TY - CHAP
T1 - Systems-Level Analysis of Physiological Regulatory Interactions Controlling Complex Secretory Dynamics of the Growth Hormone Axis
T2 - A Dynamical Network Model
AU - Chen, Lubin
AU - Veldhuis, Johannes D.
AU - Johnson, Michael L.
AU - Straume, Martin
N1 - Funding Information:
Support has been provided by the National Science Foundation Center for Biological Timing (DIR 8920162), a National Institutes of Health NICHD RCDA award to J.D.V. (1K04HD00634), the NIH NICHD Reproduction Research Center at the University of Virginia Health Sciences Center (1P30HD28934-01A1; J.D.V.), the NIH Center for Fluorescence Spectroscopy of the University of Maryland at Baltimore (RR-08119; M.L.J.), and NIH Grant GM35154 (M.L.J.).
PY - 1995/1/1
Y1 - 1995/1/1
N2 - This chapter presents systems-level analysis of physiological regulatory interactions controlling complex secretory dynamics of the growth hormone axis. Time-series data of growth hormone (GH) concentrations in the circulation of humans and of other animal models clearly demonstrate pulsatile patterns indicative of both rhythmic and episodic release from the pituitary gland. Understanding the physiological mechanisms that control the complex secretory dynamics exhibited by the GH neuroendocrine axis requires detailed appreciation of a highly regulated phenomenon—that is, dependent on functional interactions among a large number of processes comprising an exceedingly complex network of stimulatory and inhibitory feedback. The primary regulatory species responsible for mediating pituitary GH release are two hypothalamic peptides, a stimulatory factor, GH-releasing hormone (GHRH), and an inhibitory tetradecapeptide, somatostatin (SRIH). GHRH and SRIH are secreted from the median eminence of the hypothalamus into the hypophysial portal blood to be transported to the pituitary gland, where their influence on GH production and secretion is exerted. Growth hormone, after being released into the systemic circulation, stimulates production of insulin-like growth factor-I (IGF-I) in numerous peripheral tissues, including liver, bone, and muscle. It is IGF-I that serves the role of primary mediator of GHs peripheral effects. The GH neuroendocrine axis is a closed-loop system because both GH and IGF-I exert regulatory feedback on the hypothalamus in the form of decreasing GHRH and increasing SRIH signaling.
AB - This chapter presents systems-level analysis of physiological regulatory interactions controlling complex secretory dynamics of the growth hormone axis. Time-series data of growth hormone (GH) concentrations in the circulation of humans and of other animal models clearly demonstrate pulsatile patterns indicative of both rhythmic and episodic release from the pituitary gland. Understanding the physiological mechanisms that control the complex secretory dynamics exhibited by the GH neuroendocrine axis requires detailed appreciation of a highly regulated phenomenon—that is, dependent on functional interactions among a large number of processes comprising an exceedingly complex network of stimulatory and inhibitory feedback. The primary regulatory species responsible for mediating pituitary GH release are two hypothalamic peptides, a stimulatory factor, GH-releasing hormone (GHRH), and an inhibitory tetradecapeptide, somatostatin (SRIH). GHRH and SRIH are secreted from the median eminence of the hypothalamus into the hypophysial portal blood to be transported to the pituitary gland, where their influence on GH production and secretion is exerted. Growth hormone, after being released into the systemic circulation, stimulates production of insulin-like growth factor-I (IGF-I) in numerous peripheral tissues, including liver, bone, and muscle. It is IGF-I that serves the role of primary mediator of GHs peripheral effects. The GH neuroendocrine axis is a closed-loop system because both GH and IGF-I exert regulatory feedback on the hypothalamus in the form of decreasing GHRH and increasing SRIH signaling.
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U2 - 10.1016/S1043-9471(06)80037-6
DO - 10.1016/S1043-9471(06)80037-6
M3 - Chapter
AN - SCOPUS:0000549402
T3 - Methods in Neurosciences
SP - 270
EP - 310
BT - Methods in Neurosciences
ER -