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Estrogen Treatment and Estrogen Suppression: Metabolic Effects in Adolescence

Nemours Children’s Clinic and Research Programs, Jacksonville, Florida and Johns Hopkins University School of Hygiene and Public Health, Baltimore, Maryland, USA
  • Nelly Mauras , Valerie Hayes und Kimberly O. O’Brien
Veröffentlicht/Copyright: 22. Juli 2014

ABSTRACT

The metabolic consequences of reaching full reproductive maturity in humans involve not only growth hormone (GH) and insulin-like growth factor-I, but also the collaborative interaction of the gonadal sex steroids. Estrogen is critical for completing linear growth. It also inhibits bone resorption, decreases plasma lipid levels and serves as an antiatherosclerotic agent. Our studies show that, in low doses, estrogen increases GH production, increases calcium absorption and decreases bone turnover; however, unlike testosterone, estrogen has no effects as a protein-anabolic agent, at least at the whole body level. Studies of selective estrogen suppression, achieved using a potent aromatase inhibitor, show that estrogen is the main regulator of the gonadotropin axis. In boys, selective aromatase blockade may have a role in delaying epiphyseal fusion. Large placebo-controlled trials will be required to study this effect further.

Published Online: 2014-07-22
Published in Print: 2000-12-01

© 2014 by Walter de Gruyter Berlin/Boston

Artikel in diesem Heft

  1. Titelei
  2. TABLE OF CONTENTS
  3. Foreword
  4. What Happens When Growth Hormone is Discontinued at Completion of Growth? Metabolic Aspects
  5. Growth Hormone Deficiency and Peak Bone Mass
  6. Optimal Strategy for Management of Pituitary Disease in the Growth Hormone-Deficient Teenager
  7. Ethical Dilemmas in Pediatric Endocrinology: Growth Hormone for Short Normal Children
  8. Evidence-Based Approach to Growth Hormone Replacement Therapy in Adults, with Special Emphasis on Body Composition
  9. Evidence-Based Growth Hormone Therapy Prediction Models
  10. New Paradigms for Growth Hormone Treatment in the 21st Century: Prediction Models
  11. Role of Insulin-like Growth Factor Monitoring in Optimizing Growth Hormone Therapy
  12. Knockout Mice Challenge Our Concepts of Glucose Homeostasis and the Pathogenesis of Diabetes Mellitus
  13. Type 2 Diabetes Mellitus in Children: Pathophysiology and Risk Factors
  14. Emergence of Type 2 Diabetes Mellitus in Children: Epidemiological Evidence
  15. Treatment of Type 2 Diabetes Mellitus in Children and Adolescents
  16. Diagnosis of Maturity-Onset Diabetes of the Young in the Pediatric Diabetes Clinic
  17. Thrifty Genotypes and Phenotypes in the Pathogenesis of Type 2 Diabetes Mellitus
  18. Estradiol: A Protective Factor in the Adult Brain
  19. Estrogen Treatment and Estrogen Suppression: Metabolic Effects in Adolescence
  20. Estrogen, Bone, Growth and Sex: A Sea Change in Conventional Wisdom
  21. Route-Dependent Endocrine and Metabolic Effects of Estrogen Replacement Therapy
  22. Telomerase and the Cellular Lifespan: Implications for the Aging Process
  23. Human Aging and Progeria
  24. A Role for the Somatotropic Axis in Neural Development, Injury and Disease
  25. Hypothalamic Growth Hormone-Insulin-like Growth Factor-I Axis across the Human Life Span
  26. The Lost Voice: A History of the Castrato
  27. SELECTED POSTER ABSTRACTS
  28. GROWTH. FETAL GROWTH. SGA
  29. SYNDROMES: TURNER. PRADER-WILLI. NOONAN. PHP. OTHERS
  30. GHD. HYPOPITUITARISM. KIGS
  31. METABOLIC. GENETIC. ADULT. ACROMEGALY
  32. GH. IGF. IGFBPs
  33. GROWTH IN SYSTEMIC DISEASE. CRI. RICKETS. STEROIDS
Heruntergeladen am 31.10.2025 von https://www.degruyterbrill.com/document/doi/10.1515/jpem-2000-s618/pdf
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