709163
| Question | Answer |
| Hormones involved with body mass | -Insulin -Glucocorticoids -Adiponectin -Leptin |
| Hormones involved with Linear growth | -GH -IGF1, IGF2 -Insulin -Thyroid hormone -Glucocorticoids -Androgens -Estrogens |
| Where is GH secreted from? | Somatotrophs in the anterior pituitary |
| What are the forms of GH? | - 22.5 KDa -20 KDa -45 KDa (22.5 x2) |
| Hormones homologous to GH? | -pvGH -hCS1 and hCS2 -Prolactin |
| Where is GHRH released from? | small neurons of the arcate nucleus in the hypothalamus |
| General GH Pathway | Hypothalamus releases GHRH which lands on G-alpha-s receptor on somatotrophs of the Anterior Pituitary (increase cAMP and Ca+) --> release GH |
| When is GH secretion increased? | exercise, stress, fasting, high protein meal, fasting |
| When is GH secretion downregulated? | It inhibits itself. GHRH release also means Somatostatin release which inhibits GH |
| Maturation of GH protein | RER = Pre-Pro-Hormone Golgi = ProHormone -Secreted as Hormone |
| GH Secretion pattern? | Spikes when you sleep (12am-4am) |
| GH signals by which pathway? | RTK --> Jak/Stat |
| Effects of GH on target tissue | Increase lipolysis, decreased glucose uptake, increased hepatic gluconeogenesis, Insulin resistance (high doses of GH) |
| Effect of GH on the bones | -stimulates chondrocyte growth -promotes longitudinal bone growth -stimulates extracellular matrix formation |
| Ghrelin and GH | -Ghrelin involved in post meal stimulation of GH -Stimulates appetite -Interacts with GH secretogue receptor (GHRH) --- distinct from GHRH receptor |
| Somatostatin | Released from the Periventricular Nucleus of the hypothalamus. -Inhibits GH release by activated G-alpha-i pathway on somatotrophs |
| IGF interplay with GH | Made in the liver. Upregulates the Somatostatin release from the PVN in the hypothalamus which blocks GH release from anterior pituitary (Direct Effect). |
| Indirect effects of IGF-1 | supresses GHRH release from the Arcate Nucleus of the hypothalamus |
| IGF-1 is similar to what hormone in terms of receptor structure/activation? | Insulin RTK |
| IGF release in Aging | Huge spike prior to puberty and then goes down |
| IGF-2 | -Less dependent on GH -Promotes cell growth through IGF-1 receptor |
| When is IGF-2 more predominant? | During Fetal Growth |
| Describe Insulin, IGF-1, and IGF-2 receptors | Insulin and IGF-1 receptors are almost identical, except IGF-1 has longer cytosolic domain. Both are RTKs with receptors that are heterodimes (disulfide bonds) IGF-2 receptor is a singular mannose-6-phosphate receptor |
| Insulin Signaling Path | (S)tan (G)ot (R)atchet(s) (R)eady (F)or (Me) (Ma)n |
| IGF-1 Signaling pathway | homodimer signal binds to homodimer receptor -->activates IRS IRS activates RAS/RAF/MAP as well as P13K-->AKT which upregulates genes for recruiting microtubules to translocate GLUT4 to the muscle for insulin mediated uptake |
| IGF-2 signaling | activates ILK and P13K -->AKT to produce cytoskeletal reorganization (elongation of MTs) |
| De-regulation or imbalance of IGF binding proteins leads to what? | -Atherosclerosis -Cancer -Chronic kidney disease -Diabetic Neuropathy -Osteoperosis -Rheumatic disease -Type 2 Diabetes |
| Macrosomy | Mother's insulin reaches the baby's body and causes major growth. The mother will show with gestational diabetes |
| Leprochaunism | IR defect IR can bind insulin but doesn't initiate the signaling cascade |
| Factors that decrease growth | Glucocorticoids --> moves Ca+ out -Lack of T3 -IR defect |
| Factors increasing GH | Deep Sleep, exercise, Niacin, Fasting, Increased testosterone, GHRH, L-DOPA, Inhibitors of somatostatin (hypoglycemia, arginine, propanolol) |
| Decreases in HGH | DHT, Medications, high blood sugar, somatostatin (IGF-1) |
| Dwarfism | absence of GH before puberty |
| Gigantism | Excess of GH before puberty |
| Acromegaly | Excess of GH post puberty |
| How does replacement therapy with GH affect the body? | Increase in lean mass and decrease in body fat |
| Signs of GH deficiency? | Decreasing muscle strength, Osteoperosis, Increasing body fat, decreasing collagen production, wrinkles, cellulite, arthritis, decreased energy, moodiness, anxiety, depression |
| Clinical manifestations of GH Deficiency | central adioposity, Insulin resistance, ARTHEROSCLEROSIS |
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