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by: Mr. Karli Cummings

Endocrinology ZOOLOGY 603

Mr. Karli Cummings
GPA 3.57


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This 13 page Class Notes was uploaded by Mr. Karli Cummings on Thursday September 17, 2015. The Class Notes belongs to ZOOLOGY 603 at University of Wisconsin - Madison taught by Staff in Fall. Since its upload, it has received 34 views. For similar materials see /class/205126/zoology-603-university-of-wisconsin-madison in Animal Science at University of Wisconsin - Madison.

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Date Created: 09/17/15
Growth Hormone Lecture LECTURE 1A Hormones controlling normal growth 0 Growth Hormone GH 0 Insulinlike Growth Factors IGF1 and IGF2 A growth factor that functions as a hormone o Epidermal Growth Factor EGF A hormone that controls differentiation from stem cells 0 Erythropoietin Cell division is a highly regulated process growth requires the coordination of a of hormones GH stimulates the production of Insulinlike Growth Factors IGF via the JAK STAT pathway GHsomatotropin Member of a family that includes prolactin and placental lactogen Long bone growth occurs at the epiphyseal plate growth plate made of cartilaginous cells Whole animal V Cell culture Many cells involved interact with each other Compromise organ culture GH is synthesized stored and secreted by somatotroph cells within the lateral wings of anterior pituitary gland HGH is synthesized and secreted in a pulsatile fashion Somatomedins Regulated by GH regulate bone growth Insulinlike Growth Factors IGFl IGF2 Structurally resemble insulin produced in liver Direct effects of GH on bone Bone is the local producer of IGF1 If you KO IGFl totally 60 size Absent in liver 60 size 20 activity in liver normal size Production other than liver is not important and postnatal growth relatively independent of liver IGFl only need 20 functionality KO mice GH receptor KO normal size IGFl KO 60 normal size Both KO tiny Fetal development KO s KO GH 95100 normal size KO GH receptor 95100 normal size KO IGFl 60 normal size KO IGF2 60 normal size KO IGFl amp IGF2 30 normal size all die Somatomedins play a major role in fetal development GH does not GH has some functions that are separate from somatomedins Hormone V Receptor function remember things that are not the appropriate receptor CAN bind KO IGFl 60 normal size KO IGFl RECEPTOR 45 normal size 100 death KO IGF2 RECEPTOR bigger than normal neonatal death What attaches to IGFl receptor when IGFl is knocked out to prevent death IGF2 and potentially some insulin Having IGF2 KO AND IGF2 RECEPTOR K0 is BETTER than just receptor knock out If IGF2 receptor alone is knocked out very high levels of IGF2 is left in the body Insulin large affinity to insulin receptors some but small affinity to IGFl receptors IGFl large affinity to IGFl receptrs decent affinity to IGF2 receptors very small affinity to insulin receptors IGF2 Large affinity to IGF2 receptors medium affinity to IGFl receptors very small affinity to insulin receptors Revisiting Type 1 Diabetes Insulin receptor resistance leads to high levels of insulin and glucose often down regulates the insulin receptor some people experience enlarged kidneys and enlarged adrenal glands These effects may be due to the high levels of insulin acting through the IGFl receptor Insulin gtgtgtgt IGF1 and IGF2 at regulating metabolism IGFl amp IGF2 gt insulin in stimulating cell proliferation Hormone travels in the blood Growth factor cell to cell regulation epiphyseal plates 3 different hormones 3 different receptors Somatomedin is the intermediate Insulin like growth factors are binding protein that play roles in hormone delivery GH action via IGFl Remember that GHRH and GHIH SST regulated the release of GH in a pulsatile fashion GH signaling GH binds to its receptor at two sites forms a dimer Interacts with JAKZ tyrosine phosphorylation STATSb phosphorylation Dissociation of phosphorylated STATSb from GH R Dimerization of STAT 5b transport to nucleus gtactivation of target genes gt increase synthesis of IGF1 Increases transcription via STATS promotor sequences IGFl receptors are found everywhere but the liver activates an IRS complex like insulin Increases cell number and decreases apoptosis therefore promoting growth IGFl also has some antiinsulin properties and acts with GH for bone growth GHIGFl work together GH responsible for development of IGF1 responsiveness and expression of IGF1 gene then IGFl regulates clonal expansion IGFl performance enhancement but lower levels are antiaging an promote a longer life Some forms of dwarfrsm associated with a high IFGl Leron Syndrome High GH Short stature Low IGFl No GhBP 0 Some lack receptor 0 Some have a defect in the signaling pathway 0 Treatment IFGl EGF Epidermal Growth Factor 11 known family members 4 receptors Involved in cellcell regulation in cells hormone or growth factor Receptor is a tyrosine kinase acting through complex pathways EGF promotes plantshoot growth and healing of wounds via saliva receptor gets down regulated by internalization via lysosome Erythropoiesis Differentiation of all blood cells froma precursor stem cells in the bone marrow focus on the formation of erythrocytes blood cells Increases in response to hypoxic conditions Decreases when the kidney is not functioning Decreases in hypophysectomized animals Decreases in response to transfusions Increases after blood loss More red blood cells negative feedback for erythropoietin Erythropoietin Protein hormone made in the kidney Rises in hypoxic conditions Acts with receptors in the bone marrow Thyroid Hormones 1241 Synthesis control of secretion mechanism of receptor action roles and actions of thyroid hormones in metamorphosis identifying the lesion Thyroid hormones are made in the follicular cells of the thyroid gland Thyroglobulin is stored in the Colloid space of the follicle Thyroid hormone synthesis Follicular cells release thyroglobulin to the colloid space within the follicle the follicular lumen surrounded by follicle cells by exocytosis Iodide is trapped in the colloid space by a NaI symporter Iodide is transported to the lumen by a transporter Pendrin In the lumen Iodide is converted by peroxidase to a form that is incorporated onto tyrosine residues of thyroglobulin by coupling two tyrosine molecules The thyroglobulin becomes diiodo or monoiodo thyroglobulin and then further couples to become mostly T4 and a little T3 The colloid moves to follicle cells by pinocytosis the droplet joins with lysosome where enzymes separate the T3 T4 from thyroglobulin These hormones are released in response to TSH coming in from the pituitary via blood vessels Control of Thyroid Hormone Synthesis and secretion are regulated by TSH TSH is made by the anterior pituitary and is made up of two subunits of alpha and beta The TSH receptor is a Gcoupled protein that acts via cAMP cAMP regulates The sodium iodine symporter Thyroglobulin Peroxidase Proteins involved in iodine uptake TSH stimulates the immediate enhanced uptake of colloid material from the lumen into the follicular cell at the apical membrane T4 T3 More T4 is produced than T3 T3 is the physiologically relevant form Kd it is more active but has a shorter halflife TSH test if there is too much in blood 1 way to see if hypothyroidism Made in anterior pituitary Two subunits alpha common to F SH LH and TSH and beta speci c for each hormone Acts on TSH receptors on thyroid cells TRHTSHThyroid hormone Cold can increase TSH also in hypophysectomized rats cold can increase TSH Alternate sites of TSH synthesis Tyrosine based lipophillic Travels on binding proteins thyroxine binding globulin TBG and transthyretine both synthesized in liver Only free hormone is active Physiological roles Not essential for life Regulates basal metabolic rate Thermogenesis heat production Required by nervous system for early development wo is cretinism Permissive Required for some GH activity Works with glucocorticoids Important in reproductive functions Induction of prolactin synthesis Molecular Mechanism of Action Thyroid hormone receptor is a member of the steroid receptor superfamily nuclear transcription factors Important points of TR alpha and beta forms 2 forms Can act as a monomer or dimer Interact with RAR and TRAP s Thyroid hormone receptor auXillary proteins Forms of the TH receptor Two forms of the alpha TROLl and TROL2 Two forms of the beta TRBl and TRBZ TR Bl TR 32 and TR 11 are the physiologic receptors that bind with high affinity to T3 TR Bl and TR 11 are present in many cells TR 52 is only found in the pituitary Some TH regulated events don t happen in the nucleus CA ATPase activity in RBC s Uptake of amino acids Mitochondrial oxygen consumption increases in response to thyroid hormone in target cells Thyroid hormones regulate metamorphosis in amphibians TH can accelerate metamorphosis The role of the pituitary is likely to stimulate TH synthesis release Thyroid hormone stimulates TH receptor increase its own receptor T3 regulates TRB via TRE sequences Pre unoccupied TR receptor associates with DNA sequences chromosome in off con guration Post T3 binds to TR chromosome organization changes TH regulated genes involved in metamorphosis are upregulated Genes and tissues regulated by TH o TRB o Deiodinase o tail 0 Brain 0 Liver 0 Skin 0 Intestines Hyper or Hypothyroid Tired sleepy HYPO can also be hyper Gain weight HYPO Lose weight HYPER Irritable anxious HYPER Too hot HYPER Slow pulse HYPO Edema of face eyelids HYPO Depression HYPO Cold HYPO Goiter HYPO Patient X Goiter elevated T3T4 elevated TSH eyes protrude weight loss What is wrong T3 levels are high due to TSH levels there is actually a thyroid stimulating antibody that looks like TSH Autoimmune disease Grave s Disease Hyperthyroidism autoantibodies to the TSH receptor that actually function against it Treatment Use antithyroid drugs interfere with iodine uptake Patient Y T3 low TSH is low Patient is lethargic tired gaining weight Gave TRH saw an increase in the alphasubunit of TSH but not in the betasubunit Explanation T3 is low because this patient isn t making TSH functional TSH requires both subunits treatment give synthetic thyroid hormones Patient Z Goiter low T3 high TSH Symptoms feeling cold tired depression all symptoms of hypothyroidism Would we suggest the TRH test The thyroid gland is not producing T3 is this receptor problem Could be could be lots of issues iodine de ciency problems with thyroglobulin treat with synthetic thyroid hormones CASE STUDIES She will provide hormone levels and we must gure out what is wrong Including GH and adrenal hormones Map out how all hormones affect one another Hormones 0f the Adrenal Medulla 39 39 39 Lecture In your words What is the difference between a nervous system response and an endocrine response Nerve systems are fast go through nerves endocrine responses are slow go via chemicals but now we have fast chems How can two different hormones do the same thing in a cell Can you give an example Glucagon and epinephrine do Act through different receptors but do the same thing Uptake of glucose to make glycogen How about when the same hormone can do the same thing in two different cells Insulin fat and muscle cells or any other does the same thing take up glucose How can the same hormone do different thing in different cells Thyroid hormones will do totally different things in different cells different cascades activated different stuff in different cells How can the same hormone do two different things in the same cell Epinephrine can both dilate and constrict a smooth muscle cell We won t really be held responsible for parasympathetic and sympathetic nervous systems Are responsible for synthesis of catecholamines types of adrenergic receptors mechanisms a single hormone activating many responses in potentially the same cell History Epinephrine is made in the adrenal Adrenal extracts sympathetic stimulation Epinephrine is both excitatory and inhibitory can dilate and constrict a smooth muscle cell Could the opposite effects be caused by epinephrine and an inhibitor or epinephrine say norepinephrine Nope Wrongo Norepinephrine can also stimulate and relax muscle depending on the muscle Differing actions are mediated by different receptors Anatomy adrenal glands are situated above the kidneys Adrenal gland is made of two tissues Adrenal medulla and adrenal cortex cortex is made of glucocorticoids medulla is chromaffin cells epinephrine Medulla makes catecholamines cortex makes steroid hormones Adrenal medulla is under control of the sympathetic nervous system fight ight or restdigest Pre ganglion goes from the spinal cord the post ganglion goes to the end organ Pre is short post is long Para V Sympathetic Parasmpathetic RESTDIGEST Pupils constrict Heart rate decreases Bronchioles constrict Increase digestive motility Stimulates insulin No effect on adrenal No effect on kidney Major neurotransmitter is acetylcholine Sympathetic F IGHTF LIGHT Dilate Heart rate increases Bronchioles dilate Decrease digestive motility Inhibits insulin Increases rennin in kidney Major neurotransmitter is norepinephrine Sympathetic Nervous System Ganglionic chain Pre ganglionic neurons release acetylcholine Postganglionic goes to eyes heart lungs whatevs contains cholinergic receptors nicotinic receptors responds to acetylcholine by making and releasing norepinephrine Norpinephrineepinephrine NE sympathetic postganglionic neurons E Adrenal medulla really only place that can make it Epinephrine is a catecholamine meaning has 2 adjacent oh groups and an amine Postganglionic and adrenal medulla cells contain the enzymes to synthesize catecholamines Tyrosine gt LDopa gt dopa decarboxylase Dopamine gt Dopamine beta norepinephrine gt PNMT Epinephrine PNMT turns Norpinephrine into Epinephrine Catecholamines are stored in vesicles in the adrenal medulla ready for fast response upon stimulation from the sympathetic nervous system More epi is released than norepi Norepi can be converted to Epi in the cytosol by PNMT Question Most neurons make NE adrenal medulla cells make E what enzyme is differentially expressed to explain this PNMT one Hypox animals have reduced epi Adrenal medulla can make dopamine and NE in hypox animals ACTH can restore epi Glucocorticoids can restore epi What regulates what Glucocorticoids can restore epi if ACTH can restore epi glucocorticoids regulate that enzyme allow epi to be made Regulates PNMT Epinephrines halflife is 2 mintues monoamine oxidase and COMT catabolizes Epi PNMT doesn t go backwards If you had a monoamine oxidase inhibitor you would have more levels of epi Actions of E and NE Look at skin blood vessels epinephrine and norepinephrine have same effect on restriction but the drug X that looks like them does not work Does it look like E and NE are working through the same or different receptors Maybe they are doing the same thing Would you consider drug X to be an agonist or an antagonist Antagonist to skin blood vessel constriction doesn t increase it Hea1t rate drug X increases it does it better than Epi and Norepi that do the same Is an agonist Lung bronchioles is an agonist of epi antagonist of norepi norepi doesn t cause dilation of lung epi does and drug X also as well as Epi causes dilation of lung bronchioles In lung bronchioles does it seem that E and NE are acting through the same receptors No In the skin and heart Epi and Nor can act through those receptors but in lung it doesn t like norepi at all Epinephrine and Norepinephrine work through adrenergic receptors alpha 1 and 2 and beta 1 2 and 3 Don t memorize which receptors work where Just know if she gave that info alpha agonist and alpha antagonist where would it work When both receptors are present 1 At high conc of epi contraction via alpha 2 Low concof epi dilation via beta What happens to ow when arterioles constrict When they relax skin cell Alpha 1 EgtNEgtgtgtISO drug X Predominant form Found in arterioles Eye skin gut salivary glands Usually causes constriction raises bp by increasing resistence Betal igtegtNE blocked by propanalol beta blockier increases heart rate and contraction when we think of beta blockers we are thinking of blocking these receptors Beta 2 I gt E gtgt N Decrease GI motility Bronchodilation Vasodilation in skeletal and cardiac muscle Glycogenolysis in liver Works with glucagon Design the fastest endocrine response Make it where it is used Protein Stored and ready to go Second messenger system Alpha adrenergic receptors alpha receptors act through pip pathway promotes in ux of ca Beta andrenergic receptors epinephrine and ACTH act trough the same adenylate cyclase in fat cells NOT a system we want on for long fast and efficient turn it off quickly too Desensitization also assists in slowing down response if continuous hormone receptor changes conformation cAMP plateus and or decreases promotes regulation not over heartincrease in rate etc Regulation of the receptors Presence and absence of stimulation gonadol steroids will cause contraction or relaxation glucocorticoids are permissive thyroid horomes hyperthyroidism enhances adrenal catecholamines Integration of nervous and endocrine systems In response to low hemoglobin what other hormone will be increased EPO If you could only increase one in response to sudden blood lose EPO or EPI EPI is right now EPO will help in long run Need epi now CRH gt ACTH gt Glucocorticoids stress steroids What integrating center do both of these systems use The hypothalamus Adrenal Medulla makes epinephrine which circulates and acts on a number of tissues Response depends on the receptor Adrenal Medulla acts like a neural integrating center delivering epinephrine to target tissues via the blood Epinephrine can circulate in the blood Adrenal medulla and cortex are important in responding to stress Hormones 0f the Adrenal Cortex Lecture 44 Newborn presents with darker than expected skin especially scrotal skin ACTH is high Glucocorticoids are low not the whole story Genitals enlarged unusual prenatal tests show baby is XX Baby is dehydrated lethargic having seizures and heart rate is abnormal Blood tests show that sodium levels are low Adrenal glands are LARGE but adrenal hormones are wacked out Too much Andro testosterone estradiol DHEA not enough cortisole corticosterone etc Know that we are missing a key enzyme Actions of Cortisol Actions of Aldosterone Saltwater balance a coordination of hormones If the adrenal gland is removed Sodium levels in blood is low potassium level in blood is high Can t maintain glucose levels Tissues deplete glycogen easily Tissues don t breakdown proteins or fats when energy stores are low impaired gluconeogenesis Aldosterone sodium level in blood low potassium high Cortisol all the rest of those symptoms CRH gtACTH gtCortisol ACTH acts on cells in the zona fasciculate on receptors in adrenal cortex cells Acts through MCR2 receptor Uses cAMP as a second messenger Increases intracellular CA Activates StAR steroid acute regulatory protein Net effect increase in steroid synthesis ACTH regulates cholesterol uptake is part of a key step in steroid of sequestering cholesterol And steroids including cortisol are derived from cholesterol Adrenal Cortex Progesterones Glucocorticoids Andro gens Estero gens Aldosterone Adrenal Cortex hormoneswhere made Go Find Rex Make Good Sex Glomerulosa gt Mineralocorticoids Fasciculata gt Glucocorticoids Reticularis gt Sex Steroids Glucocorticoids Cortisoil Cortisone Corticosterone Travel in the blood on corticosteroid binding globulin half life is only 80 minutes Most cells have GR glucocorticoids can enter cells and bind to neuclear receptors Roles Increases glucose levels under stress Makes enzymes assosciated with gluconeogensis Makes enzymes that break down muscle and fat stressful conditions Increases PNMT in adrenal medulla Works with prolactin to promote lactation Important in proper functioning of the hippocampus memory Fetal lung development Pathophysiology of glucocorticoids Not enough Addison s disease will also result in low aldosterone low cortisol weakness increased pigmentation salt craving weight loss Too much Cushing s round face protein breakdown muscles are catabolic high insulin Excess cortisol breakdown protein Aldostemoe made in zona clomerulosa of adrenal cortex Increases in response to low blood pressure in the kidney Stimulus What is Where does it act What does it do released Low BP is Renin an In lungs Converts angiotensinogen sensed by enzyme into angiotensin I the JG cells of the kidney via baroreceptor s AN G II AN G II 1 Hypothalamus l Stimulates thirst made from releases AVPADH ANG I in 2 Vasoconstriction lungs and 2 blood vessels 3 Synthesissecretion of blood 3 adrenal cortex aldosterone vessells 4 parasympathetic NS 4 Increase cardiac output and vasoconstriction ANG II Aldosteron Aldosterone binds to receptors in Increases NA reabsorption circulates to e is made the distal tubules of the kidney K excretion via NaK and ATPase in DCT water receptors in released follows salt the adrenal from the cortex zona glomerulus a Stretch of AN P ANF 1 HypothalamusPosterior l Decrease AVPADH heart atria Atrial Pituitary 2 Vasodilation blood Natriuretic 2 Blood Vessels 3 Excrete NA and pressure too Peptide are 3 Kidney water high released 4 Adrenal Cortex 4 Decrease aldosterone from the heart Angiotensin I is converted into II by enzyme ACE this happens in lung and blood vessels throughout body Direct stimuli for aldosterone release Low plasma sodium high potassium acts in the adrenal cortex


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