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Endocrine Disorders
Published in Praveen S. Goday, Cassandra L. S. Walia, Pediatric Nutrition for Dietitians, 2022
Lisa Spence, Nana Adwoa Gletsu Miller, Tamara S. Hannon
Deficiency in growth hormone signaling is an endocrine disorder that affects 1:4,000–1:10,000 children. Without the action of growth hormone, longitudinal growth of the bones is slow or flat and the child will not follow growth curves from age 2 onwards. Other signs and symptoms of growth hormone deficiency are abnormal levels of insulin-like growth factor and insulin-like growth factor binding protein (both which are stimulated by growth hormone), as well as overweight and delayed puberty. In cases when deficiency of growth hormone is established as the cause of short stature, and if the condition is treated early, providing growth hormone by injection is effective treatment, enabling children to reach normal height. During treatment, frequent monitoring by the medical team is important to manage side effects (e.g., headache, fluid retention, muscle and joint ache, slippage of hip bones). Evaluation during treatment is also important since many cases do not respond to growth hormone therapy.
Pituitary Gland
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Growth hormone have direct effects on cellular responses and indirect effects via the stimulation of production and release of insulin growth factor-1 (IGF-1), a mediator of several of GH effects on target tissues.
An Overview of the Biological Actions and Neuroendocrine Regulation of Growth Hormone
Published in George H. Gass, Harold M. Kaplan, Handbook of Endocrinology, 2020
The large volume of data published thus far on the biological actions of growth hormone suggest a critical role not only in body growth but in maintenance of cellular function in a number of tissues of adult animals. Recent studies demonstrating the effects of growth hormone on cells of the immune system, cardiovascular system, bone, kidney, and more recently brain suggest that this hormone has an important role in maintaining cellular function within systems and coordinating the maintenance of cellular function between systems. Despite progress in identifying the biological actions of growth hormone, mechanisms responsible for the regulation of episodic growth hormone release have proceeded at a slower rate. Although it is clear that somatostatin and GHRH are necessary for episodic release, the diversity of hypothalamic peptides and the complex regulation of these peptides by neurotransmitters has complicated investigations. Nevertheless, the general consensus is that trough levels of growth hormone result from somatostatin secretion whereas peak levels are regulated by GHRH. The dynamic interaction between these peptides contributes to growth hormone secretory dynamics. Both neurotransmitter and neuropeptide levels regulate growth hormone through either inhibition or facilitation of somatostatin and GHRH secretion. Although much has been learned concerning the complex interrelationships between neurotransmitters, neuropeptides, and the secretion of somatostatin and GHRH, the specific mechanisms that interact to regulate these compounds remain unknown.
Emerging therapeutic targets for anorexia nervosa
Published in Expert Opinion on Therapeutic Targets, 2023
Growth hormone is produced in the pituitary gland and involved in numerous physiological functions such as regulation of body weight, body composition and glucose homeostasis. Since a growth hormone resistance associated with reduced downstream insulin-like growth factor-1 levels has been described in young patients with anorexia nervosa [92] likely contributing to delayed puberty onset and reduced body height, growth hormone was put into the spotlight also as a possible treatment target. One study investigated the effects of supraphysiological levels of recombinant growth hormone in patients with anorexia nervosa for 12 weeks. This treatment did not induce an increase in circulating insulin-like growth factor-1 levels but decreased fat mass without effect on body weight [93]. In adolescents with anorexia nervosa treatment with recombinant growth hormone induced an increase of insulin-like growth factor-1 and led to a stimulation of height velocity [94]. Data from this pilot study should be followed up in a larger and controlled manner.
MiR-23b targets GATA6 to down-regulate IGF-1 and promote the development of congenital heart disease
Published in Acta Cardiologica, 2022
Guo-Jin Huang, Xue-Liang Xie, Yong Zou
Numerous studies have corroborated that GATA6 is expressed during heart development [27,28]. At present, it has been found that GATA6 mutations in CHD include ASD, VSD, patent ductus arteriosus, pulmonary valve stenosis, persistent truncus arteriosus, and TOF [27,29]. GATA6 is indispensable to the normal expression of the transcription factor network during the development of cardiomyocytes. Kodo et al. [13] have confirmed that GATA6 can directly regulate the brain signal protein 3 C-plexus protein A2 signal pathway, affect the normal migration of cardiac neural crest cells, resulting in abnormal development of the cardiac outflow tract. Moreover, some studies have also confirmed that GATA6 may influence the development of the heart by regulating the signal of bone morphogenetic protein 4 [30,31]. In short, GATA6 can regulate downstream target genes, thus affecting cardiac development. In our research, we found that miR-23b can target the regulation of GATA6 in cardiomyocytes, thus affecting cell proliferation and apoptosis. As a growth hormone-dependent peptide, IGF-1 plays an indispensable role in tissue growth and differentiation. According to Carlos Stocco et al. [32] and Yvonne Y. Hui et al. [21], down-regulation of GATA6 can induce the decrease of IGF-1 expression. In this study, we also confirmed this regulatory mechanism in the CHD cells.
Hematological manifestations and complications of Gaucher disease
Published in Expert Review of Hematology, 2021
Shoshana Revel-Vilk, Jeff Szer, Ari Zimran
In children the only GD-specific therapy is ERT as SRT is only approved for adults (a clinical trial of eliglustat for children with GD is ongoing, NCT03485677). Accordingly, the decision after diagnosis is whether to start ERT and if so, at what dose. Asymptomatic patients may be followed safely untreated for many years [49] and all asymptomatic adults were once children. Symptomatic children, including relatively mildly affected patients with significant short stature, should be treated. Treatment with growth hormone is rarely needed for GD growth retardation [50]. The dose may be higher for those with more severe manifestations, i.e. bone pain, MRI evidence of a risk of bone infarction, signs of hypersplenism, etc. Like adults, if there is a poor response to low dose ERT the dose should be increased [48].