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Estrogen, Bone, Growth and Sex: A Sea Change in Conventional Wisdom

Department of Pediatrics, University of California, San Francisco, USA
  • Melvin M. Grumbach
Veröffentlicht/Copyright: 22. Juli 2014

ABSTRACT

The discovery of a man with a homozygous mutation in the estrogen receptor α gene, which results in estrogen-receptor α resistance, and of males and females with autosomal recessive mutations in the CYP19 gene encoding aromatase, which leads to a failure to synthesize estrogens, has challenged conventional wisdom about the 'unimportant' role of estrogen in the male. For example, in the male, estrogen (not androgen), derived from direct testicular secretion (~20%) and from extragonadal aromatization of testosterone and androstenedione (~80%), is the critical sex hormone in the pubertal growth spurt, skeletal maturation, accrual of peak bone mass, and the maintenance of bone mass in the adult. Estrogen stimulates chondrogenesis in the epiphyseal growth plate increasing pubertal linear growth. At puberty, estrogen promotes skeletal maturation and the gradual, progressive closure of the epiphyseal growth plate, possibly as a consequence of both estrogen-induced vascular and osteoblastic invasion and the termination of chondrogenesis. In addition, during puberty and into the third decade, estrogen has an anabolic effect on the osteoblast and an apoptotic effect on the osteoclast, increasing bone mineral acquisition in axial and appendicular bone. In the adult, estrogen is important in maintaining the constancy of bone mass through its effects on remodeling and bone turnover. Establishing a role for estrogen does not exclude a direct action of testosterone on bone in the human male (especially on cortical bone), but this action is less characterized than thought in the past and is relatively minor in comparison with the major effect of estrogen in the male.

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 21.10.2025 von https://www.degruyterbrill.com/document/doi/10.1515/jpem-2000-s619/html
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