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2,3 Bisphosphoglycerate is only made under what conditions?

Conditions of hypoxia

(Like high altitude or heavy smoking)

You don't want to do it at other times because it requires energy to do.


Describe the mechanism by which  2,3 biphosphoglycerate is activated by hypoxia

1,3 bisphophoglycerate is converted to 3 phosphoglycerate. 3 phosphoglycerate then builds up if there is no oxygen to power the electron transport chain.

When 3 phosphoglycerate builds up it actually activates bisphosphoglycerate mutase. This enzyme create 2,3 bisphosphoglycerate from 1,3 bisphosphoglcerate


If there are problems downstream of pyruvate, where does the cell get ATP from?

The cell will have to get all its ATP from glycolysis with lactic acid as the end product.


What is the turnover rate like in fatty acids?

VERY high. Turned over about 180 times per 12 hr. It's because there is a lot in storage, but only a small amount in circulation. Constantly creating and burning.


Fatty acids: Unsaturated or saturated have higher melting points? why?

Unsaturated that have a lower melting point!


Example: butter (saturated) is solid at room temp, whereas olive oil (unsaturated) is more liquid.


What is the protein in serum that transports fatty acids and transports them to needy cells.



How is adipocyte stored Fatty acids different from dietary ones in the way its transported?

Albumin takes the ones from adipocytes. There are specific molecules for the dietary ones. (Chylomicrons, i think... etc)


What do the lipase molecules in adipocyes genereally respond to?


Insulin - inhibits the lipase

Glucagon, epinephrine, and noreprinephrine - activate it


Sum up what happens to the Fatty Acid from when it arrives at the cell to when it arrives at the mitochrondria

  1. FA-albumin complex binds to receptor at surface and the FA is brought into the cell
  2. Coenzyme A is added through fatty acyl CoA synthetase (GIVE IT A HANDLE)
  3. This can then easily pass through the outer membrane of the mitochondria


How do we get the fatty-acyl CoA across the impermeable inner membrane of the mitochrondia

  1. CPT1 Switches out the CoA for a carnitine molecules that the fatty acyl group will be able to ride across the inner membrane
  2. The carnitine translocase is a symporter that trades a fatty-acyl-carnitine for a carnitine
  3. CPT2 Then switches the carnitine for a CoA and the fatty-acyl-CoA is now ready to be beta-oxidized


How does Acetyl CoA carboxylase (ACC) regulate fatty acid trasnport into the mitochrondria?

It converts acetyl CoA into malonyl CoA, which inhibits CPT1

Insulin activates it if there is a lot of glucose around because it is unecessary to make energy through beta oxidation.

AMP inactivates it if there is not a lot of excess energy around, so that more energy can be created by beta oxidation without interference from ACC


How do you get CPT 2 deficiency and what would be the problems associated?

Inherited recessive disorder

Adult onset:  Characterized by muscle pain, weakness and myoglobinuria after prolonged exercise or fasting.

Neonatal/Infant Onset: Irritabilty, failure to thrive, death


Causes problems because carb supplies just aren’t enough to meet all the caloric needs, burns up too fast and you cant use FA’s

In serum lipid profiles they will not show elevated ketone bodies like what would be seen in normal starvation because beta-oxidation is required to produce them. YOu would see a lot of acyl carnitine in their lipid profile.


4 steps of fatty acid oxidation:




Carbon-carbon bond cleavage


alpha, beta, and w-ish carbon. What are they on the fatty acid chain?

 a carbon:  first carbon away from a functional group

b carbon:  second carbon from the functional group

w carbon:  furthest carbon from the functional group


Do you get more ATO from glycolysis or fatty acid b-oxidation?

beta oxidation


Palmitic acid (16:0) is beta oxidized. How many oxidation reactions will this require? How many acetyl-CoA groups will it create?

7 oxidations (NOT 8)

8 acetly CoA 's


Let's say you have medium chain acyl CoA dehydrogenase deficiency. What is the right name for that? What are the symptoms?

Reye Syndrome


fasting hypoketotic hypoglycemia

(Not normal to be hypoketotic when you are hypoglycmeic)

Hepatic encephalopathy

sudden infant death syndrome

Diagnosed by lipid profiles of mutation identification


What would you see in the blood serum of someone with Reye Syndome?

A lot of medium length fatty-acyl-CoA 's


Why should you watch out for unripe fruit in Jamaica?

Ackee fruit that is not ripe has a chemical called hypoglycin.

Ingesting a lot can inhibit acyl-CoA-dehydrogenase similar to MCAD(REYE)

So you could get Jamaican vomiting sickness.

Usually not fatal, but also not fun.



Are cis or trans double bonds needed in order for fatty acid catabolism to occur?


Enoyl-CoA hydratase only accepts trans double bodns


What has to be done to catabolize a fatty acid with unsaturation?

Enoyl-CoA isomerase can move the double bond to the right positiion and 2,4-Dienoyl CoA reductase can reduce the fatty acid

(This is a crappy answer...)


What can be done in the case of odd-chain lengthed fatty acids?

Basically the oxidation is all the same until the very last cycle when instead of 2 acetyl-CoA's you get 1 acetyl-CoA and 1 Propionyl-CoA


Downstream the propionyl CoA can be converted to succinyl CoA (An exact intermediate in the TCA cycle)

That's wild.


What happens to all those ridiculously long fatty acid chains?

They are degraded in peroxisomes in a similar manner to beta-oxidation. Once they hit a 4-6 carbon chain then they are trasnferred to mitochondria for the regular beta oxidation


What about  fatty acid chains with branches coming off of the chain? waht happens to them?

They are beta oxidized the same way but can produce different end prodcucts. For example, any carbons with methyl chains will make propionyl CoA, whereas the ones without branches can still prodcue normal propionyl CoA.


What is w oxidation?

It is a sosrt of inefficient way of doing oxidation where they make both ends carboxylic acids and then metabolize from both ends. 

Cytochrome P450 enzymes do it.

I think this happens when there is a disruption of normal metabolism and things have to go down in the endoplasmic reticulum instead


Outline where these parts of your body can get energy and where they prefer to get energy:

Red Blood Cells:


Skeletal Muscle:

Red Blood Cells: Glucose ONLY (no mitochondria)

Brain: Prefers glucose, can use ketone bodies

Skeletal Muscle: Glucose/ Fatty Acids/ Ketone Bodies



Where in the body are ketone bodies produced from fatty acids?

the liver! yep.


If a patient comes in with ketoacidosis, what would you expect is their condition?

Also, what is Ketoacidosis?

Starvation or diabetes


Ketoacidosis is a depression in blood pH caused by excessive ketone body prodcution


A couple examples of ketone bodies that can be used as fuel by brain heart and skeletal muscle?

3-hydroxybutyrate and acetoacetate


They are first converted to acetly CoA and then go into the TCA cycle