Lecture 4 Flashcards
Where is lipoprotein lipase absent
brain and liver
Where is LPL attached to?
sulfate proteoglycan on surface of capillary endotheliium
which chylomicrons bind to as they pass
When chylomicrons bind to LPL as they pass through sulfate proteoglycan on surface of capillary endothelium; the TG are hydrolyzed to what?
what happens to them?
FFA and 2-Monoacylglycerols
They diffuse freely into tissues
Each tissue has its own isoenzyme of LPL
Does LPL activity increase or decrease in fasting state?
Decrease
Except in skeletal muscle and myocardium; they stay moderate in either state
Following a fatty meal TG’s enter where?
adipocytes
In the transition period between meal and fasting TG’s are sent where?
Skeletal muscle and myocardium
What solubilizes LPL when injectedin skin?
Heparin, increasing LPL activity
The assessment is based on serumlipase activity level pre/and post heparin injection
When TAG is hydrolyzed and a glycerol is released, it does what?
Provides substrate for gluconeogenesis
What’s the primary regulation of gluconeogenesis
Availibility of substrates (glycerol)
Circulating level of glucagon
What’s the secondary regulation of gluconeogenesis?
Adaptive changes in the rate of enzyme synthesis, degradation or both
How many amino acids in glucagon?
Is it alpha or beta?
It’s made as a large precursor and converted to glucagon how?
29
alpha
By series of proteolytic enzyme cleavage
What’s the role of glucagon?
maintain normal blood glucose level
Epinephrine and Norepinephrine is made where?
Adrenal medulla which is mediated by autonomic nervous system
and triggered by Hypothalamic glucoreceptors
Cortisol is made where?
Adrenal Zona Fasciculata and Reticularis
What triggers growth hormone
adrenal corti co tropic hormone & anterior pituitary glands stored in somatotroph cells
What secretes norepinephrine?
Pancreatic symppathetic innervations in adrenal medulla
What stimulates glucagon?
Low blood glucose (rises at night due to overnight fast)
AA in meals (stimulates insulin too)
IMplication in diabetes therapy (Byetta=exenatide
EPI/NorEPI
During severe exercise what happens?
EPI overrides inhibitory effects of substrates and glucagon will remain high
What inhibits glucagon?
elevated glucose
elevated insulin
What does glucagon do to lipids?
stimulate liver oxidation of FA and the product of ketones via acetyl-CoA
minimal effect on adipocytes
What does GLucagon do to carbs?
Increases blood glucose via mobilization of liver glycogen and increase gluconeogenesis (not muscle stored glycogen)
Free glycerol from adipocytes ends up where? What happens to it?
LIver
Glycerol kinase turns glycerol into glycerol phophate (GPO4) where it is oxidized by dehydrogenase to turn to dehydroxyacetone phosphate
What can’t adipocytes metabolize glycerol?
They lack glycerol kinase thus not being able to phosphorylate glycerol
WHat are irreversible steps of gluconeogenesis?
Glucose 6 phophatase
Fructose 1,6 Bisphophatase
Pyruvate carboxylase
Phosphoenolpyruvate carboxykinase
In gluconeogensis What is the irreversible step of phosphofructokinase-1 in glycolysis?
D-Fructose 1,6bisphophate is hydroylyzed in the next step by fructose 1,6 bisphophatase
Because adipocytes lack glycerol kinase they cannot phosphorylate and sent to liver where what happens?
Glycerol is phophorylated making Glycerol 3 P which; forms TAG or convert to DHAP by G3P dehydrogenase
What signals low energy state?
High AMP/ADP
AMP/ADP inhibit what?
Fructose 1,6 bisphosphatase but activates 1,6 phophofructokinase
What activates fructose 1,6 bisphosphatase?
HIgh citrate
What stimulates GLuconeogenesis?
High ATP and citrate levels and low amp
