The Experts below are selected from a list of 303 Experts worldwide ranked by ideXlab platform
Kunju Sathishkumar - One of the best experts on this subject based on the ideXlab platform.
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prenatal testosterone exposure leads to Gonadal Hormone dependent hyperinsulinemia and Gonadal Hormone independent glucose intolerance in adult male rat offspring
Biology of Reproduction, 2016Co-Authors: Amar S More, Jay S Mishra, Kathirvel Gopalakrishnan, Chellakkan S Blesson, Gary D V Hankins, Kunju SathishkumarAbstract:Elevated testosterone levels during prenatal life lead to hyperandrogenism and insulin resistance in adult females. This study evaluated whether prenatal testosterone exposure leads to the development of insulin resistance in adult male rats in order to assess the influence of Gonadal Hormones on glucose homeostasis in these animals. Male offspring of pregnant rats treated with testosterone propionate or its vehicle (control) were examined. A subset of male offspring was orchiectomized at 7 wk of age and reared to adulthood. At 24 wk of age, fat weights, plasma testosterone, glucose homeostasis, pancreas morphology, and gastrocnemius insulin receptor (IR) beta levels were examined. The pups born to testosterone-treated mothers were smaller at birth and remained smaller through adult life, with levels of fat deposition relatively similar to those in controls. Testosterone exposure during prenatal life induced hyperinsulinemia paralleled by an increased HOMA-IR index in a fasting state and glucose intolerance and exaggerated insulin responses following a glucose tolerance test. Prenatal androgen-exposed males had more circulating testosterone during adult life. Gonadectomy prevented hyperandrogenism, reversed hyperinsulinemia, and attenuated glucose-induced insulin responses but did not alter glucose intolerance in these rats. Prenatal androgen-exposed males had decreased pancreatic islet numbers, size, and beta-cell area along with decreased expression of IR in gastrocnemius muscles. Gonadectomy restored pancreatic islet numbers, size, and beta-cell area but did not normalize IRbeta expression. This study shows that prenatal testosterone exposure leads to a defective pancreas and skeletal muscle function in male offspring. Hyperinsulinemia during adult life is gonad-dependent, but glucose intolerance appears to be independent of postnatal testosterone levels.
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prenatal testosterone exposure leads to hypertension that is Gonadal Hormone dependent in adult rat male and female offspring
Biology of Reproduction, 2012Co-Authors: Vijayakumar Chinnathambi, Meena Balakrishnan, Chandrasekhar Yallampalli, Kunju SathishkumarAbstract:Prenatal testosterone exposure impacts postnatal reproductive and endocrine function, leading to alterations in sex steroid levels. Because Gonadal steroids are key regulators of cardiovascular function, it is possible that alteration in sex steroid Hormones may contribute to development of hypertension in prenatally testosterone-exposed adults. The objectives of this study were to evaluate whether prenatal testosterone exposure leads to development of hypertension in adult males and females and to assess the influence of Gonadal Hormones on arterial pressure in these animals. Offspring of pregnant rats treated with testosterone propionate or its vehicle (controls) were examined. Subsets of male and female offspring were gonadectomized at 7 wk of age, and some offspring from age 7 to 24 wk received Hormone replacement, while others did not. Testosterone exposure during prenatal life significantly increased arterial pressure in both male and female adult offspring; however, the effect was greater in males. Prenatal androgen-exposed males and females had more circulating testosterone during adult life, with no change in estradiol levels. Gonadectomy prevented hyperandrogenism and also reversed hypertension in these rats. Testosterone replacement in orchiectomized males restored hypertension, while estradiol replacement in ovariectomized females was without effect. Steroidal changes were associated with defective expression of Gonadal steroidogenic genes, with Star, Sf1, and Hsd17b1 upregulation in testes. In ovaries, Star and Cyp11a1 genes were upregulated, while Cyp19 was downregulated. This study showed that prenatal testosterone exposure led to development of gonad-dependent hypertension during adult life. Defective steroidogenesis may contribute in part to the observed steroidal changes.
Cheryl L Sisk - One of the best experts on this subject based on the ideXlab platform.
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Gonadal Hormone contributions to individual differences in eating disorder risk
Current Opinion in Psychiatry, 2019Co-Authors: Megan E Mikhail, Kristen M Culbert, Cheryl L Sisk, Kelly L KlumpAbstract:PURPOSE OF REVIEW Females experience eating disorders at substantially higher rates than males. Although sociocultural factors have traditionally been thought to underlie this sex disparity, accumulating evidence implicates differential exposure to Gonadal Hormones early in life. Gonadal Hormones also impact within-sex variability in disordered eating, helping to explain why not all women develop an eating disorder, and some men do. We review recent findings regarding these Gonadal Hormone effects and their implications for the etiology of eating disorders. RECENT FINDINGS Males are exposed to significantly higher testosterone levels than females perinatally, and this exposure appears to protect against later binge eating in males relative to females. Within-sex, higher estradiol levels among females and higher testosterone levels among males appear to be protective. Progesterone exhibits minimal direct phenotypic effects on disordered eating but appears to counteract the protective effects of estrogen in adult females. Importantly, Gonadal Hormone effects may be moderated by psychosocial factors. SUMMARY Evidence suggests that Gonadal Hormones play a critical role in the etiology of disordered eating. Overall, higher testosterone and estrogen appear to be protective across development. Additional research is needed to identify mechanisms underlying these effects and further explore interactions between hormonal and psychosocial risk.
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sex differences in binge eating Gonadal Hormone effects across development
Annual Review of Clinical Psychology, 2017Co-Authors: Kelly L Klump, Kristen M Culbert, Cheryl L SiskAbstract:Eating disorders are highly sexually differentiated disorders that exhibit a female predominance in risk. Most theories focus on psychosocial explanations to the exclusion of biological/genetic influences. The purpose of this descriptive review is to evaluate evidence from animal and human studies in support of Gonadal Hormone effects on sex differences in binge eating. Although research is in its nascent stages, findings suggest that increased prenatal testosterone exposure in males appears to protect against binge eating. Although pubertal testosterone may exert additional protective effects, the prenatal period is likely critical for the decreased risk observed in males. By contrast, studies indicate that, in females, it is the lack of prenatal testosterone coupled with the organizational effects of pubertal ovarian Hormones that may lead to increased binge eating. Finally, twin data suggest that changes in genetic risk may underlie these Hormone influences on sex differences across development.
Kelly L Klump - One of the best experts on this subject based on the ideXlab platform.
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Gonadal Hormone contributions to individual differences in eating disorder risk
Current Opinion in Psychiatry, 2019Co-Authors: Megan E Mikhail, Kristen M Culbert, Cheryl L Sisk, Kelly L KlumpAbstract:PURPOSE OF REVIEW Females experience eating disorders at substantially higher rates than males. Although sociocultural factors have traditionally been thought to underlie this sex disparity, accumulating evidence implicates differential exposure to Gonadal Hormones early in life. Gonadal Hormones also impact within-sex variability in disordered eating, helping to explain why not all women develop an eating disorder, and some men do. We review recent findings regarding these Gonadal Hormone effects and their implications for the etiology of eating disorders. RECENT FINDINGS Males are exposed to significantly higher testosterone levels than females perinatally, and this exposure appears to protect against later binge eating in males relative to females. Within-sex, higher estradiol levels among females and higher testosterone levels among males appear to be protective. Progesterone exhibits minimal direct phenotypic effects on disordered eating but appears to counteract the protective effects of estrogen in adult females. Importantly, Gonadal Hormone effects may be moderated by psychosocial factors. SUMMARY Evidence suggests that Gonadal Hormones play a critical role in the etiology of disordered eating. Overall, higher testosterone and estrogen appear to be protective across development. Additional research is needed to identify mechanisms underlying these effects and further explore interactions between hormonal and psychosocial risk.
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sex differences in binge eating Gonadal Hormone effects across development
Annual Review of Clinical Psychology, 2017Co-Authors: Kelly L Klump, Kristen M Culbert, Cheryl L SiskAbstract:Eating disorders are highly sexually differentiated disorders that exhibit a female predominance in risk. Most theories focus on psychosocial explanations to the exclusion of biological/genetic influences. The purpose of this descriptive review is to evaluate evidence from animal and human studies in support of Gonadal Hormone effects on sex differences in binge eating. Although research is in its nascent stages, findings suggest that increased prenatal testosterone exposure in males appears to protect against binge eating. Although pubertal testosterone may exert additional protective effects, the prenatal period is likely critical for the decreased risk observed in males. By contrast, studies indicate that, in females, it is the lack of prenatal testosterone coupled with the organizational effects of pubertal ovarian Hormones that may lead to increased binge eating. Finally, twin data suggest that changes in genetic risk may underlie these Hormone influences on sex differences across development.
Rosa Catalan - One of the best experts on this subject based on the ideXlab platform.
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Do FSH/LH ratio and Gonadal Hormone levels predict clinical improvement in postmenopausal schizophrenia women?
Archives of Women's Mental Health, 2017Co-Authors: Alexandre González-rodríguez, Miquel Bernardo, Rafael Penades, Barbara Arias, Mary V Seeman, Victoria Ruiz Cortés, Rosa CatalanAbstract:Menopause is a process characterized by a decline in estrogen levels and is therefore a period of biological vulnerability for psychotic relapse in women with schizophrenia. Our goal was to correlate not only Gonadal Hormone levels but also follicle-stimulating Hormone (FSH) and luteinizing Hormone (LH) levels with improvement in specific clinical symptoms. Thirty-seven acutely ill postmenopausal schizophrenia women with a newly initiated, clinically determined change in antipsychotic medication participated in a 12-week prospective observational outcome study. Scales used were the PANSS scale for psychotic symptoms, the PSP for functioning, and CGI for global clinical impression. Circulating FSH, LH, estradiol, progesterone, and testosterone serum levels were determined by chemiluminescent immunoassay. Partial correlational analyses were performed along with a Bonferroni significance correction ( p
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do fsh lh ratio and Gonadal Hormone levels predict clinical improvement in postmenopausal schizophrenia women
Archives of Womens Mental Health, 2017Co-Authors: Alexandre Gonzalezrodriguez, Miquel Bernardo, Rafael Penades, Barbara Arias, Victoria Ruiz Cortes, Mary V Seeman, Rosa CatalanAbstract:Menopause is a process characterized by a decline in estrogen levels and is therefore a period of biological vulnerability for psychotic relapse in women with schizophrenia. Our goal was to correlate not only Gonadal Hormone levels but also follicle-stimulating Hormone (FSH) and luteinizing Hormone (LH) levels with improvement in specific clinical symptoms. Thirty-seven acutely ill postmenopausal schizophrenia women with a newly initiated, clinically determined change in antipsychotic medication participated in a 12-week prospective observational outcome study. Scales used were the PANSS scale for psychotic symptoms, the PSP for functioning, and CGI for global clinical impression. Circulating FSH, LH, estradiol, progesterone, and testosterone serum levels were determined by chemiluminescent immunoassay. Partial correlational analyses were performed along with a Bonferroni significance correction (p < 0.0007). After adjustment for confounding factors, the FSH/LH ratio correlated positively with mean changes in PANSS positive scores, and there was a correlation with worsening of CGI total and cognitive scores. Testosterone was also positively associated with improvement in PANSS positive scores. However, after correction for multiple testing, the initial correlations were no longer statistically significant. In summary, while the Hormone assays we did in this small sample did not prove to be significantly linked to clinical improvement in any of the schizophrenia symptom domains, we recommend further investigation of pituitary, adrenal, and Gonadal Hormone ratios as potential markers of clinical improvement in this population.
Hannsmartin Lorenz - One of the best experts on this subject based on the ideXlab platform.
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adrenal and Gonadal Hormone variations during a febrile attack in a woman with tumor necrosis factor receptor associated periodic syndrome
The Journal of Clinical Endocrinology and Metabolism, 2005Co-Authors: Rainer H Straub, Peter Harle, Martin A Kriegel, Jurgen Scholmerich, Hannsmartin LorenzAbstract:CONTEXT: TNF-receptor-associated periodic syndrome (TRAPS) is a hereditary fever syndrome that results from mutations in the TNF-receptor superfamily 1A gene (TNFRSF1A). It is characterized by periodic fever, arthralgia, abdominal pain, myalgia, headache, and skin lesions. OBJECTIVE: Because adrenal and Gonadal Hormone cascades are modulated by TNF, this study aimed to investigate specific Hormones and enzyme steps during an attack phase in a woman with TRAPS. DESIGN: Morning blood samples were taken from a 38-yr-old woman before, during, and after the febrile episode in the late luteal, menstrual, and early follicular phase of the menstrual cycle, respectively. RESULTS: Serum cortisol levels were markedly increased throughout the entire observation period and demonstrated a dip during the attack phase. In contrast, serum levels of dehydroepiandrosterone and 17-hydroxyprogesterone demonstrated a sharp rise during the febrile episode. Dehydroepiandrosterone in relation to androstenedione or cortisol was increased. Indicative of aromatase activation, estrone and 17beta-estradiol demonstrated a marked increase during the attack phase. CONCLUSION: This study suggests that some important steroid Hormone-conversion steps are activated (aromatase) and inhibited (second step of the P450c17 and the 3beta-hydroxysteroid dehydrogenase) during the inflammatory attack phase in a TRAPS patient. These changes of enzyme pathways are typical on the basis of increased TNF signaling.
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clinical case seminar adrenal and Gonadal Hormone variations during a febrile attack in a woman with tumor necrosis factor receptor associated periodic syndrome
2005Co-Authors: Rainer H Straub, Martin A Kriegel, Hannsmartin LorenzAbstract:Context: TNF-receptor-associated periodic syndrome (TRAPS) is a hereditary fever syndrome that results from mutations in the TNFreceptor superfamily 1A gene (TNFRSF1A). It is characterized by periodic fever, arthralgia, abdominal pain, myalgia, headache, and skin lesions. Objective: Because adrenal and Gonadal Hormone cascades are modulated by TNF, this study aimed to investigate specific Hormones and enzyme steps during an attack phase in a woman with TRAPS. Design: Morning blood samples were taken from a 38-yr-old woman before, during, and after the febrile episode in the late luteal, menstrual, and early follicular phase of the menstrual cycle, respectively. Results: Serum cortisol levels were markedly increased throughout the entire observation period and demonstrated a dip during the attack phase. In contrast, serum levels of dehydroepiandrosterone and 17-hydroxyprogesterone demonstrated a sharp rise during the febrile episode. Dehydroepiandrosterone in relation to androstenedione or cortisol was increased. Indicative of aromatase activation, estrone and 17-estradiol demonstrated a marked increase during the attack phase. Conclusion: This study suggests that some important steroid Hormone-conversion steps are activated (aromatase) and inhibited (second step of the P450c17 and the 3-hydroxysteroid dehydrogenase) during the inflammatory attack phase in a TRAPS patient. These changesofenzymepathwaysaretypicalonthebasisofincreasedTNF signaling. (J Clin Endocrinol Metab 90: 5884–5887, 2005)