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Chapter 11

Chapter 11. Endocrine Glands - Secretion & Action of Hormones. 11-1. Chapter 11 Outline Overview Chemical Classification of Hormones Hormonal Actions & Interactions Mechanisms of Hormone Action Pituitary Gland Adrenal Gland Thyroid Gland Islets of Langerhans

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Chapter 11

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  1. Chapter 11 Endocrine Glands - Secretion & Action of Hormones 11-1

  2. Chapter 11 Outline • Overview • Chemical Classification of Hormones • Hormonal Actions & Interactions • Mechanisms of Hormone Action • Pituitary Gland • Adrenal Gland • Thyroid Gland • Islets of Langerhans • Miscellaneous Glands & Hormone • Autocrine & Paracrine Regulation 11-2

  3. Overview 11-3

  4. Endocrine Glands • Are ductless & secrete hormones into bloodstream • Hormones go to target cells that contain receptor proteins for it • Neurohormones are secreted into blood by specialized neurons • Hormones affect metabolism of targets Fig 11.1 11-4

  5. 11-5

  6. Chemical Classification of Hormones 11-6

  7. Chemical Classification of Hormones • Amine hormones are derived from tyrosine or tryptophan • Include NE, Epi, thyroxine, melatonin • Polypeptide/protein hormones are chains of amino acids • Include ADH, GH, insulin, oxytocin, glucagon, ACTH, PTH • Glycoproteins include LH, FSH, TSH • Steroids are lipids derived from cholesterol • Include testosterone, estrogen, progesterone & cortisol 11-7

  8. Fig 11.2 11-8

  9. Chemical Classification of Hormones continued • Steroid & thyroid hormones are lipids • Can diffuse into target cells • The 2 major thyroid hormones are shown in Fig 11.3 11-9

  10. Prohormones & Prehormones • Prohormones are precursors of hormones • E.g. proinsulin • Prehormones are precursors of prohormones • E.g. preproinsulin • Some hormones are inactive until activated by target cells • E.g. thyroxine (T4) is inactive until converted to T3 in target cells 11-10

  11. Hormonal Actions & Interactions 11-11

  12. Common Aspects of Neural & Endocrine Regulation • Both NS & endocrine system use chemicals to communicate • Difference between NTs & hormones is transport in blood & more diversity of effects in hormone targets • Some chemicals are used as hormones & NTs • Targets for both NTs & hormones must have specific receptor proteins • Must be way to rapidly inactivate both 11-12

  13. Hormone Interactions • A tissue usually responds to # of hormones • 2 hormones are synergistic if work together to produce an effect • Produce a larger effect together than individual effects added together • A hormone has permissiveeffect if it enhances responsiveness of a target organ to 2nd hormone • If action of 1 hormone inhibits effect of another, it is antagonistic 11-13

  14. Hormone Levels & Tissue Responses • Half-life is time required for blood level to be reduced by half • Ranges from mins to hrs for most (days for thyroid hormones) • Normal tissue responses are produced only when hormones are in physiological range • High (pharmacological) doses can cause # of side effects • Probably by binding to receptors of other hormones 11-14

  15. Hormone Levels & Tissue Responses continued • Priming effect (upregulation) occurs when a hormone induces more of its own receptors in target cells • Results in greater response in target cell • Desensitization (downregulation) occurs after long exposure to high levels of polypeptide hormone • Subsequent exposure to this hormone produces a lesser response • Due to decrease in # of receptors on targets • Most peptide hormones have pulsatilesecretion which prevents downregulation 11-15

  16. Mechanisms of Hormone Action 11-16

  17. Mechanisms of Hormone Action • Target cell receptors show specificity, high affinity, & low capacity for a hormone • Lipid hormones have receptors in target's cytoplasm &/or nucleus because can diffuse thru plasma membrane • Receptors for water-solubles are on surface of target cell 11-17

  18. Hormones That Bind to Nuclear Receptor Proteins • Lipid hormones travel in blood attached to carrier proteins • They dissociate from carriers to pass thru plasma membrane of target • Receptors are called nuclear hormone receptors Fig 11.4 11-18

  19. Nuclear Hormone Receptors • Serve as transcription factors when bound to hormone ligands • Activate transcription • Constitute a "superfamily" composed of steroid family & thyroid hormone family (which includes vitamin D & retinoic acid) 11-19

  20. Nuclear Hormone Receptors • Have ligand (hormone)-binding& DNA-binding domains • Binds hormone & translocates to nucleus • Binds to hormone-response element (HRE) on DNA located adjacent to target gene Fig 11.5 11-20

  21. Mechanisms of Steroid Hormones • HRE consists of 2 half-sites • 2 ligand-bound receptors have to bind to each HRE (dimerization) • This stimulates transcription of target gene Fig 11.5 11-21

  22. Mechanism of Thyroid Hormone Action • Thyroid secretes 90% T4 (thyroxine) & 10% T3 • 99.96% of T4 in blood is bound to carrier protein (thyroid binding globulin - TBG) • Only free can enter cells, so bound is reservoir • T4 converted to T3 inside cell • T3 binds to receptor protein located in nucleus 11-22

  23. Mechanism of Thyroid Hormone Actioncontinued • T3 & receptor bind to 1 half-site • Other half-site binds retinoic acid • Two partners form heterodimer that activates HRE • Stimulates transcription of target gene Fig 11.7 11-23

  24. Hormones That Use 2nd Messengers • Water soluble hormones use cell surface receptors because cannot pass through plasma membrane • Actions are mediated by 2nd messengers • Hormone is extracellular signal; 2nd messenger carries signal from receptor to inside of cell 11-24

  25. Adenylate Cyclase-cAMP • Mediates effects of many polypeptide & glycoprotein hormones • Hormone binds to receptor causing dissociation of a G-protein subunit Fig 11.8 11-25

  26. Adenylate Cyclase-cAMP continued • G-protein subunit binds to & activates adenylate cyclase • Which converts ATP into cAMP • cAMP attaches to inhibitory subunit of protein kinase Fig 11.8 11-26

  27. Adenylate Cyclase-cAMP continued • Inhibitory subunit dissociates, activating protein kinase • Which phosphorylates enzymes that produce hormone’s effects • cAMP inactivated by phosphodiesterase Fig 11.8 11-27

  28. Phospholipase-C-Ca2+ • Serves as 2nd messenger system for some hormones • Hormone binds to surface receptor, activates G-protein, which activates phospholipase C Fig 11.9 11-28

  29. Phospholipase-C-Ca2+ • Phospholipase C splits a membrane phospholipid into 2nd messengers IP3 & DAG • IP3 diffuses through cytoplasm to ER • Causing Ca2+ channels to open Fig 11.9 11-29

  30. Phospholipase-C-Ca2+ continued • Ca2+ diffuses into cytoplasm & binds to & activates calmodulin • Ca2+-Calmodulin activates protein kinases which phosphorylate enzymes that produce hormone's effects 11-30

  31. Epi Can Act Via Two 2nd Messengers Fig 11.10 11-31

  32. Tyrosine Kinase 2nd Messenger System • Is used by insulin & many growth factors to cause cellular effects • Surface receptor is tyrosine kinase • Consists of 2 units that form active dimer when insulin binds Fig 11.11 11-32

  33. Tyrosine Kinase 2nd Messenger System • Activated tyrosine kinase phosphorylates signaling molecules that induce hormone/growth factor effects Fig 11.11 11-33

  34. Pituitary Gland 11-34

  35. Pituitary Gland • Pituitary gland is located beneath hypothalamus at base of forebrain Fig 8.16 11-35

  36. Pituitary Gland continued • Is structurally & functionally divided into anterior & posterior lobes • Hangs below hypothalamus by infundibulum • Anterior produces own hormones • Controlled by hypothalamus • Posterior stores & releases hormones made in hypothalamus Fig 11.12 11-36

  37. Anterior Pituitary • Secretes 6 trophic hormones that maintain size of targets • High blood levels cause target to hypertrophy • Low levels cause atrophy 11-37

  38. Anterior Pituitary continued • Growth hormone(GH) promotes growth, protein synthesis, & movement of amino acids into cells • Thyroid stimulating hormone (TSH) stimulates thyroid to produce & secrete T4 & T3 • Adrenocorticotrophic hormone (ACTH) stimulates adrenal cortex to secrete cortisol, aldosterone • Follicle stimulating hormone (FSH) stimulates growth of ovarian follicles & sperm production • Luteinizinghormone (LH) causes ovulation & secretion of testosterone in testes • Prolactin (PRL) stimulates milk production by mammary glands 11-38

  39. Anterior Pituitary continued • Release of A. Pit. hormones is controlled by hypothalamic releasing & inhibitingfactors & by feedback from levels of target gland hormones 11-39

  40. Anterior Pituitary continued Fig 11.15 • Releasing & inhibiting hormones from hypothalamus are released from axon endings into capillary bed in median eminence • Carried by hypothalamo-hypophyseal portal system directly to another capillary bed in A. Pit. • Diffuse into A. Pit. & regulate secretion of its hormones 11-40

  41. Feedback Control of Anterior Pituitary • Involves short feedback loop in which retrograde flow of blood & hormones from A. Pit. to hypothalamus inhibits secretion of releasing hormone • Involves negative feedback of target gland hormones • & during menstrual cycle, estrogen stimulates “LH surge” by positive feedback Fig 11.17 11-41

  42. Higher Brain Function & Anterior Pituitary Secretion • Hypothalamus receives input from higher brain centers that can affect A. Pit. secretion • E.g. psychological stress affects circadian rhythms, menstrual cycle, & adrenal hormones 11-42

  43. Stores & releases 2 hormones produced in hypothalamus: Antidiuretic hormone (ADH/vasopressin) which promotes H20 conservation by kidneys Oxytocin which stimulates contractions of uterus during parturition & contractions of mammary gland alveoli for milk-ejection reflex Posterior Pituitary 11-43

  44. Hypothalamic Control of Posterior Pituitary • Supraoptic nuclei of hypothalamus produce ADH • Paraventricular nuclei produce oxytocin • Both transported along hypothalamo-hypophyseal tract to posterior pituitary • Release controlled in hypothalamus by neuroendocrine reflexes Fig 11.13 11-44

  45. Adrenal Gland 11-45

  46. Adrenal Glands • Sit on top of kidneys • Each consists of outer cortex & inner medulla • 2 arise differently during development Fig 11.18 11-46

  47. Adrenal Glands • Medulla synthesizes & secretes 80% Epi & 20% NE • Controlled by sympathetic • Cortex is controlled by ACTH & secretes: • Cortisol which inhibits glucose utilization & stimulates gluconeogenesis • Aldosterone which stimulate kidneys to reabsorb Na+ and secrete K+ • & some supplementary sex steroids 11-47

  48. Adrenal Cortex Fig 11.19 11-48

  49. Adrenal Medulla • Hormonal effects of Epi last 10X longer than NE • Innervated by preganglionic Symp fibers • Activated during "fight or flight" response • Causes: • Increased respiratory rate • Increased HR & cardiac output • General vasoconstriction which increases venous return • Glycogenolysis & lipolysis 11-49

  50. Stress & the Adrenal Gland • Stress induces a non-specific response called general adaptation syndrome (GAS) • Causes ACTH & cortisol release • Often affects physiology negatively Fig 11.20 11-50

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