NUTR 600 Exam 1 Hormones 2 & 3

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NUTR 600 Exam 1 Hormones 2 & 3
2012-10-01 21:59:32
nutr600 hormones

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  1. What are the three main types of hormones?
    Peptide, steroid, amino acid derived 
  2. Name the 12 peptide hormones (4 categories)

    • 1. Pancreatic hormones: insulin, glucagon, somatostatin
    • 2. Gut hormones: GLP-1, GIP
    • 3. Growth hormones: GH, prolactin, placental lactogen
    • 4. Glycoprotein hormones: FSH, LSH, chorionic gonadotropin, TSH
  3. Name the 5 steroid hormones
    • 1. Cortisol
    • 2. Estradiol
    • 3. Testosterone
    • 4. Aldosterone
    • 5. Progesterone
  4. Name the 4 amino-acid derived hormones.

    Which use external receptor?
    • 1. Thyroid hormones: thyroxines (T3 and T4)
    • 2. Catecholamines: Epinephrine & norepinephrine

    Catecholamines use external receptor, whereas thyroid hormones can interact within cell. 
  5. Basically, what is the overview of hormone synthesis for peptides, steroids, and amino-acid derived?
    1. Peptides: DNA --> mature mRNA --> preprohormone -->prehormone --> hormone

    2. Steroids: derived from cholesterol

    3. Amino acids: derived from the AAs tyrosine, tryptophan, and histidine. 
  6. Which 3 amino acids are the precursors for hormones?
    tyrosine, tryptophan, histidine
  7. How are protein hormones synthesized? (6)
    • 1. DNA --> mRNA --> protein
    • 2. Pre-prohormones are processed in ER (removing N-terminal signal sequence (directs protein for secretion), glycosylation, cleavage)
    • 3. Prohormones: packed into membrane-bound secretory vesicles and secreted via exocytosis in response to specific signals; often have superfluous amino acid residues that used to direct folding, but are useless now since everythign is folded. 
    • 4. Endopeptidases w/i cell cleave prohormone just before release, generating mature peptide hormone form of molecule
    • 5. Mature peptide hormones travel in blood
    • 6. Interact w/ specific receptors on surface of target cells
  8. How is insulin specifically synthesized? (3)
    • 1. Signal peptide removed from preproinsulin to form proinsulin.
    • 2. Formation of disulfide bonds between A&B components
    • 3. Removal of intervening C chain --> mature hormone
  9. What hormones are secreted by anterior pituitary? 6 posterior pituitary? 2
    Anterior pituitary:

    • LH, FSH (gonadotropins) --> ovaries, testes
    • GH --> bones, tissues
    • PRL --> mammary glands
    • ACTH --> adrenal cortex
    • TSH --> thyroid

    • ADH --> kidney
    • Oxytocin --> uterus, mammary glands

    ADH & oxytocin are syn in hypothalamus. 
  10. Where are releasing hormones produced? What type of hormone are they? Where are they synthesized? Where are they secreted to?

    What do they do?
    Produced in central nervous system (brain, spinal cord) in hypothalamus. Secreted through axons to anterior pituitary gland.

    Peptide hormones that initiate signaling pathways that result in exocytosis of vesicles containing specific anterior pituitary hormones. 
  11. What are the steps of the hormone pathway from CNS to final hormone? 8
    CNS --> neurotransmitters --> hypothalamus --> releasing hormones --> anterior pituitary gland --> anterior pituitary releasing hormones --> target gland --> target hormone
  12. Name the 4 important releasing hormones and their anterior pituitary releasing hormone and their final target hormones
    1. Gonadotropin RH --> LH & FSH --> Testosterone & estrogen

    2. Thyroid RH --> TSH --> Thyroid hormone

    3. Corticotropin RH --> ACTH --> Cortisol

    4. Growth hormone RH --> GH --> IGF-1
  13. Describe how glycoprotein hormone family is secreted: 

    1. name the members of glycoprotein hormone family 4
    2. Pathway 3, 3, 7 
    1. FSH, LH, TSH, and chorionic gonadotropin

    Pathway: GnRH (hypothalamus) --> FSH/LH (ant pit) --> testosterone, estrogen, and dihydrotesosterone (ovaries and testes)

    FSH/LH --> CG (embryo/placenta); earliest sign of pregnancy, maintains implantation and pregnancy. 

    TSH: Thyroid RH (hypothalamus) --> TSH (ant pit) --> binds to receptors on cells of thyroid gland --> cAMP --> PKA --> secretion of T4 and T3 --> T3 interacts with IC receptors, altering transcription. 
  14. How does GRH (Growth hormone releasing hormone) work?

    How is this pathway regulated?
    GRH (hyp) --> GH release (ant pit) --> IGF-1 released (liver)(principal regulator of tissue growth, regulates hypothalamic and pituitary targets)

    Negative feedback loops:(1) IGF-1 inhibits GHRH release from hypothalamus, inhibiting GH release from pituitary (2) IGF-1 directly inhibits GH release from pituitary. 

    Positive feedback loop:  (1) IGF-1 activates SS release from hypothalamus which inhibits GH release from pituitary. 
  15. What is the principle regulator of tissue growth?

    Insulin-like Growth Factor 1
  16. Where are growth hormones synthesized? Stimulated by? Inhibited by what from where? What metabolic pathways does it promote? (3)
    GH produced by somatotroph cells in ant pituitary

    Stimulated by GRH from hypothalamus

    Inhibited by Somatostatin from hypothalamus

    Promotes glucose production, amino acid uptake, lipolysis to support protein synthesis 
  17. What is gigantism caused by? What doesn't happen that happens in normal people?
    Gigantism is caused by excess production of GH before epiphyseal closure of long bones, usually caused by pituitary tumor.

    Bones grow at ends (growth plate) and eventually fuses with end of bone, but if you have excess GH before growth ends, bones keep getting large. 
  18. What are 2 diseases caused by excess GH?
    Gigantism - excess GH production before epiphyseal closure

    Acromegaly --> excess GH production after epiphyseal closure --> acral bone growth (jaw, brow, hands, feet, enlarged heart)
  19. When insulin & glucagon are secreted, where do they first go? What is their circulating half-life?
    into portal vein --> liver. 5 minutes.
  20. Where is somatostatin secreted from? (2)

    What does it do? (3)
    Somatostatin is secreted by delta cells of pancreas (as well as hypothalamus).

    In pancreas, acts as a paracrine inhibitor of glucagon and insulin

    In pituitary gland, prevents GH release. 
  21. What is the mechanism behind insulin secretion? 4
    • 1. G enters B-cell and is phosphorylated
    • 2. G6P activates release of ATP, closing ATP-sensitive K+ channels
    • 3. Increased IC K+ causes depolarization/opening of voltage-gated Ca2+ channels
    • 4. Increased IC Ca2+ causing granules containing insulin & C-peptide to move to surface, fuse with membrane and release contents into blood. 

    K+ closes, Ca2+ opens
  22. Do high Km transporters function at rates close or far from maximal velocity?

    What influences rate of glucose uptake?

    Number of transporters at cell surface. 
  23. What are the gut hormones? (2) Another name for them? What do they do?
    GLP-1 (L cells in ileum & colon)  & GIP (K cells in duodenum and proximal jejunum)


    Enhance insulin synthesis & secretion when circulating glucose concentrations are high, reduce postprandial glucose levels. 
  24. What does GLP-1 do? 3

    What does GIP do?

    What is a blocker that is used for T2D?
    GLP-1: (1) stimulates glucose-dep insulin release from B-cells (2) inhibits glucose-dep glucagon secretion and thus (3) suppresses hepatic glucose output 

    GIP: stimulates glucose-dep insulin release from B-cells

    Something that blocks DPP-4, which is a protease in blood that degrades GLP-1!!
  25. What is insulin syn/secretion inhibited by? 3
    starvation, stress, norepinephrine (secreted by adrenal medulla in respone to stress, trauma, or extreme exercise). 
  26. What does glucagon activate? What is secretion of glucagon activated by? (3) What is secretion of glucagon inhibited by? (3)
    Glucagon activates hepatic glycogenolysis & gluconeogenesis

    Secretion of glucagon is activated by low blood glucose, AA, epinephrine

    Inhibited by elevated blood glucose, insulin, and GLP-1
  27. What are steroid hormone receptors also? 2
    Nuclear transcription factors (IC receptors)
  28. Explain EC signaling pathway with more emphasis on G protein (5 steps)
    • 1. Unoccupied receptor does not interact w/ Gs protein
    • 2. Occupied receptor changes shape and interacts w/ Gs protein
    • 3. Gs protein releases GDP and binds GTP
    • 4. A-subunit of Gs protein dissociates and activates adenylyl cyclase
    • 5. When hormone is no longer present, receptor reverts to resting state, GTP on a-subunit is hydrolyzed to GDP and adenylyl cyclase is deactivated.
  29. What is the pathway of steroid hormone synthesis? (7)
    Cholesterol --> Pregnenolone --> Progesterone

    Progesterone can turn into cortisol (glucocorticoid), aldosterone (mineralcorticoid), and testosterone (androgen).

    Estradiol (estrogen) is made from testosterone. 
  30. What are all steroid hormones produced from? Where are they stored?
    Cholesterol. Not stored!
  31. Cortisol:

    (1) site of syn (2) regulation of syn (3) bio effect - 6
    • 1. adrenal cortex
    • 2. ACTH, stress
    • 3. (1) inhibits DNA, RNA, protein synthesis (not in liver); (2) anti-inflammatory (3)adipose: stim TAG lipolysis (4) Liver: stim glucose production (5) Muscle: stim lactate release (6) muscle/fat: inhibit glucose uptake.
  32. Aldosterone

    (1) site of syn (2) regulation of syn (3) bio effect -2
    • 1. Adrenal cortex
    • 2. Angiotensin
    • 3. Blood pressure, electrolyte balance
  33. Progesterone
    (1) site of syn (2) regulation of syn (3) bio effect 2
    • 1. Corpus luteum, placenta
    • 2. FSH, LH
    • 3. Implantation, gestation
  34. Estradiol
    (1) site of syn (2) regulation of syn (3) bio effect - 2
    • 1. Theca cells (ovaries), fat
    • 2. FSH, LH
    • 3. Feminization, ovulation 
  35. Testosterone
    (1) site of syn (2) regulation of syn (3) bio effect - 2
    • 1. Leydig cells
    • 2. FSH, LH
    • 3. Masculinization, spermatogenesis
  36. What three hormones do LH and FSH regulate synthesis of?
    • 1. Progesterone
    • 2. Estradiol
    • 3. Testosterone
  37. Which 2 hormones are made in adrenal cortex?
    • 1. Cortisol
    • 2. Aldosterone
  38. Do steroid hormones have a long-term effect or short-term effect on metabolism? Why?
    Long-term, bc they affect gene transcription and protein synthesis. 
  39. Describe the steps of the steroid hormone cell signaling pathway 7
    • 1. SH enters cell via diffusion
    • 2. Binds to LBD of receptor and enters nucleus or first enters then binds
    • 3. Hormone binding causes structural change --> activation
    • 4. Dimerization (receptor-hormone complex binds with another one)
    • 5. DBD binds to specific sequence upstream of gene called HORMONE RESPONSE ELEMENT!!
    • 6. This causes suppression/stimulation of gene transcription
    • 7. Long-term effects on metabolism via changes in mRNA expression. 

    • 1. SH enters cell via passive diffusion
    • 2. Bind to LBD of their specific receptor in cytosol and enter nucleus OR enter nucleus THEN bind to specific receptor
    • 3. Hormone binding causes structural change in steroid receptors --> activation
    • 4. Dimerization: activated receptor-hormone complex pairs w/ another receptor-hormone complex
    • 5. DBD of dimerized RHcomplex binds to specific sequence on DNA called HRE (hormone respones element)
    • 6. Binding of dimerized RHcomplex upsream of specific genes either stimulates/suppresses transcription
    • 7. Changes in mRNA exp of different genes alters abundance of proteins they encode leading to long-term regulation. 
  40. Estrogen action: three types of estrogen-like compounds
    • 1. Circulating estrogen: estriol <estrone<estradiol
    • 2. Dietary estrogens - plant-derived compounds w/ similar chemical structure as circulating estrogen (phytoestrogens); lignans/isoflavins
    • 3. Xenoestrogens - environmental compounds that can activate ER
  41. Name circulating estrogens from least potent to most potent
    estriol, estrone, estradiol
  42. What does SERM stand for? What do they do? What's the point? What's an example?
    SERM - selective ER modulators block circulating estrogens from binding to ER, so cells don't get signals they need to multiply

    ex. Tamoxifen - blocks growth of ER-dep breast cancer cells
  43. How do estrogens affect bones and uterine endothelia?
    Estrogen strengthens bones and stimulates growth of uterine endiotheliam cells increasing risk of endometrial cancer!
  44. What is tamoxifen's mode of action? (3)
    Competitive inhibitor to estrogen: binds to estrogen receptor, receptor doesn't change form, receptor cannot bind coactivators. 
  45. How can the effects of ligand binding to ER be regulated? 4
    1. When ligand binds to receptor, receptor undergoes conformational change allowing it to exist in a spectrum of forms from active to inactive, depending on ligand.

    2. Conformation regulates recruitment of specific transcriptional co-regulatory proteins. 

    3. Coactivators bind to the active (agonist-bound) form of receptor and activate transcription.

    4. Corepressors bind to inactive (antagonist-bound) form of receptor and repress transcription.
  46. What does estrogen do with breast cancer? 2
    Increases risk of breast cancer. If DNA in breast cell mutates, estrogen amplifies that effect, increasing population of mutant cells and increased risk of additional mutations that lead to uncontrolled proliferation and onset of cancer.
  47. How does estrogen relate to other types of cancer? Ovaries, prostates, breast?
    ER antagonists inhibit ovarian tumor growth

    Estradiol disrupts normal prostate morphogenesis and prostate growth

    ERs are primary mediators of of estrogen-dep breast cancer 
  48. How does estrogen relate to osteoporisis? 

    Decreased estrogen leads to osteoporosis in men and women, as well as obesity (increased central body fat accumulation). 
  49. Which hormones are derived from tyrosine? 4
    Thyroid hormones (T3 and T4) and catecholamines (ep, NE)
  50. How is thyroid hormone synthesis/secretoin regulated? 3
    • 1. TSH (ant pit) binds to receptors on thyroid epithelial cells stimulating synthesis of iodide transporter, thyroid peroxidase, and thyroglobulin. 
    • 2. High [TSH] cause more rapid endocytosis & more rapid release of TH into circulation
    • 3. Negative feedback control: TRH --> TSH --> thyroid hormone release. Thyroid hormones inhibit TRH and TSH.
  51. How is thyroid hormone synthesized & secreted? 7
    • 1. Organification: Iodide uptaken --> converted to iodine --> condensed onto tyrosine residues on thyroglobulin (mono-iodinated tyrosine MIT or DIT) in thyroid.
    • 2. Iodotyrosine molecules are coupled together to form T4 or T3 (T3 more biologically active)
    • 3. T4 and T3 accumulate on colloid (pool of TH bound to thyroglobulin) on surface of thyroid epithelialc ells. 
    • 4. Thyroid ep cells ingest colloids via endocytosis
    • 5. Colloid-laden endosomes fuse w/ lysosomes, containing hydrolytic enzymes which digest thyroglobulin, freeing TH. 
    • 6. Free THs diffuse out of lysosomes --> basal plasma mebrane of cell --> blood
    • 7. Bind to carrier proteins for transport to target cells
  52. How does TH act on target cell?
    Like steroid hormone, diffuses in and binds to receptor, activating transcription
  53. What is function of TH? 5
    • 1. Regulates fetal development of nervous/skeletal systems
    • 2. Increases basal metabolic rate (increases body heat production from increased oxygen consumption & rates of ATP hydrolysis)
    • 3. Lipolysis and B-oxidation
    • 4. TH stimulates insulin-independent entry of glucose into cell, gluconeogenesis, and glycogenolysis to increase plasma glucose. 
    • 5. Physiological effects: cardiovascular system (increases heart rate, promotes vasodilation), CNS (alterations in mental state, too little --> lethargy, too much --> anxiety), Reproductive systems (too little --> infertility). 
  54. How does TH affect physiological systems? 3
    • 1. Cardiovascular system (4) - increases heart rate, cardiac contractility, cardiac output, vasodilation
    • 2. CNS (2) alterations in mental state; too much--> anxiety, too little --> lethargy
    • 3. Reproductive system - too little --> infertility
  55. How does TH affect carb metabolism? 3

    Fat metabolism? 3
    Stimulates almost all aspects of carb metabolism

    • 1. Enhances insulin-independent glucose uptake into cells
    • 2. Gluconeogenesis
    • 3. Glycogenolysis

    Fat: Increases lipolysis and B-oxidation, plasma levels of cholesterol & TAGs are inversely proportional to levels of TH
  56. Name the 3 catecholamines. What are they made from? Where are they synthesized?
    Dopamine, epinephrine, norepinephrine

    made from tyrosine

    synthesized in brain and automatic nervous system. E and NE are both synthesized in adrenal medulla too. 
  57. What secretes E and NE? 5
    Exercise, hypoglycemia, medical stresses (angina), daily life stress, and anxiety
  58. What are the effects of E and NE? 6
    • Fight or flight
    • 1. Increases amount of glucose/FA fuel (GNG, lipolysis, glycogenolysis in muscle)
    • 2. Increases heart rate and contractility
    • 3. Vasodilation that supply skeletal muscle & skin
    • 4. Increases blood pressure
    • 5. Increases oxygen consumption and 6. heat production
  59. What is made from tryptophan? (2) When is 2nd one made?
    Serotonin (NT) synthesized from L-tryptophan.

    Melatonin is syn from serotonin in pineal gland when light stimulation is low. 
  60. What is the effect of histidine? Is it essential?
    Causes swelling, reddening in many inflammations & allergic rxns

    YES, it's essential
  61. What is the primary source of circulating NE? 
    Spillover form sympathetic nerves innervating blood vessels.

    Most NE released by sympathetic nerves is taken back up and metabolized. 

    Some diffuses into blood & circulates around body. At times of high sympathetic nerve action, amounts of NE increases dramatically.
  62. What happens to NE released by sympathetic nervous system?

    What causes high levels of NE in blood?
    It is reuptaken and metabolized, but some can spill over and circulate. 

    High sympathetic nervous activatoin. 
  63. What is a pheochromocytoma?
    It's a chromaffin cell tumor that secretes high amounts of catecholamines sporadically, causing episodic hypertension.