Startseite Hypothalamic Growth Hormone-Insulin-like Growth Factor-I Axis across the Human Life Span
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Hypothalamic Growth Hormone-Insulin-like Growth Factor-I Axis across the Human Life Span

Department of Internal Medicine, Division of Endocrinology, University of Turin, Turin, Italy
  • Ezio Ghigo , Emanuela Arvat , Laura Gianotti , Fabio Lanfranco , Fabio Broglio , Gianluca Aimaretti , Mauro Maccario und Franco Camanni
Veröffentlicht/Copyright: 22. Juli 2014
Journal of Pediatric Endocrinology and Metabolism
Aus der Zeitschrift Journal of Pediatric Endocrinology and Metabolism Band 13 Heft s2

ABSTRACT

The activity of the growth hormone (GH)- insulin-like growth factor-I (IGF-I) axis undergoes marked variations across the human life span, mainly reflecting age-related changes in the neural control of somatotroph function. IGF-I secretion generally reflects GH status, except in newborns, who secrete high levels of GH but low levels of IGF-I. Changes in the gonadal steroid milieu, particularly estradiol, play a major role in the enhanced activity of the GH-IGF-I axis at puberty and probably reflect further changes in the neuroendocrine control of somatotroph secretion. The change in responsiveness of somatotrophs to various stimuli, including GHRH, is not as marked as the spontaneous secretion of GH at puberty. However, in childhood, somatotrophs are unusually refractory to the somatostatin-mediated negative GH autofeedback mechanism. Normal children show normal responsiveness to the stimulatory influence of α-adrenergic and cholinergic agonists, galanin and arginine, but the activating effect of these stimuli on somatotroph secretion is reduced in elderly individuals, with the notable exception of arginine. Arginine potentiates both spontaneous and GHRH-induced GH secretion to the same extent in normally growing children, adults and elderly individuals, indicating that the releasable pool of GH is generally preserved across the human life span. Thus, the reduction in spontaneous and GHRH-induced GH secretion in the elderly probably reflects age-related changes in neurotransmitter control, leading to GHRH hypoactivity and absolute or relative somatostatin hyperactivity in the aged hypothalamus. Cholinergic impairment in the aging brain probably involves hypothalamic pathways and leads to decreased activity of the GH-IGF-I axis in normal and elderly individuals, as well as in individuals with premature brain aging. However, there is evidence indicating that age-related variations in the activity of the natural GH-secretagogue ligand(s) at the hypothalamic level could also play a role in the age-dependent changes in the GH-IGF-I axis.

Keywords: growth hormone; human life span; insulin-like growth factor-I; neurotransmitters
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
https://doi.org/10.1515/jpem-2000-s624
Schlagwörter für diesen Artikel
growth hormone; human life span; insulin-like growth factor-I; neurotransmitters

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
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