UW BIOCHEM Wk2

glucose transport in APICAL face of intestinal cells

secondary active transport

glucose transport in BASAL face of intestinal cells

GLUT2

properties of GLUT1

low Km, low Vmax, basal uptake for all tissues

properties of GLUT2

high Km, high Vmax, liver and pancreas - high intake after eating to trap with glucokinase

properties of GLUT3

low Km, low Vmax - brain

properties of GLUT4

low Km, high Vmax, translocated to plasma membrane in response to insulin, muscle and adipose tissue

properties of glucokinase

acts as glucose censor in pancreatic β cells

mechanism for insulin release

high ATP → K+ channels close → depolarization → insulin release

when glucose is high

insulin will be high

when glucose is low

glucagon will be high

NADH:ATP from ETC

1:3

Glucose:ATP from glycolysis

costs 2 during investment phase, gains 4 during production phase

hexokinase is inhibited by

glucose-6-phosphate

phosphofructokinase is inhibited by

ATP, citrate

pyruvate kinase is inhibited by

ATP, acetyl-CoA, alanine

action of pyruvate kinase

phosphoenolpyruvate (PEP) → pyruvate

insulin action on PFK2/FPBase

dephosphorylation (cruelly activates KINASE)

glucagon/epinephrine action on PFK2/FPBase

phosphorylation (cruelly activates PHOSPHATASE)

action of PFK2/FBPase

Fructose-6-Phosphate ←→ Fructose-2,6-bisphosphate

role of F26BP

drives glycolysis while insulin is high

reason for anaerobic glycolysis

not speedy enough; mitochondria are slow

citrate synthase is inhibited by

NADH, succinyl-CoA, citrate, ATP

isocitrate dehydrogenase is inhibited by

ATP

α-ketoglutarate dehydrogenase complex is inhibited by

succinyl-CoA, NADH

TCA is driven by

low energy conditions (AMP) and muscle use (Ca2+)

TCA is inhibited by

high energy conditions (NADH, ATP)