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28 Cards in this Set

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Where does Betta oxidation occur?
Mostly in the mitochondria.

The first step is to activate the fatty acid to fatty acyl CoA in the cytisol and have carnitine transfer it into the mitochondria for the remainder of oxidation.
Where does fatty acid synthesis occur?
Mostly in the cytoplasm.

The acetyl CoA is inside the mitochondria and must be shuttled out of the mitochondria
When glucagon is released how are the following
enzymatic processes effected?

1.) acetyl CoA carboxylase
2.) hormone sensative lipase
3.) pyruvate dehydrogenase
1.) acetyl CoA carboxylase will be inhibited since its activation would synthesize fats.

2.) would be activated as it would break down TG to make ATP.

3.) pyruvate dehydrogenase would be inhibited to preserve pyruvate for gluconeogenesis.
When acyl CoA or palmitoyl CoA are high what can we expect to be ALLOSTERICALLY regulated?
Decrease in Fatty acid BS by regulation of the enzyme Acetyl CoA carboxylase.

When there are lots of fatty acid you block the pathway to make fatty acids.
When acetyl CoA and other fatty acids are high, what Allosteric regulation can we expect with respect to Fructose 2,6 disphosphate.
A decrease in the enzyme and phosphofructokinase 1 and all enzymes that promote glycolysis because there is no need for energy. Expect increases in fructose bisphosphotase activity (gluconeogenic pathway).
Insulin concentration is high what can you expect of the following enzymes:

1.)acetyl coa carboxylase
2.)hormone sensative lipase
3.)pyruvate dehydrogenase
4.) How is it that insulin activates/inactivates an enzyme?
High insulin means that glucose is high and no need to break down TG or FA.

1.) makes FA so wed expect an increase in expression of the enzyme. (dephosphorylation activates)
2.) we would expect a decrease in lipases as there is no need for TG oxidation there is plenty of glucose (dephosphorylation = inactivation).
3.) activated. Lots of glucose becomes lots of pyruvate and dehydrogenase begins converting to Acetyl CoA.
4.) dephosphorylation
acetyl coa carboxylase is activated/inactivated by citrate? what about epinephrine?
Like insulin, citrate activates acetyl coa carboxylase to make FA. Insulin suggest plenty of sugar and no need for FA oxidation AND citrate means plenty of activity through TCA store some FA.

Epinephrine on the other hand deactivates the action of acetyl coa carboxylase.
Carnitine palmitoyl transferase is activated/inhibited by malonyl CoA.
Inhibited. Why???
What happens when a person fasts (low carbohydrate diet or high fat)
Glucagon increaess

Insulin decreases

Betta oxidation stimulated in liver (acyl CoA dehydrogenase)

Acetyl CoA carboxylase is deactivated (no synthesis)

Fatty acid synthase decreases

Malonyl CoA (synthesis) decreases and in turn Carnitine transferase (oxidation) activity increases

oxaloacetate increasingly used for gluconeogenesis since no glycolytic energy demands. Thus TCA cycle slows meaning Citrate concentration will decrease and Acetyl CoA will accumulate.

Alternative uses for Acetyl CoA begin including production of ketone bodies and thier increased use in the brain. Ketone production increases found in urine and result in urine acidosis and loss of Na ions.
Phosphotidyl choline made from..
CDP Choline and a diacyl glycerol.
How is cholesterol synthesized?
3 Acretyl CoA form HMG CoA by the enzyme HMG CoA synthase. then by the enzyme HMG CoA reductase HMG CoA is converted to mevalonate (MVA). 3 MVAs come together with 3 ATP to form Farnesyl pyrophosphate (15 carbons). 2 of these dimerize forming C30 squalene which in the presence of O2 undergoes cyclization to C27 cholesterol (a cross roads molecule).
What is the precursor to bile salts and steroid hormones?
Choleterol
Cholesterol and sunlight can form...
Vitamin D
Reduction of cholesterol and the presence of O2 can produce
Progesterone
Oxidation of cholesterol gives progesterone what 2 products are made by further oxidation?
Aldosterone, Cortisol, Estrone and Testosterone
What is cholic acid and how is it derived.
Cholic acid is a detergent to emulsify fats. it is synthesized from cholesterol.
What are the 4 classes of lipoproteins?
Very low density lipids
Low density lipids
intermediate density lipids
high density lipids

HDL, IDL, LDL, VLDL
which lipoproteins are highest in lipids and lowest in protein?
VLDL and chylimicrons.
Chylomicrons are made in __________________ and function to _____________________
the intestines;
function to transport TG to peripheral tissue (adipose tissue) where TG are broken into glycerol and fatty acids to be taken up by the cell.
What is the function of Lipoproteins?
Function to transport lipids in the blood.
HDL is made in the ____________. its primary function is to __________________ because it can _________________.
It is made in the liver and intestines. main fxn is to collect cholesterol from periphery and perform esterification to fatty acids and then transfer them back to the liver. It has the enzyme LCAT which allows it to transfer fatty acyl groups from Phosphotidyl choline to cholesterol.
When cholesterol is low what enzyme do we KNOW FOR SURE is being inactivated...
HMG CoA reductase (1st step in cholesterol synthesis).
Which of the lipoproteins serve to deliver cholesterol? How can it do this?
LDL; because it has APOb100 protein
which lipoprotein fuctions to collect cholesterol and esterifies it.
HDL
Which class of lipoprotein deliver TG to peripheral tissue.
Chilomicrons
Which lipoprotein class serve to deliver a broad range of lipids to the tissue
VLDL
Other than HMG CoA reductase activity what result do you expect to accompany high cholesterol?
Synthesis of LDL receptors should decrease. Recall that LDL serve to "deliver cholesterol to peripheral tissue" since it contains the APOb100 protein.
Summary of TG metabolism as it relates to lipoproteins.
Original TG are broken down to FA and glycerol. Upon entering the intesting TG are reformed and absorbed by lipoproteins for transport throughout the body.