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143 Cards in this Set

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  • Back
Which has a higher melting point, saturated or unsaturated fatty acids?
saturated has a higher MP (e.g. butter is solid at room temp, veg oil is liquid)
Is animal fat or vegetable fat more saturated?
Animal fat is more saturated.
What are the essential fatty acids for humans?
lineoleate (w-6) and linolenate (w-3)
Fatty acids are stored as ____.
triacylglycerols (aka triglycerides)
Why are TAGs more efficient energy stores than glycogen?
1. TAGs are more reduced, so more energy is released when they are oxidized.

2. TAGs are water insoluble. Glycogen on the other hand, stores quite a bit of water with it.
TAG + lipase --->
glycerol + fatty acid
If you have a 16C fatty acid, how many times will this FA need to be oxidized for it to be completely broken down to Ac-S-CoA?
It will need to go through the process 7 times.
What coenzymes are required to break an acetylCoA off a FA?
one of each:
FAD
NAD+
CoA
H20
About how much more ATP per gram do you get from the oxidation of FAs than that of glucose?
about 2.5 times more ATP from fatty acids
Where does fatty acid synthesis occur?
In the cytoplasm.
What cells carry out fatty acid synthesis?
Mostly liver cells, but also adipocytes
What is ACP?
acyl carrier protein
What is the major coenzyme of fatty acid synthesis?
NADPH (this is a common coenzyme of biosynthetic pathways)
FAs are synthesized two carbons at a time. What carries these two carbons?
They are attached to an acyl carrier protein (ACP)
How is acetyl ACP activated?
It is carboxylated to make it malonyl ACP.

The carboxyl group will be removed during the first step of synthesis.
The acyl carbon is completely ____ during FA synthesis.
reduced
What rxn does acetyl CoA carboxylase catalyze?
The synthesis of malonyl CoA from acetyl CoA.

(NB: This is counter-intuitive for me!! Try to remember that this "carboxylase" ADDS a carboxyl group to the acetyl CoA.)
Higher levels of what might increase FA synthesis?
Insulin and citrate, which both indicate a high energy state.
The presence of what hormones might stop FA synthesis?
Epinephrine and glucagon (among others). These both indicate a low energy state. FAs will be broken down, not synthesized.
FA degradation occurs where?
In the matrix of the mitochondria.
The acyl group of acyl CoA must attach to what protein to get into the mitochondrial matrix?
carnitine
What happens to acyl carnitine once is enters the mitochondrial matrix?
It is converted right back to acyl CoA.
What inhibits acyl carnitine formation?
malonyl CoA
How does malonyl CoA affect FA degration and synthesis?
High levels of malonyl CoA indication that FA synthesis is occuring.

They also indicate that FA degradation is being inhibited by blocking the formation of acyl carnitine for transport into the mitochondrial matrix.
What is beta oxidation?
It is the process by which acyl CoA is broken down into acetyl CoA during fatty acid degration.
What is the first organ to break down fat droplets in the intestines?
Bile salts of the gall bladder emulsify the drops into smaller "emulsion droplets".
What role does the pancreas play in breaking down emulsion droplets?
Pancreatic lipase breaks the fat into monoglycerides and free fatty acids.
Monoglycerides and free fatty acids will combine with bile salts in what form in the intestines?
mixed micelles
Mixed micelles can interact with the ____ in the intestines.
microvilli
What happens to the fatty acids of the micelles after they enter the intestinal epithelial cells?
They form back into TAGs.
What happens to TAGs in intestinal epithelial cells?
They combine with lipoprotein to make chylomicrons, which exit the cell.
Lipoproteins and triacylglyerides combine to form ____.
chylomicrons
What is on the interior of the chylomicron?
cholesterol and TAGs
What is on the surface of the chylomicron?
phospholipids and proteins
Why does the blood of a person who has just eaten appear milky?
chylomicrons
What does LPL (lipoprotein lipase) do to the chylomicron?
It breaks down most of the TAGs into FAs and glycerol, which are taken up by tissues.
What is the main component of the chylomicron remnant? Where does the remnant go?
cholesterol ester. It goes to the liver.
What is serum albumin?
It is a protein that binds FAs in blood and prevents them from acting as soaps in the blood.


(Serum albumin does a lot of other stuff too that I don't care about right now.)
What is the precursor for the backbone of TAGs? What pathway is the source of this molecule?
Glycerol-3-phosphate (not glycerol) is the precursor. Glucose metabolism is the only source of this molecule.
Adipocytes can both ____ and ____ TAGs.
synthesize; degrade
The adipocyte makes TAGs from what two components?
Glycerol-3-phosphate and fatty acyl CoA.
When the adipocyte breaks down TAGs, it breaks them into what two components?
glycerol and free fatty acids
When insulin is high, would you expect hormone-sensitive lipase to be high or low?
It would be low. The cell is synthesizing TAGs for storage, not breaking them down for more energy.
Hormone sensitive lipase is stimulated by ___ levels of glucagon and ___ levels of insulin.
high; low
During fasting, TAGs will be broken into glycerol and FAs. What happens to these in the liver?
Glycerol can become glucose. FAs enter the matrix of the mitochondria.
Fatty acids are beta oxidized into ____.
acetyl CoA
In the liver, acetyl CoA can be converted into ______, which are easily converted back to acetyl CoA in other tissues.
ketone bodies
What are the two main ketone bodies?
acetoacetate (can be reduced to acetone) and 3-hydroxybutyrate
Why does the body convert acetyl CoA to ketone bodies (i.e. what are the benefits over acetyl CoA)?
They are easier to transport and absorb, and they don't need to be bound by serum albumin in the blood.
What is the problem with ketone bodies?
They are acids. They can acidify the blood.
Explain the relationship between glucose, ketone bodies, and fatty acids during fasting.
Glucose stores are very limited. The body turns to other sources, including FAs. However, only so much FA can be carried in the blood, so the body uses ketone bodies instead.
Oxaloacetate levels in the liver drop during starvation because it is being used in ____.
gluconeogenesis
When oxaloacetate is used for gluconeogenesis during starvation, it cannot be used in the TCA cycle. What is then used for energy?
FAs are degraded via beta oxidation. (but the levels may be high and acetyl CoA is then converted to ketone bodies)
Low levels of insulin in Type 1 cause diabetic ketoacidosis. Why?
Although there is a lot of glucose in the blood, the tissues cannot take it up, and react as they do during starvation, which results in production of ketone bodies.
Hypoketotic hypoglycemia is a genetic disorder characterized by what?
Inability to efficiently oxidize fatty acids. They can't, therefore, make acetyl CoA for ketones, and rely almost exclusively on glucose, so there are low levels of both.
How does the body catabolize cholesterol?
It does not. It can only convert them to bile salts, which are excreted.
What is a cholesteryl ester?
It is a cholesterol molecule with a fatty acid attached at the hydroxyl group.
Where is cholesterol synthesized in the body?
Mostly in the liver. Also in the intestines.
Where is cholesterol synthesized in the cell? What are the building blocks?
In the cytoplasm. Acetyl CoA
What synthetic pathway most resembles the cholesterol synthetic pathway?
Ketone bodies. (In fed as opposed to fasting conditions.)
What is the common intermediate in the ketone and cholesterol synthetic pathways before they split?
HMG-CoA (in cholesterol, it is reduced to mevalonic acid)
What is the precursor to mevalonic acid? Mevalonic acid loses CO2 to become what?
HMG-CoA; isopentenyl PP
Isopentenyl PP condenses with with DMA PP to increase by how many carbons?
5 (10 total)
What intermediate in cholesterol synthesis can be used to make dolichol, CoQ, and phrenylated proteins?
Farnesyl PP
What kind of hormones are made of cholesterol?
steroids
From isopentenyl PP, 5 carbons are added at a time until what step? What is unique about this step?
Until farnesyl condenses with farnesyl to form squalene in a head to head reaction (no more PP).
Cholesterol is only one of numerous _____ compounds to be synthesized by the biosynthetic pathway we discussed.
isoprenoid
What is HMG-CoA?
Two acetyl CoA's condensed (one loses CoASH)
How many carbons does squalene lose to become cholesterol?
3 carbons (30 ---> 27)
Remember the G protein Ras? How does is relate to cholesterol?
It is a phrenylated protein. The cholesterol precursor farnesyl attaches to a protein and anchors it in a membrane.
The cholesterol synthesis pathway from the beginning to isopentenyl PP
1. Acetyl CoA + Acetyl CoA
2. HMG-CoA
3. mavelonic acid
4. Isopentenyl PP / DMA PP
What is the RDS for cholesterol synthesis?
HMG-CoA reduced by HMG CoA reductase to mavelonic acid.
The cholesterol synthesis pathway from isopentenyl to squalene.
1. isopentenyl PP + DMA PP
2. geranyl PP
3. farnesyl PP
4. squalene
Cholesterol synthesis intermediates from squalene to cholesterol.
1. squalene
2. lanosterol
3. 7-dehydrocholesterol (converted to vit D)
4. cholesterol
Transcription of HMG CoA reductase is mediated by the binding of _____.
a transcription factor called sterol response element binding protein (SREBP)
SREBP is in the ER. How does it get to the Golgi where it is cleaved and activated?
SCAP escorts it
How might high levels of cholesterol inhibit cholesterol synthesis (in relation to expression of HMG CoA reductase)?
Sterols inhibit SCAP. Without SCAP, SREBP cannot activate, and so, HMG CoA reductase will not be synthesized. HMG CoA will not be reduced to malevonic acid, and so, cholesterol will not be synthesized.
What does insulin do to SREBP?
It increases activity of SREBP-1, the form that will upregulated fatty acid synthesis.

(More insulin means more enery must go into storage form.)
SREBP-2 allows expression of what two things?
LDL-R and HMG CoA reductase
What is the major regulatory enzyme of cholesterol synthesis?
HMG-CoA reductase
What effect will insulin have on SREBP-1?
It will upregulate it. SREPB-1 expresses FA synthetic enzymes.
What is LDL?
Cholesterol rich, low density lipoprotein.
Reduction of SREBP-2 will cause downreglation of HMG-CoA reductase and what else?
LDL receptor

(LDL receptor and HMG-CoA reductase expression go in tandem.)
How does LDL enter the cell?
It binds to LDL-R and enters through endocytosis.
In a lysosome, LDL is broken into what constituent parts?
fatty acids, proteins, and cholesterol
What enzyme converts cholesterol to cholesterol ester?
ACAT
How does a large concentration of cholesterol inhibit further cholesterol synthesis?
Cholesterol inhibits SCAP, the protein that transports SREBP to the Golgi for activation. Without SREBP-2, HMG-CoA reductase and LDL-R will not be expressed.

Without HMG-CoA reductase, mevalonic acid cannot be formed and cholesterol will not be synthesized.

Without LDL-R, LDL cannot be taken into the cell.
What will happen if there is a deficiency of LDL receptors?
This will lead to high levels of cholesterol in the blood. This can be genetic.
Adding ___ to normal cells suppresses cholesterol synthesis by repressing expression of ____, but not when added to cells from an FH patient.
LDL; HMG-CoA reductase
Why is the tandem expression of LDL-R and HMG-CoA reductase a problem for those with mutations on LDL-R?
LDL-R admits LDL to cells. It also binds to and inhibits SCAP. This inhibits activation of SREBP, which inhibits expression of HMG-CoA reducatse.

This means that cholesterol synthesis will continue unabated. This is a problem for someone who already has high cholesterol.
What is PCSK9?
It is an enzyme that increases degradation of LDL-R.
If PCSK9 activity increases, what would you expect to happen to blood levels of LDL?
They would go up. PCSK9 degrades LDL-R, so LDL cannot be absorbed into the cells.
Why are LDL receptors on liver cells particularly important?
These cells are the only ones that can get cholesterol out of the body as bile salts.
Cholesterol can be converted to ______ bile acids, with both a hydrophilic and hyrophobic domain.
amphipathic
Statins inhibit what?
HMG-CoA reductase.
Describe the pathway of bile salts in enterohepatic circulation.
Liver --> gall bladder --> duodenum --> illeum --> hepatic portal vein --> liver

(About 3% lost in feces.)
Why are statins and bile acid sequestering resins successful in combination?
Statins decrease de novo synthesis of cholesterol without interfering with LDL-R production. The bile acid sequestering resins help to excrete cholesterol already in the blood.
Why might statins cause myopathy?
Farnesyl PP, one of the intermediates in cholesterol synthesis, is used to make CoQ, which is used in electron transport, which makes ATP.
Cells, especially _____, have receptors on their surface that recognize and bind LDL.
hepatocytes
Excess cholesterol is removed from the ER by ______ (via ACAT) for storage in cytoplasmic droplets.
esterification
What does FH stand for? Is it an autosomal dominant or recessive condition?
Familial hypercholesteremia. Autosomal dominant. Heterozygous better than homozygous.
In the mitochondria, HMG-CoA will be used to synthesize ____, while in the cytosol, HMG-CoA will be used to synthesize _____.
ketone bodies; cholesterol
Smith-Lemli-Opitz syndrome (SLOS) results from a defect in synthesizing what? What are some symptoms?
Cholesterol. Retardation and cranio-facial malformations. May be stillborn.
How does mutation of the ras proto-oncogene affect its function?
GTP cannot be hydrolyzed, so the protein is in a perpetually active state.
What is our major source of nitrogen?
protein (food)
In terms of nomenclature, how can you tell that an enzyme is in its inactive zymogen form?
It will begin with "pro" or end with "ogen".
What foods can provide the body with carbs?
Carbs themselves, glycerol (from TAGs), or proteins, with the latter two converted to carbs via gluconeogenesis.
Amino acid catabolism starts one of two ways:
1. The transfer of NH2 to keto acids to form new amino acids or
2. the release of ammonia (NH3)
Carbon skeletons of amino acids can be ____, ____, or both.
glucogenic; ketogenic
We cannot synthesize glucose from ____.
fat/acetyl CoA
Gluconeogenesis results in net energy ___, meaning that _____.
loss; it costs more energy to do than it will ever make back.
Which major animal protein is not "complete"?
Collagen. It does not contain all the essential amino acids.
Most ____ proteins are incomplete.
plant
What happens to amino groups cleaved off digested proteins?
They form urea and are excreted.
What happens to the carbon skeleton of digested amino acids?
A number of things. The can become acetyl CoA or glucose, or they can enter the TCA cycle as intermediates.
How are amino acids transported across the intestinal epithelium.
An active transport process driven by the sodium gradient.
How are proteins degraded intracellularly?
Proteins are marked for digestion by ubiquitin in the cytosol. They then enter a proteasome, where they are digested.
Which part of the ubiquitin-proteasome pathway requires energy?
ubiquitinylation
Glutamic acid has the same carbon skeleton as what TCA cycle intermediate?
a-ketoglutarate
Nitrogen atoms can be moved from one C-skeleton to another in a process called _____.
transamination
N atoms can be removed from glutamate by a process called _______.
oxidative deamination.
N atoms can be carried in the blood in the form of free ______, especially ____ and _____.
amino acids; glutamine; alanine
____ can become pyruvate when it loses its amino group during transamination.
Alanine
_____ can become aspartate when it gains an amino group during transamination.
Oxaloacetate
Transamination causes amino acids to become _____ and vice versa.
keto acids
Which vitamin is a cofactor during the "ping-pong" step of transamination?
pyridoxine (B6)
What might high levels of transaminases in the blood indicate?
Cell damage (e.g. after heart attack)
Where is urea formed (what tissue and where in the cell)? Of what?
in the liver (cytosol and mitochondria). ammonia and CO2
When there is too much N, the brain tends to synthesize _____, while muscle cells synthesize ____.
glutamine; alanine
In the mitochondria, NH4+ and CO2 will combine to form _____.
carbamoyl phosphate
Carbamoyl phosphate combines with ____, which will eventually be regenerated.
ornithine
How much energy is required to form one carbamoyl phosphate?
2 ATP
Which amino acid is split to form urea?
Arginine
Ornithine transcarbamoylase (OTC) deficiency will lead to what?
Inability to make urea resulting in ammonia build up.
What regulates the urea cycle?
1.Energy availability.
2. Substrate availability.
3. Carbamoylphosphate synthetase 1 (CPS1).
How are CPS1 and NAG an example of feed forward regulation?
CPS1 is activated by NAG. NAG is activated by arginine. Arginine is a product of the urea cycle, which requires CPS1 to function.
How does starvation upregulate the urea cycle?
The body starts mining proteins for their carbon skeletons, resulting in ammonia needing to be excreted.
Amino acids whose carbon fragments can only be converted to _____ cannot be used to form glucose, but can be used to make fatty acids. They are termed ______.
acetyl CoA; ketogenic
What are the three main substrates for gluconeogenesis?
1. lactate
2. glucogenic amino acids
3. glycerol
PEP can be formed from pyruvate in a two step process with _____ as an intermediate.
oxaloacetate
If there is an abundance of pyruvate and NADH, what might happen?
The pyruvate will become lactate.
If there is an abundance of NAD+ and lactate, what might happen?
The lactate will become pyruvate.
"Fat burns in the flame of carbohydrate." Explain.
To optimally burn fat, the TCA cycle should be running at full blast. Without enough carbs, TCA intermediates will start to be used for gluconeogenesis.