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Hormones, FSH, LH -gonadotrophs ->gonads -common a-subunit -highly glycosylated -activin also stims. -pulsatile, circadian (-) gonadal ster. hors. (-)inhibin (+)activin Female LH->theca cells->inc. cAMP chol->androstenedione FSH->gran. cells->inc. cAMP Andro.->aromatase->est. high est->(+) whole axis low est->(-) whole axis -also select follic to mature, Calcium/Phosphate Regulation ???? Parathyroid Hormone (PTH) -made, secreted by CHIEF cells -stored in secretory granules -cleaves C-terminal fragment Activate Ca-sensing receptor-> Chief cells dec. PTH synth via G_aq, G_ai Vit. D/RXR receptor activated-> Dec. PTH synth 15% PTH release not regulated by Ca, vit. D beta-agonists, histamine, glucocorticoids: all increase PTH release Transport: water-sol., few min. half-life metabolized in kidney/liver, elim in urine, Calcium/Phosphate Regulation ???? Calcitonin-not key in humans -parafollic. cells of Thyroid -stored in sec. granules -responds to high EC Ca. -7-transmemb domain rec. couples to G_as, G_aq Bone-osteoclasts DEC resorption Kidney-DEC PO4 resorption at PCT, Corticotropin Releasing (CRH) -cortisol(-), hypoglycemia(+), stress(+) Peptide Hormones Growth Hormone (GH) -somatotroph (50% of Ant. Pit) ->*liver*, tissues (JAK/STAT) ->prot., IGF, IGFBP synth; gly'gen'lysis -pulsatile, nocturnal peak -50 min half-life -GNRH (+) from hypothal. -(-) fdbk to hypoth by GH -(-) fdbk to hypoth, AP by IGF-1 -somatostatin (-) -most in plasma bound to GHBP -cleared by liver/kidney actions->lipolysis, inc. glucose, prot. synth, Thyroid Stim. Hormone (TSH) -thyrotrophs (% of AP) -glycosylated dimer -a-subunit same as LH, FSH, b-diff -TRH (+) from hypoth. (-) by FREE T3, T4, som'statin, DA pulsatile (2hr), circadian (midnight peak) (+) hypoth pulse gen. -(-)FREE T3,T4 Thyroid Hormones Action:Sim to Steroid Hs a,b nuclear receptors -T3>>>T4 receptor affinity hormone-pro complex->DNA promoter ->O2 consumption, heat production all tissues but brain, spleen, testes ->inc Na/K ATPase, ATP & NAD+ generation -->inc. BMR, core body temp, heat dissipation EFFECTS-> favor energy utilization, catabolism ->inc. lean body mass -> HR, CO, cardiac hypertrophy -inc. b-adrenergic sensitivity ->THYROID STORM if stressed hyperthyroid pt. ->stim. gut motility ->stim. bone formation and resorption ->low/high levels disrupt reproductive fcn, Hormones Steroid Hormones Androgens -androstenodione, DHEA -regulation-ACTH, no fdbk -not nec. for life, but for: puberty convert to estrogen after menopause female sexual responses -in excess w/ adrenal hyperplasia, or if no glucocorticoids to reduce ACTH, Glucagon-3-6 min half-life -a-cells of islets, single chain -cleavage of proglucagon by PROPROTEIN CONVERTASE (PC2) -removed by liver (80% on 1st pass), kidney -stim'd by dec. glucose, inc. AAs, Sympa NS -inhibit by somatostatin, insulin, high gluc. -cortisol, epi-enhance glucagon action -control long-term hypoglycemia response Glucagon-Like Peptides (GLPs)-sm. intestine increased after meals->B cells->insulin Receptor -7trans domains -G_s, G_q Glucagon Action-oppose insulin -insu/gluca ratio->phos. states -at liver, mm, adipose->mobilize fuel, Growth Hormone (GH) -somatotroph (50% of Ant. Pit) ->*liver*, tissues (JAK/STAT) ->prot., IGF, IGFBP synth; gly'gen'lysis -pulsatile, nocturnal peak -50 min half-life -GNRH (+) from hypothal. -(-) fdbk to hypoth by GH -(-) fdbk to hypoth, AP by IGF-1 -somatostatin (-) -most in plasma bound to GHBP -cleared by liver/kidney actions->lipolysis, inc. glucose, prot. synth ???? Somatostatin -d-cells of islets & hypothal ->dec. GH release ->slow fuel mvmt from GI tract to circ. ->dec. insulin, glucagon release Pancreatic Polypeptide-unknown fcn. -produced by F cells of islet, Corticotropin Releasing (CRH) -cortisol(-), hypoglycemia(+), stress(+) Peptide Hormones Calcium/Phosphate Regulation, Hormones Steroid Hormones Cortisol-glucocorticoid -from ad. cortex Z. fasc,Z. retic. -CYP17, CYP11B1 present, so pregnenolone -> cortisol, some androgens -pulses w/ ACTH, peak right before waking -primary CRH, ACTH modulator (-)fdbk *synthetics-prednisone, hydrocort., dexamethasone ->lead to adrenal atrophy via (-)fdbck CRH,ACTH ->type II GR-higher affinity for cortisol than aldo. -travels in blood bound to proteins CBG/transcortin, albumin, free - 80 min half life -CBG-75%-produced in liver -cortisol converted to c'sone, glucuronides-excreted -actions:inflammation, stress, CNS fcn, circ system -maintain NL serum glucose-catabolic (use fuel) -protein->glucose -suppress inflammation before-not good after it starts