Growth Hormone - HBF3 Exam 2

#separator:tab #html:true #tags column:3 GH SynthesisGrowth hormone is a {{c1::peptide}} hormone that is synthesized and secreted by {{c1::somatotroph}} cells in the {{c2::anterior pituitary}}. "" HBF3::Exam2::Physiology::GrowthHormone(28) GH SynthesisGrowth hormone is stored in {{c1::granules}} unt...

#separator:tab #html:true #tags column:3 GH SynthesisGrowth hormone is a {{c1::peptide}} hormone that is synthesized and secreted by {{c1::somatotroph}} cells in the {{c2::anterior pituitary}}. "" HBF3::Exam2::Physiology::GrowthHormone(28) GH SynthesisGrowth hormone is stored in {{c1::granules}} until {{c2::GHRH}} from the {{c1::hypothalamus}} stimulates secretion.  "GHRH: Growth hormone releasing hormone" HBF3::Exam2::Physiology::GrowthHormone(28) GH SynthesisGH is a member of the {{c1::somatotropin}}/{{c1::prolactin}} family of hormones. These include GH itself, the {{c2::placental lactogens}}, also known as placental chorionic somatomammotropins, and prolactin.  "Except for prolactin, all on same locus on chr 17" HBF3::Exam2::Physiology::GrowthHormone(28) GH RegulationTwo hypothalamic hormones control growth hormone secretion: {{c2::GHRH}} and {{c1::somatostatin}}. {{c2::GHRH}} stimulates GH secretion while {{c1::somatostatin}} suppresses its release. "" HBF3::Exam2::Physiology::GrowthHormone(28) GH Regulation{{c1::GHRH}} is produced in the {{c2::arcuate nucleus}} of the hypothalamus. It {{c1::activates::activates/suppresses}} GH release and synthesis via a specific GPCR and the {{c2::cAMP/PKA}} signaling pathway. "" HBF3::Exam2::Physiology::GrowthHormone(28) GH Regulation{{c1::Somatostatin (SS)}} is produced in the {{c2::periventricular}} region of the hypothalamus. It {{c1::suppresses::activates/suppresses}} GH release and synthesis by inhibiting the {{c2::cAMP/PKA}} signaling pathway. "" HBF3::Exam2::Physiology::GrowthHormone(28) GH SecretionGrowth hormone secretion spikes throughout the day, but overall secretion follows a {{c1::diurnal}} pattern with elevated secretion at {{c1::night}}--particularly during {{c2::non-REM deep sleep}}. "" HBF3::Exam2::Physiology::GrowthHormone(28) GH SecretionHalf-life of GH: {{c1::20-25}} minutes "" HBF3::Exam2::Physiology::GrowthHormone(28) GH SecretionFactors that {{c1::suppress::stimulate/suppress}} GH secretion:1. {{c2::Growth hormone}}2. {{c2::IGF-1}}3. {{c3::Hyperglycermia}}4. {{c3::Cortisol}}5. {{c4::Xenobiotics}}, e.g. certain endocrine disruptors "" HBF3::Exam2::Physiology::GrowthHormone(28) GH SecretionFactors that {{c1::stimulate::stimulate/suppress}} GH secretion:1. {{c2::Energy deficiency}}: {{c4::hypoglycemia}}, vigorous exercise, {{c4::fasting}}2. {{c2::Certain amino acids}}: protein-rich meal, infusion of arginine3. {{c3::Hormones}}: sex steroids, {{c4::glucagon}}4. {{c3::Deep sleep}} (later stages of non-REM sleep) "" HBF3::Exam2::Physiology::GrowthHormone(28) GH ActionGH acts directly on its target cells by binding to and activating the GH receptor, or GHR. This initiates a {{c1::JAK/STAT}} based intracellular signaling cascade that leads to the activation the STAT family of {{c2::transcription factors}}. These proteins induce transcription of GH target genes, including {{c2::IGF1}}. "" HBF3::Exam2::Physiology::GrowthHormone(28) GH ActionIn the {{c1::liver}}, one of the primary GH target organs, GH action leads to {{c1::IGF-1}} production and release. "" HBF3::Exam2::Physiology::GrowthHormone(28) GH EffectsGH produces indirect, long-term effects through IGF-1, such as increasing {{c1::linear growth}}.  "" HBF3::Exam2::Physiology::GrowthHormone(28) GH EffectsIn addition to GH's chronic effects on growth, GH also has direct, {{c1::acute}} effects that shift energy metabolism to a more {{c2::prodiabetic}} state. These changes include increasing {{c3::gluconeogenesis}}, increasing {{c4::lipolysis}}, and decreasing {{c3::glucose uptake}} by muscle.  "Pathological circumstances - chronic GH excess can promote diabetes" HBF3::Exam2::Physiology::GrowthHormone(28) IGFsIGF-1 and IGF-2 are both {{c1::peptide}} hormones with insulin-like activities. {{c3::IGF-2}} has a less well understood physiological role but may be important for {{c2::fetal}} and {{c2::neonatal}} growth. {{c3::IGF-1}} is produced by the liver in response to GH signaling and exerts GH's growth-promoting effects. "IGF: Insulin-like growth factor" HBF3::Exam2::Physiology::GrowthHormone(28) IGFsThe majority of IGFs in circulation are bound to carrier proteins, {{c1::IGFBPs}}. {{c1::IGFBPs}} {{c2::prolong}} the biological half-life of the hormones and {{c2::blunt}} their biological effects by slowly releasing small amounts of free hormone. HBF3::Exam2::Physiology::GrowthHormone(28) IGF SignalingThe IGF-1 receptor is structurally similar to the {{c1::insulin}} receptor and can bind {{c1::insulin}} with lower affinity. The IGF-1 signaling cascade is similar to that of {{c1::insulin}} binding to its receptor.  "" HBF3::Exam2::Physiology::GrowthHormone(28) IGF-1 and GrowthIGF-1 levels are {{c1::low}} at birth and gradually {{c1::rise}} during childhood. Levels peak at {{c2::puberty}} and gradually decline during adulthood.  "" HBF3::Exam2::Physiology::GrowthHormone(28) Regulation of GH/IGF-1Regulation of GH and IGF-1 occurs through multiple negative feedback loops:Hypothalamus: IGF-1 {{c2::suppresses::increases/suppresses}} {{c1::GHRH}} release and {{c2::increases::increases/suppresses}} {{c1::somatostatin}} releaseAnterior pituitary: GH and IGF-1 both {{c3::negatively::negatively/positively}} feedback on the somatotrophs in the anterior pituitary, {{c3::decreasing::increasing/decreasing}} GH release  "" HBF3::Exam2::Physiology::GrowthHormone(28) Pathologies - GH{{c3::Hypersecretion}} of GH can lead to {{c1::acromegaly}} or {{c1::gigantism}}, depending on whether these high levels occur before or after post-{{c2::puberty}} closure of the {{c2::epiphyseal plate}}. The most common cause of {{c3::elevated}} growth hormone release is a {{c3::benign pituitary adenoma}}. "AcromegalyGigantism" HBF3::Exam2::Physiology::GrowthHormone(28) Pathologies - GHHyper-secretion of GH during {{c1::childhood}} leads to excessive linear body growth: {{c1::gigantism}}. If this occurs post-puberty, the outcome is {{c2::acromegaly}}, in which the bones become {{c2::deformed}} rather than elongated. Both conditions can be accompanied by {{c3::insulin resistance}} and {{c3::type 2 diabetes}}. "AcromegalyGigantism" HBF3::Exam2::Physiology::GrowthHormone(28) Pathologies - GHAcromegaly is characterized by a coarsening of facial features including an increased size of the mandible, which can cause the jaw to {{c2::protrude}} (prognathism). Cartilage in the larynx may thicken, making the voice {{c1::deep}} and {{c1::husky}}.  "AcromegalyGigantism" HBF3::Exam2::Physiology::GrowthHormone(28) Pathologies - GHLow GH production or defects in the signaling pathway can cause {{c2::dwarfism}}. An example of dwarfism caused by a genetic defect in GH signaling is {{c1::Laron syndrome}}. This syndrome is categorized as a {{c2::Growth Hormone Insensitivity Syndrome (GHIS)}} and is caused by inactivating mutations in the GH receptor. "" HBF3::Exam2::Physiology::GrowthHormone(28)