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Growth
Growth Hormone
| Question | Answer |
|---|---|
| growth definition | lengthening of long bones, hypertrophy and hyperplasia of cells in soft tissue |
| hypertrophy definiton | growing of cell size |
| hyperplasia definition | increase number of cells/multiply |
| what is growth dependent on | genetics, diet, environmental stress, presence/absence of disease, fetal factors (not GH), and postnatal (GH and GHRH) |
| t/f: being malnourished increases growth | false |
| t/f: excess food intake increase vertical growth | false |
| t/f: excess food intake increases weight | true |
| t/f: low stress causes increased growth | true |
| how does high stress decrease growth | high stress increases cortisol to cause protein breakdown, inhibit long bone growth, and inhibit GH |
| puberty | time when individuals become reproductively mature and individuals experience a mild growth spurt |
| when do girls hit puberty | age 11 |
| when do boys hit puberty | age 13 |
| what do girls starting puberty depend on | adrenal androgens and ovarian estrogens |
| what do boys starting puberty depend on | testicular androgens |
| t/f: estrogen halts growth once mature | true |
| what does the aromatase enzyme do | convert testosterone to estrogen |
| GH signal transduction | JAK/STAT |
| GH is released from | somatotrophs in anterior pituitary |
| GH is triggered for release by | growth hormone releasing hormone (GHRH) |
| GH is inhibited by | GHIH, ↑ levels of IGF-1 and GH |
| GH functions of liver | ↑ production of IGF-1 to ↑ hyperplasia, ↑ protein synthesis, and ↑ bone growth |
| GH function- metabolic actions unrelated to growth | ↑ fat breakdown, ↓ glucose uptake by muscles, ↑ glucose output by liver |
| Overall GH functions | ↑ free fatty acids, ↑ glucose, ↓ amino acids (↑ protein synthesis) |
| IGF-1 growth promoting factors | ↑ cell division, ↑ protein synthesis, ↑ bone growth |
| major inputs of HPG Axis | exercise, stress, ↓ blood glucose, and diurnal rhythm |
| minor inputs of HPG Axis | ↑ blood amino acids, ↓ blood fatty acids, and Ghrelin |
| major and minor inputs that stimulate the hypothalamus inhibit what hormone and what does this cause? | inhibit somatostatin which inhibits anterior pituitary somatotrope to secrete GH which stimulates liver functions and metabolic actions unrelated to growth |
| major and minor inputs that stimulate the hypothalamus stimulate what hormone and what does this cause? | stimulate GHRH which stimulates anterior pituitary somatotrope to secrete GH which stimulates liver functions and metabolic actions unrelated to growth |
| what factors inhibit the hypothalamus in the HPG Axis | GH and IGF-1 |
| what factors inhibit anterior pituitary somatotropes | GH and GHIH |
| Hormones that use cAMP pathway | LH, FSH, TSH, ACTH, vasopressin, epinephrine, norepinephrine, glucagon, PTH, CRH, GHRH, somatostatin, calcitonin |
| hormones that use IP3 and DAG pathway | THR, GnRH, oxytocin, IGF-1, and IGF-2 |
| hormones that use JAK/STAT pathway | GH and PRL |
| hormones that use hormone-response elements in DNA | all lipophilic hormones: TH, cortisol, aldosterone, testosterone, estrogen, progesterone, and vitamin D |
| IGF-1 | acts directly on target cells for growth of soft tissue and bone |
| IGF-2 | used for fetal development |
| bone growth thickness | osteoblasts in periosteum ↑ bone deposition & osteoclasts dissolve bone on the inside which ↑ bone marrow cavity |
| bone growth lengthening | chondrocytes in epiphyseal plates multiply and enlarge which pushes the epiphysis and lengthens the bone |
| JAK/STAT pathway # of ligands and receptors | 1 ligand and a 2-receptor complex |
| t/f: JAK is a type of protein kinase | true |
| STAT meaning | signal transducer and activator of transcription |
| what does the dimer produced by the JAK/STAT pathway do | enter nucleus to bind to DNA and stimulate transcription to produce IGF-1 |
| what does GHRH do to cAMP and how | increase cAMP via Gstimulatory |
| what does GHIH do to cAMP and how | decrease cAMP via Ginhibitory |
| when GH is secreted by anterior pituitary what does it bind to | GH binding protein (GHBP) which binds to GHR on liver |
| what does GHR (growth hormone receptor) consist of | 1 ligand and 2 receptors |
| When the liver is stimulated by IGF-1 what happens? | activates gene transcription to make tri-molecular complexes to increase stabilization and half like of IGF-1 |
| after IGF production, what do proteases do | cut trimolecular complexes to make free IGF-1 that binds to IGF-1R on target tissues |
| IGF-1 pathway | tyrosine kinase; homodimer, 2 ligands |
| what does increased insulin do for growth | excessive growth; stimulate protein synthesis and can act like IGF-1 |
| what does decreased insulin do for growth | stunted growth |
| what do sex steroids do for growth | stimulate growth via androgens to ↑ muscle mass in males |
| reasons why boys grow taller than girls | 2 years of growth before puberty, longer growth spurt during puberty, and ↑ cyclic patterns of GH |
| decreased GH in children | dwarfism |
| types of dwarfism | laron dwarfism, and african pygmies |
| laron dwarfism | abnormal GH rceptor |
| increased GH in children | gigantism- extreme and uncontrolled growth |
| decreased GH in adults | can lead to low muscle mass, bone mass, and heart failure |
| increased GH in adults | acromegaly |
| why does acromegaly occur | epiphyseal plates have already closed- only cartilage hypertrophies and cartilaginous features like ears and nose become enlarged |
| GH affect on adipose tissue | ↓ glucose uptake, ↑ lipolysis, ↓ adiposity |
| GH and IGF affects on kidney, pancreas, intestine, islets, parathyroids, skin, connective tissue, bone, heart, and lungs | ↑ protein synthesis, ↑ RNA synthesis, ↑ DNA synthesis, ↑ cell size and number, ↑ organ size, ↑ organ function |
| GH affect on the liver | ↑ RNA synthesis, ↑ protein synthesis, ↑ gluconeogenesis, ↑ IGFBP, and ↑ IGFs |
| GH and IGF affects on muscle | ↓ glucose uptake, ↑ amino acid uptake, ↑ protein synthesis, ↑ lean body mass |
| GH and IGF affects on chondrocytes | ↑ amino acid uptake, ↑ protein synthesis, ↑ RNA synthesis, ↑ DNA synthesis, ↑ collagen, ↑ chondroitin sulfate, ↑ cell size and number, ↑ linear growth |
| IGF-1 affect on chondrocyte proliferation in epiphyseal plate | 1. chondrocytes undergo cell division 2. grow old chondrocytes 3. EC matrix calcifies to entrap chondrocytes that will die 4. dead chondrocytes eaten by osteoclasts 5. osteoblasts come from diaphysis and deposit bone over dying chondrocytes |
Created by:
k.murski
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