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Physiology Unit 6 > Growth Hormone > Flashcards

Growth Hormone Flashcards

1
Q

growth hormone

A
  • single chain polypeptide hormone
  • produced in anterior pit
  • half life of 20 minutes
  • excess in childhood-gigantism
  • adult- acromegaly
  • deficiency during childhood-dwarism
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2
Q

regulation of GH secretion

A
  • hypothalamus- GHRH, somatostatin
  • stomach and pancreas- ghrelin
  • all activate G protein coupled receptors
  • targets in most tissue
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3
Q

hypothalamic control of GH secretion

A
  • GHRH-dominant signal
  • somatostatin inhibits
  • integration results in episodic, pulsatile secretion
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4
Q

GHRH

A
  • increases GH gene transcription
  • promotes GH release
  • stimulates production of GHRH
  • stimulates somatostatin release (brakes no out of control)
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5
Q

somatostatin

A
  • decreases pulse frequency
  • decreases pulse amplitude
  • no impact on GH synthesis
  • inhibits GHRH release
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6
Q

ghrelin

A
  • stomach and pancreas
  • stimulates hunger
  • levels increase before meals and decrease after
  • acts on growth hormone secretagogue receptor
  • feeding behavior, energy regulation, sleep?
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7
Q

pulsatile secretion of growth hormone over lifespan

A
  • pulses primarily at night
  • number of pulses per day stays nearly constant
  • larger pulse amplitude during puberty
  • strenuous exercise can cause surger
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8
Q

ritalin

A
  • can cause short stature
  • because disrupts sleep and secretion of GH
  • can catch up if good nutrition is maintained
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9
Q

stimulation of GH secretion

A
  • deep sleep
  • exercise
  • sex steroids
  • fasting/ hypoglycemia
  • amino acids
  • stress-like severe stress/nutritional loss
  • alpha adrenergic
  • dopamin agonists (suppress in acromegaly)
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10
Q

inhibitors of GH secretion

A
  • IGF-I
  • obesity
  • glucocorticoids
  • hyperglycemia
  • free FA
  • GH
  • beta adrenergic agonists
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11
Q

effect of nutrient state

A
  • obesity decreases- number of GH pulses, duration of pulse

- fasting increases-number of pulses, amplitude of pulses

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12
Q

insulin induced hypoglycemia

A
  • used as a clinical test to provoke GH secretion in suspected GI-deficient individuals
  • aa increase GH primarily by decreasing somatostatin release
  • GH binds to GH binding protein which prolongs life
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13
Q

GH Regulation/effects

A
  • GHRH from hypothal increases GH, somatostatin decreases
  • GH important in child development and metabolism
  • some effects mediated by somatomedins-IGF1 produced by liver or target tissues
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14
Q

actual release of GH

A
  • GHRH stimulates Gs protein receptors in somatotroph cells
  • increases cAMP and calcium, causes release of GH
  • cAMP activates PKA, phosphorylates CREB, upregulates Pit-1 which upregulates GH
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15
Q

paraventricular region

A
  • synthesize somatostatin

- inhibits through Gi

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16
Q

GH activation of its receptor

A

-transmembrane receptor in cytokine receptor family
-must dimerize for signal transduction
-major sites of action:
bone, liver adipocyte, muscle
-JAK/STAT
-binding causes dimerization of receptor and binding of JAK tyrosine kinase 1, induces phosphorylation of JAK kinases as well as receptor 2
-activated JAKs subsequently P the STATs- which go to the nucleus and act as TFs
-leads to expression of CISH and established GH target gene

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17
Q

effects of GH

A
  • postnatal longitudinal growth

- direct and indirect effects

18
Q

GH in liver

A
  • stimulates IGF1

- stimulates hepatic glucose production

19
Q

adipose tissue

A
  • GH stimulates release and oxidation of free FA, especially during fasting
  • mediated by the reduction in activity of lipoprotein lipase
  • lipogenesis reduced
20
Q

skeletal muscle-GH

A
  • anabolic actions
  • stimulates aa uptake and incorporation into protein
  • suppresses protein degradation
  • stimulates cell proliferation, increases metabolism and changes muscle fiber distribution
21
Q

brain effects of GH

A

-mood and behavior

22
Q

gh overall

A

counteracts action of insulin on lipid and glucose metabolism by decreasing skeletal muscle glucose use, increasing lipolysis and stimulating hepatic glucose production

23
Q

effect of GH on bone

A
  • increase aa uptake
  • increase protein syn
  • inc DNA and RNA syn
  • inc chondroitin sulfate
  • inc collagen
  • inc cell size and number
  • supports differentiation of mesenchymal stem cells into chondrocytes
  • local IGF1 induces clonal expansion of early chondrocytes and maturation of later
  • leads to synthesis of ECM proteins including typ II collagen, hyaluronic acid and mucopolysaccharides
  • as cells move toward trabecula they become calcified
24
Q

GH and food

A
  • stimulate the liver to secrete IGF1
  • some made by kidney and skin but don’t contribute to circulation
  • circulates all day at relatively constant level
  • GH doesn’t induce growth in animals that lack insulin, also wont work without carbs, anorexia will curtail IGF 1 and decrease growth
25
Q

IGF1

A
  • stimulates growth
  • endocrine, paracrine and autocrine
  • negative feedback to hypothal and pit to downregulate GH
  • clinical use-primary screening test fo GH def, more stable and reflective of GH
26
Q

IGF I and II

A
  • share 3 domains, aa seq homology (with insulin too)
  • C region is cleaved from insulin, but not IGFs
  • IGFs have D domain
27
Q

IGF I and II receptors

A
  • insulin and IGF1 are heterotetramers joined by disulfide bonds
  • cytoplasmic portion of beta subunits have tyrosine kinase domains and auto-P sites
  • IGFII-single polypeptide chain with no kinase domain, cellular function poorly understood
28
Q

signaling pathways from IGF1

A
  • dimerization of receptor leads to auto-P
  • recruits two major phosphotyrosine binding proteins IRS-1 and SHC
  • phosphorylated by IGF1 receptor
  • recruits other proteins to the membrane leading to activation of the phosphoinositol 3 kinase and Ras/MAp kinase pathways that regulate transcription
29
Q

pubertal growth spurt

A
  • sex hormones contribute to rapid increase in stature
  • girls earlier and boys later
  • IGF peak in puberty
30
Q

GH def and replacement

A
  • several rare causes of def
  • any defect affecting HPA
  • mutation ins GH1 gene (can’t treat because they’ve never seen it so they will have a rxn)
  • children have extremely slow growth- less than 2 inches/year
  • severe post natal growth factor
  • giving extra hormone doesn’t increase rate of growth to above normal levels
31
Q

organic causes of GH def

A

congenital absence of pit stalk, TBI, cranial radiation therapy

32
Q

idiopathic causes of GH def

A

-can be functional of developmental state, which resolves mid puberty

33
Q

laron syndrome

A
  • GH insensitivity
  • point mutation/deletion in GH receptor
  • low IGF concentration
  • normal/elevated GH
  • severe post natal growth failure
  • treatable with IGF
  • AR
  • heterozygotes mild growth retardation
  • out of 230 worldwide, none have cancer
  • no diabetes/ acne
  • mutation of Stat5b gene similar
  • treatment with IGF before puberty can compensate for short stature
  • ecuador
34
Q

gigantism

A
  • pituitary giants
  • exposed to too much GH throughout life
  • hyperglycemia/ diabetes
  • degeneration of beta cells
35
Q

acromegaly

A
  • GH secreting adenomas
  • effects vary depending on size and growth rate and invasiveness
  • large tumors cause destruction of pit and deficiency of other pit hormones can affect optic chiasm and vision
  • protrusion of jaw, macroglossia (big tongue), enlarged hands and feet, carpal tunnel, reduced strength
36
Q

GH def in adults

A
  • usually caused by pit probs
  • can be result of surgery or radiation
  • causes increase in interstitial fat
  • reduced strength and bone loss
  • feelings of anxiety and depression
  • treatment with GH remediates issues
  • found by using insulin to stimulate secretion
  • increases visceral fat-carotid intima media thickness, IF markers of CV disease, clotting factors, insulin resistance
  • decreases myocardial function- HDL
37
Q

GH and aging

A
  • 5-20, 5 ng/ml
  • 20-40, 3
  • 40-70, 1.6
  • replacement therapy:
  • restores muscle mass, reduces fat deposits, feeling of increased energy
  • side effects include insulin resistance, diabetes, edema, carpal tunnel
38
Q

FDA approved use of GH

A
  • GH def, idiopathic short stature, turner syndrome
  • prader willi syndrome
  • chronic renal insufficiency
  • small for gestational age
  • nutrition- first few generations in america are taller because parents weren’t nourished
39
Q

other causes of growth problems

A
  • celiac, hypothyroidism
  • reduced levels of IGF
  • replacement of thyroxin restore growth to normal height
  • thyroid response element upstream of GH transcriptional start site- hypothyroid reduces GH
40
Q

short stature with normal hormones

A

-turner, down syndrome

41
Q

tuner syndrom

A
  • haploinsufficiency of SHOX gene
  • SHOX is developmentally regulated
  • concentrated in the hypertrophic region of the growth plate zone during childhood
  • pseudoautosomal region of Xp
  • missing 1 X
  • 45, X in about 50%
  • isochomosome Xp or q, or mosaic
  • 45X, 46XX
  • slower velocity during childhood, scant pubertal growth spurt
  • treated with GH and sex steroids- height improved but not restored
42
Q

SHOX locus

A
  • developmentally regulated
  • expressed throughout fetal growth plate, concentrated in hypertrophic zone
  • pseudoautosomal region of Xp
  • can have mutation that causes short stature

Physiology Unit 6 (12 decks)

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