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glycogensis
glucose—→ glycogen
activated by insulin
glycogenolysis
glycogen—→ glucose
activated by glucagon
gluconeogensis
glycerol and amino acids—→ glucose
activated by glucagon
control of blood glucose
if blood sugar too high
insulin
insulin secreted from B cells in islets of langerhans
binds to specific receptors on liver/ muscle cells
increases permeability to glucose
more glucose moves in by facilitated diffusion- more channel proteins
activates an enzyme that converts glucose to glycogen (glycogenesis)
increased glycolysis
controlling blood glucose
low blood sugar
glucagon
glucagon secreted from a cells of islets of langerhans
binds to receptors on liver cells
activates enzymes that hyrolyse glycogen into glucose (glycogenolysis)
activates enzymes that convert amino acids and glycerol into glucose (gluconeogensis)
inhibits glycolysis
second messenger model
adrenaline
secreted from adrenal glands when blood sugar levels are low
binds to receptors on liver cells
activates glycogenolysis
inhibits glycogenesis
activates glucagon secretion
inhibits insulin secretion
activates adenylate cyclase
converts ATP into cAMP (second messenger)
activates enzymes that hydrolyse glycogen into glucose
cascade reaction
type 1 diabetes
immune system attacks B cells so they can’t produce insulin anymore
may be genetic or triggered by infection
kidneys can’t reabsorb glucose so some urinated out
treay with insulin injections
type 2 diabetes
risk factors= obesity
b cells don’t produce enough insulin or body doesn’t respond to it
insulin receptors don’t work properly
colorimetry to determine glucose conc
serial dilution
benedict’s
colorimeter
calibration curve
kidneys
ultrafiltration
happens in bowman’s capsule
under high pressure
efferent end is narrower- higher hydrostatic pressure
forces liquic out of capillary into bowmans capsule
past three layers
capillary endothelium
basement membrane
epithelium of capsule
larger molecules e.g proteins too big so stay in blood
kidneys
selective reabsorption
PCT- proximal convoluted tubule
Na+ pumped out of cell into blood by sodium potassium pump
conc gradient
Na+ move from filtrate into cell by cotransporter protein
bringing amino ancids and glucose along too
amino acids move out into blood by fac diff
high w.p
some water follows by osmosis
adaptattions of PCT
microvilli- large SA
many mitochondria- ATP
many channel/ carrier proteins
loop of Henle
Na+ and Cl- actively trasnported out of ascending limb into medulla
lowers w.p in medulla
water moves out of descending limb by osmosis
descending has aquaporins, ascending doesn’t
water reabsorbed into blood by capillary network
lower w.p at bottom of medulla
water moves of of DCT and collecting duct by osmosis and reabsorbed into blood
controlling water potential
ADH
low w.p detected by osmoreceptors in hypothalamus
increased ADH production by posterior pituitary gland
ADH in capillary
binds to complementary receptors
activates phsophorylase
vesicles move and fuse with membrane so cell now has aquaporins- more permeable to water
higher w.p in collecting duct
water moves into capillary by osmosis through cell and intersitial fluid