Things I don't know: Phys Flashcards
superior hypophysial arteries
supply pars tuberalis, median eminence, infundibulum
arise from internal carotid and posterior communicating artery of circle of Willis
inferior hypophysial artieries
supply pars nervosa
arise from internal carotid
primary capillary plexus
drain into hypophysial portal veins
arise from superior hypophysial arteries
give rise to secondary capillary plexus
11B-hydroxysteroid dehydrogenase 2
- converts cortisol to cortisone in cells where aldosterone is active
kidney, colon, salivary gland
cortisone does NOT bind aldosterone receptor - local neg. feedback on cortisol, CRH and ACTH
permissive effects
TH/GC increase response of fat cells to Epi/NE ability to do lipolysis
second messengers
amplify and disperse signal of hormone once hormone binds the receptor
Factors that alter TBG levels
- increase
- decrease
- hepatitis, heroin, pregnancy
2. steroids (depends on type)
5’/3’ vs 5/3 monodeoiodinase
5’/3’: active T3 (outer iodine chopped off)
5/3: rT3 (inner iodine chopped off)
What can decrease uptake of I- into the follicular cell?
ClO-, TcO-, SCN
hypocholorite, technetium (oxidized), thiocynate
How does TSH (thyrotropin) increase TH secretion?
- increase Na/I symporter activity
- stimulates iodination of thyroglobulin
- stimuates conjugation of iodinated tyrosine to generate T4, T3
- increases endocytosis of iodinated thyroglobulin into follicular cells
- stimulates proteolysis of iodinated thyroglobulin in lysoendosomes
- increase T4, T3 into circulation
- exerts growth factor effects on thyroid cells (hypertrophy, hyperplasia)
glycogen synthase
glycogenesis
add activated UDP glucose (made from glucose to G1P) to glycogen
increased by: G6P
phosphorylation: inactive
glycogen phosphorylase
glycogenolysis releases G1P that can be dephosphorylated to glucose activated by: stress (increase in AMP) inhibited by: G6P phosphorylation: active
gluconeogenesis
liver
glucose made from amino acids, lactate, FA oxidation products
rate limiting enzymes in gluconeogenesis
- phophoenolpyruvate carboxykinase (PEPCK)
- fructose-1,6-bisphosphatase (FBPase)
- glucose-6-phosphatase (G6Pase)
Order that we use energy stores (fed)
- circulating glucose
- glycogen breakdown
- gluconeogenesis
insulin receptor cascade
- receptor TK
- transautophaosphorlate itself
- PI3K binds
- PIP3 (second messenger) is generated
- recruit PDK1 (kinase)
- PDK1 and mTORC2 phosphorylate and activate Akt
Akt
INSULIN
- MOST important protein kinase in mediating insulin function
- phosphorylates and inactivates FOXO (decreases gluconeogenesis)
- activate mTORC1: protein synthesis
AS160 and RGC 1/2
Akt activates (via insulin) proteins that regulate activity of small GTPases involved in GLUT4 translocation
AMPK and GSK-3
phosphorylate glycogen synthase and inactivate it
inactivated by: INSULIN
phosphorylation of glycogen synthase and glycogen phosphorylase
glycogenolysis
dephosphorylation of glycogen synthase and glycogen phosphorylase
glycogenesis
protein phosphatase
removes phosphate from glycogen synthase
activated by: INSULIN
fructose-2,6-bisphosphate
increases in glycolysis
inhibits FBPase
FOXO
transcription factor forG6Pase and PEPCK