FSH signaling pathway and the molecular interactions that occur upon FSH receptor activation. Our effort yielded 64 reactions comprising 35 enzyme-substrate reactions, 11 molecular association events, 11 activation events and 7 protein translocation events that occur in response to FSH receptor activation. We also cataloged 265 genes, which were differentially expressed upon FSH stimulation in normal human reproductive tissues.ConclusionsWe anticipate that the information provided in this resource will provide better insights into the physiological role of FSH in reproductive biology, its signaling mediators and aid in further research in this area. The curated FSH pathway data is freely available through NetPath (http://www.netpath.org), a pathway resource developed previously by our group.
| S-EPMC3204250 | biostudies-literature
Project description:Elevated follicle-stimulating hormone (FSH) activity is proposed to directly cause bone loss independent of estradiol deficiency in aging women. Using transgenic female mice expressing human FSH (TgFSH), we now reveal that TgFSH dose-dependently increased bone mass, markedly elevating tibial and vertebral trabecular bone volume. Furthermore, TgFSH stimulated a striking accrual of bone mass in hypogonadal mice lacking endogenous FSH and luteinizing hormone (LH) function, showing that FSH-induced bone mass occurred independently of background LH or estradiol levels. Higher TgFSH levels increased osteoblast surfaces in trabecular bone and stimulated de novo bone formation, filling marrow spaces with woven rather than lamellar bone, reflective of a strong anabolic stimulus. Trabecular bone volume correlated positively with ovarian-derived serum inhibin A or testosterone levels in TgFSH mice, and ovariectomy abolished TgFSH-induced bone formation, proving that FSH effects on bone require an ovary-dependent pathway. No detectable FSH receptor mRNA in mouse bone or cultured osteoblasts or osteoclasts indicated that FSH did not directly stimulate bone. Therefore, contrary to proposed FSH-induced bone loss, our findings demonstrate that FSH has dose-dependent anabolic effects on bone via an ovary-dependent mechanism, which is independent of LH activity, and does not involve direct FSH actions on bone cells.
| S-EPMC3012495 | biostudies-literature