Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0848255 (female puberty)
 121 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Insulin resistance (IR) and polycystic ovarian syndrome (PCOS) appear as linked phenomena, although this is not easy to obviate in common forms of PCOS while it is evident in the rare cases of extreme IR and hyperinsulinism (HI). Experimental data indicate that insulin could interfere with the local insulin-like growth factor systems in ovaries, and presumably in adrenals and in the hypothalamic pituitary system. The female puberty system offers a physiological model to explain the gonadotropic action of insulin. In patients with IR, HI could induce a state of hyperpuberty, leading to the constitution of PCOS during adolescence.
 ...
PMID:Insulin resistance and polycystic ovarian syndrome. 130 14

Lead (Pb) can delay sexual maturation; however, the mechanism and critical time of insult are not clearly defined. Therefore, we assessed maternal Pb levels during low-level gestational and/or lactational exposure, as well as blood and tissue Pb in developing fetuses in relation to the subsequent detrimental effects of Pb on puberty-related hormones and the onset of female puberty. Adult Fisher 344 female rats were gavaged daily with either a 1-ml solution of PbAc containing 12 mg/ml Pb or an equal volume of sodium acetate (NaCl), for the controls, from 30 days prior to breeding until their pups were weaned at 21 days. By cross-fostering at the time of birth, the pups were either exposed to PbAc or NaAc during gestation only, lactation only, or during both gestation and lactation. Pb delayed the timing of puberty and this delay was associated with suppressed serum levels of insulin-like growth factor-1 (IGF-1), luteinizing hormone (LH), and estradiol (E(2)). Liver IGF-1 mRNA was not affected, suggesting that Pb altered translation and/or secretion of IGF-1. We reported previously that peripherally derived IGF-1 acts at the hypothalamic level to facilitate LH release at puberty; hence, we suggest that the action of Pb in decreasing circulating IGF-1 contributes to the delayed puberty. The detrimental effects occurred regardless of the developmental time of exposure, although gestational exposure appeared more sensitive to the effects of Pb. Also, the effects noted were with blood Pb levels less than previously reported and these levels are relevant to human health concerns.
 ...
PMID:Effects of lead (Pb) exposure during gestation and lactation on female pubertal development in the rat. 1222 May 94

The major drug of abuse among teenagers in the United States continues to be ethanol (EtOH), but use is seen in children as young as nine. In the studies reported here, the impact of EtOH on biologic and hormonal parameters of puberty was assessed in female rats. Rats were fed a liquid diet containing EtOH, pair fed an identical liquid diet containing dextrimaltose instead of EtOH, or fed a liquid diet not containing EtOH ad libitum. Feeding was started at 21, 25, or 28 d of age. EtOH markedly delayed the age at vaginal opening (34.5 +/- 0.5 d in controls vs 48.5 +/- 2.4 d in EtOH animals; p < 0.001), delayed the age at first estrous (40.9 +/- 0.6 d in controls vs 61.2 +/- 2.6 d in EtOH animals; p < 0.001), increased the length of the estrous cycle, and decreased the number of proestrous days. EtOH, concomitant with reduced ovarian and uterine weight, decreased serum estradiol and progesterone. Associated with these changes in ovarian hormones there was a selective increase in follicle-stimulating hormone, but not luteinizing hormone. EtOH consistently reduced insulin-like growth factor-1. In general, EtOH-induced disruption was more severe the younger the animals were at the start of feeding. Opiate receptor blockade with naltrexone completely prevented the EtOH-induced delay in vaginal opening. The impact of EtOH on female puberty is dramatic, is an emerging public health problem, and deserves more study.
 ...
PMID:EtOH disrupts female mammalian puberty: age and opiate dependence. 1245 Mar 16

Several studies suggest an interrelationship between estradiol (E2) and insulin-like growth factor-1 (IGF-1) at the hypothalamic level. The present study was designed to discern if the capability of IGF-1 to release LH and influence the timing of female puberty is influenced by E2. Twenty-eight-day-old female rats were ovariectomized (OVEX), then implanted with a third ventricular (3V) cannula. Two weeks later, these animals received subcutaneous (s.c.) injection of oil, or either one or two injections of E2 in the form of estradiol benzoate (1 microg). Forty-eight hours later, four basal blood samples were drawn then the animals received IGF-1 (200 ng) or saline via the 3V and four more blood samples were taken. Results indicated that E2 replacement lowered basal LH levels and IGF-1 induced a significant LH release in only animals that had E2 levels above 20 pg/ml. These levels of E2 were also associated with increases (p<0.05) in the expression of both IGF-1 receptor (IGF-1R) mRNA and protein. In order to further support the hypothesis that the action of IGF-1 at the time of puberty is influenced by E2, 24-day-old intact female rats received s.c. injection of sesame oil or 0.1 microg of E2. The next day, the E2-treated animals also received twice daily s.c. injections of either IGF-1 (500 ng) or saline until vaginal opening (VO) occurred. The animals that received E2 plus IGF-1 showed VO at 31.1 days, which was 2.5 days earlier (p<0.01) than E2-treated animals and 4 days earlier (p<0.001) than IGF-1-treated and saline control animals. Taken together, these results indicate that the hypothalamic action of IGF-1 to stimulate LH release and advance female pubertal development is dependent upon the influence of E2.
 ...
PMID:Influence of estradiol on insulin-like growth factor-1-induced luteinizing hormone secretion. 1519 71

Because prepubertal female rats maternally exposed to lead (Pb) exhibit suppressed serum levels of insulin-like growth factor-1 (IGF-1) and delayed puberty, we investigated the ability of centrally administered IGF-1 to stimulate luteinizing hormone (LH) release in vivo and LH-releasing hormone (LHRH) release in vitro from maternally Pb-exposed prepubertal female rats. Additionally, we assessed whether IGF-1 replacement could affect the timing of female puberty. Results demonstrated that IGF-1 stimulated significantly LH release in both control and Pb-exposed animals. When median eminences from control and Pb-exposed females were incubated with rat IGF-1 in vitro, they responded similarly with significant peptide-induced LHRH release. Lastly, we showed IGF-1 replacement reversed the delay in puberty caused by Pb. These results indicate the central LHRH response to IGF-1 is intact and that Pb-induced delayed puberty is due, at least in part, to suppressed circulating IGF-1 available to the hypothalamus.
 ...
PMID:IGF-1 administration to prepubertal female rats can overcome delayed puberty caused by maternal Pb exposure. 1615 99

Puberty is initiated by hormonal changes in the adolescent body that trigger physical and behavioral changes to reach adult maturation. As these changes occur, some adolescents experience concerning pubertal symptoms that are associated with dysfunction of the autonomic nervous system (ANS). Vasovagal syncope (VVS) and Postural Orthostatic Tachycardia Syndrome (POTS) are common disorders of the ANS associated with puberty that are related to orthostatic intolerance and share similar symptoms. Compared to young males, young females have decreased orthostatic tolerance and a higher incidence of VVS and POTS. As puberty is linked to changes in specific sex and non-sex hormones, and hormonal therapy sometimes improves orthostatic symptoms in female VVS patients, it is possible that pubertal hormones play a role in the increased susceptibility of young females to autonomic dysfunction. The purpose of this paper is to review the key hormonal changes associated with female puberty, their effects on the ANS, and their potential role in predisposing some adolescent females to cardiovascular autonomic dysfunctions such as VVS and POTS. Increases in pubertal hormones such as estrogen, thyroid hormones, growth hormone, insulin, and insulin-like growth factor-1 promote vasodilatation and decrease blood volume. This may be exacerbated by higher levels of progesterone, which suppresses catecholamine secretion and sympathetic outflow. Abnormal heart rate increases in POTS patients may be exacerbated by pubertal increases in leptin, insulin, and thyroid hormones acting to increase sympathetic nervous system activity and/or catecholamine levels. Given the coincidental timing of female pubertal hormone surges and adolescent onset of VVS and POTS in young women, coupled with the known roles of these hormones in modulating cardiovascular homeostasis, it is likely that female pubertal hormones play a role in predisposing females to VVS and POTS during puberty. Further research is necessary to confirm the effects of female pubertal hormones on autonomic function, and their role in pubertal autonomic disorders such as VVS and POTS, in order to inform the treatment and management of these debilitating disorders.
 ...
PMID:Pubertal Hormonal Changes and the Autonomic Nervous System: Potential Role in Pediatric Orthostatic Intolerance. 3179 99