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Endocrine System

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imissyou419's version from 2017-04-01 00:34

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Endocrine systemtissues and cells capable of secreting and responding to hormones, communication system
Hormonea chemical substance, formed in 1 organ or part of the body and carried in the blood to another organ or part; depending on the specificity of their effects, hormones can alter the functional activity of just ONE ORGAN or of VARIOUS NUMBER OF ORGANS (GnRH vs T3);
Hormones are regulators of physiologic events, effective in minute quantities, synthesized by cells/endocrine glands, from Greek hormon
Endocrine hormonechemical mediators produced in 1 part of the body and act on a distant part
Paracrine hormonechemical mediators produced in 1 cell that act on a neighbouring cell
Autocrine hormonechemical mediators produced in 1 cell and act on that same cell e.g. pancreas producing insulin which act on itself
Nervous vs. Endocrine systemaction potential vs chemicals;
fraction of second vs. minute, hours, days;
frequency vs. amplitude modulation;
"wiring" vs receptors
functions mediated by electrochemical conduction along nerves vs functions meditated by chemical messengers called hormones
Peptide/polypeptidesmall monomers e.g. TRH, 3 a.a. or large multimeric proteins e.g. TSH, FSH, LH, 200 a.a+
water soluble
Steroidderived from cholesterol metabolism, 4 hydrocarbon rings with various side chains,
lipid soluble (requires binding protein in serum)
e.g. testosterone, estrogen, vitamin D
Amino acid derivativese.g. epinephrine, thyroxine (T4) - tyrosine residues have large aromatic rings which make it lipid soluble
Most cells producelocally-acting growth factors and cytokines and hormones that can go systemically
Gut secreteregulate food intake and digestion (CCK, ghrelin, gastrin, secretin, NPY)
Heart secreteANP, regulate vascular tone and volume
Kidneys secreteEPO, increase erythrocyte formation
Liver secreteAngiotensinogen, IGF-I and thrombopoietin (increase platelets)
Fat secreteadipokines e.g. leptin
Negative feedback between 2 hormonesTSH and T3 (TSH stimulate release of T3 and high T3 negatively feedback shut down TSH)
Negative feedback between a hormone and a metabolitePTH and Ca2+ (PTH act on bone, bone increases Ca2+ (metabolite) in blood, high Ca2+ stop production of PTH due to Ca2+ sensing receptors in parathyroid gland)
Negative feedback between antagonist pairs of hormonesInsulin, glucose, glucagon (if glucose level is high => sensed by beta cells, secrete insulin which lower circulating blood glucose; if glucose level low => sensed by alpha cell, secrete glucagon which increase circulating blood glucose)
Positive feedforward and negative feedback for reproductive hormonesPositive feedforward: estrogen on LH & FSH; Negative feedback: progesterone on LH & FSH
Receptor specificityonly certain cells respond to a given hormone, some cells are targets for more than 1 hormone, a cell must have the appropriate receptor to respond to a hormone
T/F - a single hormone may elicit different responses in each target tissueT - each cell expresses its own unique complement of receptors and second messengers (testosterone passes through cell and bind to androgen receptor to elicit classic responses, testosterone can be converted to DHT if encounters 5a-reductase (intracellular enzyme) and become more potent and elicit different response (anabolism muscle mass)
T/F - single processes can be altered by multiple hormonesT, e.g. serum glucose homeostasis (glucagon, insulin, catecholamines, cortisol affect serum glucose)
5 Factors affecting hormone action1. hormone production/release,
a) regulation of gene expression by other hormones & cytokines, b) availability of necessary substrates, enzymes & energy, c) innervation
2. serum carrier proteins e.g. SHBG, CBG, IGFBP3,
3. converting/deactivating enzymes e.g. ACE, COMT (enzymes conduct hormone into more potent form or inactivate hormone before it gets to receptor),
4. metabolic clearance - kidney/liver (if poor -> activate more target tissues),
5. receptor and signal transduction
Hormone production/releaseregulation of gene expression by other hormones and cytokines; availability of necessary substrates, enzymes, and energy; innervation (neuro-endocrine organ affected by cells from NS)

In response to another hormone, synthesis of mRNA, mRNA translated into prohormone, post-translationally processed (glycosylation, myristolation, enzymatic cleavage) to become hormone and in response to stimulus, Ca2+ released and hormone exocytosed
Effect of hormone concentrationmore at target cell -> activate more receptors until saturated; constant exposure to high levels of hormone -> downregulation of receptors in target cell
Variable release rate into bloodfine tunes physiological response, prevent receptor down regulation, attenuates negative feedback due to constant exposure, i.e ultradian secretion
Example of Ultradian Secretion
KNOW THIS
GnRH, LH (GnRH secreted on minute to minute basis, LH released by min to min from anterior pituitary in response to GnRH)
Example of Circadian/Diurnal rhythm release
KNOW THIS
CRH, cortisol released in response to CRH (released once a day @ 4AM; naps do not increase cortisol), GHRH
Serum Carrier proteinse.g. SHBG (sex hormone binding globulin), CBG (corticosteroid binding globulin), IGFBP3;
Binding proteins regulate: solubility, stability, metabolic clearance, bioavailability (how many carrier proteins present affect steroid, amino acid derivative tyrosine actions; if not bound to carrier proteins, liver/kidney clear it out)
Signal amplificationeach hormone/receptor complex produces multiple 2nd messenger molecules (e.g. cAMP, PKC, Ca2+), each 2nd messenger activates different signal cascade (protein phosphorylation), end result is generation of multiple copies of an mRNA, functional phosphorylated protein, etc
Water soluble ligands & receptorspeptide, cytokines, a.a derivatives, ions can bind to PM receptors: GPCR, tyrosine-kinase associated receptor, tyrosine kinase receptor, receptor-mediated ion channels
GPCR influence intracellular cell processes such asgrowth, secretion, protein synthesis, differentiation, apoptosis
Gsalpha↑ cAMP
Gialpha↓ cAMP, ion channels, PLs
Gqalpha↑ PLC
G12,13 alphaRho activation
Lipid soluble ligandssteroids, thyroid hormones, vitamin D, retinoic acid bind to receptors present in cytosol (cytosolic/nuclear receptors), translocate into nucleus and act as transcription factor which bind to promotor sequences of genes (other intracellular proteins recruited i.e. co-activators => increase gene transcription, co-repressors => decrease gene transcription)
Steroid synthesisderived from cholesterol, different enzymes can interconvert hormones and it influences which hormone is made (can upregulate enzymes in making that specific hormone)
Steroid secretion bound to what,
how does it get into cell
passive diffusion down the concentration gradient (since lipid soluble), circulate in plasma bound to carrier protein
Steroid hormone receptors (transcription factors)
Amplification of hormone action
amplification of hormone action occurs when 1 hormone molecule induces formation of multiple copies of mRNA
What regulates the activation of cytosolic NR?HSPs (they bind to receptor until receptor binds to ligand and then acts as transcription factor)
Steroid inactivation1. subtle changes in ring structure of molecule (oxidation, hydroxylation); 2. conjugation to organic acids (more polar), thereby increasing aqueous solubility -> excreted in urine
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