Flashcards in biochem - feast/starve cycle Deck (50)
brain derives energy from...
glucose and ketone bodies only
cannot use FA
glucose levels for
-normal 8 mM
-renal threshold at 10mM --> glucosuria, excess urination
-diabetic coma 60 mM
-overnight = 5 mM
after a meal
glucose from where
up to 24 hrs
starting at 8 hrs
gluconeogenesis - dominant process at 16 hrs
polypeptide secreted by beta cells in pancreas in response to elevated blood glucose
SIGNALS well fed state and promotes increased transport of glucose into adipose and muscle, glycogen synthesis, de novo TG synthesis, deposition of fat, and protein synthesis
-inhibits breakdown of fat, protein, and glycogen
made from alpha cells in pancreas in response to low blood glucose, low insulin
signals fasting state and promotes glycogenolysis, lipolysis, and gluconeogenesis
where is there no glucagon receptor (so no effect on)?
in pancreas glucose binds and causes
glucagon to go down, and insulin to go up
liver fat production
in liver glucose can be converted to triacylglycerols and packged into VLDLs and released into blood --> FAs of VLDLs are stored in adipose tissue
intestinal triacylglycerol absorption
packaged into chylomicrons and secreted into lymph into blood
insulin activates which transporter?
GLUT4 on muscle and fat tissue
oxidize it to pyruvate and lactate
what vessel transports aa and glucose to liver
hepatic portal vein
in liver, what activates...
1- glucose transport
5- FA oxidation
7 - gluconeogenesis
1 - insulin and glucagon both have no effect on transport
2 - insulin activates glycogen storage
3 - glucagon activates glycogen breakdown
4 - insulin activates FA synthesis
5 - glucagon activates FA oxidation
6 - insulin activates glycolysis
7 - glucagon acivates gluconeogenesis
in adipose, what inhibits
1- glucose transport
2 - TG deposition
3- TG mobilization
1 - glucagon inhibits glucose transport in fat
2 - glucagon inhibits TG deposition in fat
3 - insulin inhibits TG mobilization; glucagon ACTIVATES TG mobilization
in muscle, what enzyme works? what is its effect on...
activates - glucose transport, glycogen synthesis, protein synthesis
inhibits - glycogen breakdown and protein breakdown
TGs of chylomicrons and VLDL
where are each produced? and where are they digested/by what?
chylomicrons are made from dietary fat and VLDL is made from glucose in liver
digested in capillaries by lipoprotein lipase to form FAs and glycerol --> stored by adipose as TGs
as blood glucose decreases...insulin? and glucagon?
insulin decreases and glucagon increases --> stimulating release of stored fuels into blood
when in fasting state, the liver...
supplies glucose and KB to the blood
it maintains blood glucose via glycogenolysis and gluconeogenesis and makes ketone bodies from FAs of adipose
2 ketone bodies?
ketone bodies have a _____ ______ effect
what happens 2-3 hrs after a meal to release glucose into blood
glycogenolysis - glycogen is broken down;
glycogen stores deplete within 30 hrs
what happens 4-6 hrs after a meal?
gluconeogenesis carbon sources
lactate from RBCs or exercising muscle
glycerol from TGs of adipose breakdown
AAs (alanine) from muscle protein
propionate from oxidation of odd chain FAs
ketone body formation
adipose tissue breaks down TGs in response to rising glucagon
FAs and glycerol are released
B oxidation converts the FAs to acetyl coA which is used in liver to make KBs
muscle release ____ in fasting state
the carbons are used for gluconeogenesis and the nitrogen is converted to urea
muscles decrease use of KBs so KB [ ] in blood goes up and brain can use them for energy so that it requires less glucose
gluconeogenesis slows down which spares muscle protein and produces less urea than an overnight fast!
body uses mostly fat when in starvation
two places where gluconeogenesis occur?
liver and kidney cortex
cycling of Lactate produced by red blood cells during anaerobic respiration in the muscles back into glucose.
The lactate produced by the muscle anaroebic glycolysis (glucose to lactate to produce atp) is cycled into the liver through the blood. In the liver it is converted to pyruvate by lactate dehydrogenase. The pyruvate is then cycled back into glucose by gluconeogenesis (using atp) and recycled back into the blood for use by red blood cells and muscles.
The Cori Cycle is significant two fold; it is neccesary to prevent lactic acidosis and in the conservation of oxygens being carried by erythrocytes(red blood cells). Because erythrocytes do not contain mitochondria, any aerobic respiration they would undertake would require the use of the oxygen they are transporting, which would negate the transport.
major gluconeogenesis precursors?