Growth hormone-releasing hormone (GHRH) receptor mutation and dwarfism: after the mouse, the human
Jérôme Bertherat
Abstract
Jérôme Bertherat
Abstract
Synthesis and secretion of growth hormone by the anterior pituitary gland is mainly controlled by two antagonist hypothalamic neuropeptides: the stimulatory hormone GHRH and the inhibitory hormone somatostatin. The GHRH receptor (GHRH-R) is a member of the seven-transmembrane G-proteincoupled receptor superfamily. It interacts with Gs protein to stimulate adenylate cyclase activity and cyclic AMP (cAMP) production. Both GHRH and cAMP are known to be involved in somatotroph proliferation and differentiation. Growth hormone-releasing hormone was purified for the first time in 1982 from a pancreatic tumor responsible for acromegaly and pituitary hyperplasia. In transgenic mice, overexpression of GHRH causes also gigantism and somatotroph hyperplasia or tumor.
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Synthesis and secretion of growth hormone by the anterior pituitary gland is mainly controlled by two antagonist hypothalamic neuropeptides: the stimulatory hormone GHRH and the inhibitory hormone somatostatin. The GHRH receptor (GHRH-R) is a member of the seven-transmembrane G-proteincoupled receptor superfamily. It interacts with Gs protein to stimulate adenylate cyclase activity and cyclic AMP (cAMP) production. Both GHRH and cAMP are known to be involved in somatotroph proliferation and differentiation. Growth hormone-releasing hormone was purified for the first time in 1982 from a pancreatic tumor responsible for acromegaly and pituitary hyperplasia. In transgenic mice, overexpression of GHRH causes also gigantism and somatotroph hyperplasia or tumor.
Key concepts: Endocrinology, Internal medicine, Growth-hormone-releasing hormone receptor, Somatotropic cell, Growth hormone–releasing hormone, Acromegaly, Somatostatin, Gigantism