1,721,286 research outputs found
Luteal responses to gonadotropin-releasing hormone during the luteal phase: relation to the age of corpus luteum.
No full textThe pituitary and luteal responsiveness of GnRH were studied in 20 normal women at different stages of the luteal phase (LP). Blood samples were collected every 15 min for 180 min before and 120 min after the iv injection of 25 μg GnRH. The studies were performed in the early LP (ELP; days 2–3 of LP; n = 5), mid-LP (MLP: days 4–8 of LP; n = 11), late LP (LLP; days 9–12 of LP; n = 13), and premenstrual phase (PMP; days 13–14 of LP; n = 3). Plasma LH, FSH, progesterone (P), and estradiol (E) levels were assayed by RIA. The data were analyzed as integrated secretory area before (ISAb) and after GnRH stimulation (ISAs) and in terms of their percent increase with respect to the basal value. In all studies, GnRH elicited increases in plasma LH and FSH (P < 0.001). On the other hand, in the ELP, GnRH did not alter steroid ISAs compared to their ISAb, while significant increases in plasma P and E levels were found in the MLP (P, P < 0.01; E, P < 0.02) and LLP (P and E, P < 0.01). In the PMP, two women had no increase in steroid secretion; in the remainder of the subjects, both P and E ISAs markedly increased. This different pattern was not related to basal steroid levels. All women who had a blunted steroid response in the ELP or PMP had a normal secretory response of both P and E when studied at the other LP stages of the same cycle. Furthermore, there was a positive linear correlation between plasma P and E for the ISAb and ISAs values, while the secretory patterns of gonadotropins and steroids were not related to each other. In conclusion, the corpus luteum is able to respond to GnRH at a well identified period of the LP. This pattern indicates variable dependence of the corpus luteum on the functional activity of the hypothalamic-pituitary axis. © 1987 by The Endocrine Society
Role of opioid antagonists in the treatment of women with glucoregulation abnormalities
No full textBeta-endorphin were detected in the endocrine pancreas and seem able to influence insulin and glucagon release. Hence, endogenous opioids could have a role in glucoregulation and in the pathogenesis of obesity beyond the previously detected effects on appetite. Metabolic abnormalities, such as hyperinsulinemia, insulin-resistance and obesity, are common features of polycystic ovary syndrome (PCOS), and seem to have a pathogenetic role in this disorder. A link between opioids and PCOS-related hyperinsulinism is suggested by the finding of altered central opioid tone and elevated β-endorphins levels, directly correlated with body weight, in these patients. Furthermore, naloxone and naltrexone significantly reduce the insulin response to glucose load only in hyperinsulinemic PCOS patients. This effect is obtained chiefly through an improvement of insulin clearance. Naltrexone is also able to ameliorate the abnormal gonadotrophins secretion and to improve the ovarian responsiveness in obese PCOS women undergoing ovulation induction with exogenous GnRH. Such effects are believed to be obtained through an amelioration of hyperinsulinemia. Gonadal steroids modulate the opioid system both centrally and in peripheral districts. Nevertheless, the decline of ovarian function does not abolish the opioidergic control of glucoregulation. Post-menopausal period is characterised by a high prevalence of hyperinsulinemia and insulin-resistance. In particular, an association between hyperinsulinemia and increased opioid activity was found in postmenopausal women showing a central body fat distribution. Both naloxone and naltrexone ameliorate the metabolic imbalance also when it appears in the climacteric period, and mainly by increasing insulin clearance. The benefits of naltrexone may represent in the future a useful tool for the treatment of women with hyperinsulinism in the clinical practice. © 2006 Bentham Science Publishers Ltd
Implications of Gestational Weight Gain in Studies of Gestational Diabetes
No full textA research article published in JAMA Pediatrics, “Associations of Maternal Diabetes and Body Mass Index With Offspring Birth Weight and Prematurity,” asserts that maternal insulin-treated diabetes and obesity in mothers with type 2 diabetes appeared to be associated with increased risks for the offspring being large for gestational age (LGA) and preterm births. Increased LGA risks were found also for mothers with diabetes with insulin treatment, with type 2 diabetes and gestational diabetes (GDM) not treated with insulin. In addition, prematurity rose for mothers with type 2 diabetes, independent of prepregnancy body mass index (BMI). Prepregnancy BMI, with no diabetes, was associated with the risk for LGA and prematurity.
Large for gestational age is a stronger marker for risk of being overweight/obese in early childhood. Rates of being overweight/obese in childhood were highest in LGA children born to mothers with GDM.2 Gestational weight gain (GWG) is an important risk factor for macrosomia.3 The GWG is calculated as the difference between weight at the last prenatal visit and the prepregnancy self-reported weight. The research by Kong et al1 would have been enhanced by including the use of self-reported prepregnancy weight. In an important and significant study such as this, it would have been appropriate to indicate not only the pregravidic weight of women but also the GWG. If the GWG is not mentioned, the risks associated with it could be underestimated. The GWG may influence the grade of insulin resistance and subclinical inflammation that accompanies GDM. It is known that prepregnancy BMI is important, but perhaps it becomes even more important than the GWG. It is not certain that only nondiabetic women with an overweight prepregnancy BMI develop a GDM. It is possible that even normal-weight women before pregnancy, if they become overweight during pregnancy, can develop a GDM, which in turn may be associated with having an LGA infant.
It would be appropriate to stress from the beginning of pregnancy, not only in overweight or obese women, to avoid excessive GWG to reduce the risks of GDM and morbid obesity. In these women, adequate GWG may prevent fetal overgrowth
Long-term naltrexone treatment reduces the exaggerated insulin secretion in patients with polycystic ovary disease.
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Longitudinal metabolic observation of metformin effects during pregnancy in hyperinsulinemic women with polycystic ovary syndrome: A case report
No full textObese hyperinsulinemic women with polycystic ovary syndrome (PCOS) present a markedly increased risk of developing glycaemic alterations during pregnancy, commonly recognized as a "diabetogenic" condition. This risk seems to be safely reduced by the administration of metformin during gestation. We analyzed the metabolic changes in two hyperinsulinemic PCOS women, who became pregnant after 8 weeks of metformin therapy and continued taking the drug till delivery. An oral glucose tolerance test and an euglycemic hyperinsulinemic clamp were performed at baseline and, during metformin therapy, in pre-conceptional state and at each trimester of gestation. A pronounced decrease in peripheral insulin sensitivity occurred as the pregnancies proceeded (at the third trimester 51.7% and 41.1% of pregestational values in patient 1 and 2 respectively), along with an increase in stimulated insulin secretion (at the third trimester 120% and 50.6% of pregestational values in patient 1 and 2 respectively). Despite these findings, none of the studied subjects developed gestational diabetes or impaired glucose tolerance. This confirms that metformin may exert a protective role against such disturbances in hyperinsulinemic PCOS patients, probably by avoiding the gestational physiologic changes leading to a loss of the metabolic balance achieved by these subjects out of pregnancy. © 2004, Editrice Kurtis
The impact of dosage on ovulation induction by pulsatile gonadotropin-releasing hormone (Gn-RH) in hypothalamic amenorrhea.
No full textTwenty-four-hour urinary cortisol levels in Alzheimer disease and in dysthymia
No full textDuring senescence, homeostatic and stress-response capacities are impaired particularly in patients with dementia and depression. Therefore, the study of the hypotalamic-pituitary-adrenal (HPA) axis function, involved in the physiological adaptation processes to environmental stimuli, appears to be relevant. In this study, we evaluated the 24-hour urinary free cortisol in a group of 20 normal young adults (C) (12 males and 8 females, mean age 46 ± 4 years); in a normal elderly group of 23 subjects (15 males and 8 females, mean age 68 ± 9 years); in a group of 15 patients with Alzheimer disease (AD) (8 males and 7 females, mean age 70 ± 8 years) and in a group of 22 dysthyrnic elderly patients (8 males and 14 females, mean age 69 ± 4 years), to evaluate the mutual influence between these states and the HPA axis function. Subjects with depression different from dysthymia, under drug treatment or with acute illness or in chronic conditions, which could influence HPA axis function, were not included. The diagnoses of AD and dysthymia were established according to the DSM-IV criteria. We evaluated the 24-hour urinary cortisol using commercial RIA Kits (Radim, Pomezia, Italy) in all subjects. Statistical analysis was performed by means of the Student's t-test, in the normal elderly urinary cortisol values are 34.18 ± 13.85 μg/day, higher, but not significantly, than those of C, whose urinary cortisol is 27.78 ± 10.36 μg/day. In AD the urinary cortisol is 53.18 ± 17.49 μg/day and in dysthymic patients is 55.31 ± 26.93 7mu;g/day. Hyperactivity of HPA axis in AD (p<0.001) and in dysthymic patients (p<0.01) both compared to normal elderly and to C is evident. Our data confirm those of the literature and emphasize a low increase in 24-hour urinary cortisol in normal elderly compared to young adults and an involvement of the HPA axis in AD, with values of the 24-hour urinary cortisol significantly higher than those of C. Moreover, our data show a HPA axis hyperactivity in dysthymic patients, as reported in the literature for major depression. This hyperactivity of the HPA axis function, according to the "glucocorticoid cascade hypothesis", indicates that dysthymia might be considered as a very important risk factor for AD
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