M1-C1-L77 --> Lipid Metabolism
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- In the fasted state, what happens with glucagon?
- Goes up.
- In the fasted state, what happens with epinephrine?
- Goes up.
- In the fasted state what happens with insulin?
- Decreases
- Triglyceride breakdown requires the stimulation from what molecules?
-
Glucagon
Epinephrine - What are the generalized sequence of events that occurs with triglyceride breakdown?
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1. Intracellular cAMP INCREASES and ACTIVATES protein kinase A.
2. Phosphorylation and activation of hormone sensitive lipase.
3. Degradation of triglyceride to free fatty acids and glycerol. - Post degradation of triglycerides, what happens to FFA and glycerol in the fasted state?
- Both will diffuse into blood, where FFA will bind to serum albumin. Glycerol is soluble.
- In the liver, glucagon and epinephrine stimulate WHAT to form WHAT products for what process?
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Beta Oxidation
Ketones and Glycerol
Gluconeogenesis - What must happen for hormone sensitive lipase to act?
- Phosphorylation of perilipin
- What is perilipin?
- Protein that coats the lipid droplets in adipocytes
- What happens to the majority of the FFA that are mobilized from adipocytes to be taken up by the liver?
- In the liver, 60% of FFA is repackaged into lipoproteins and sent back to the adipocytes
-
What is this? - Glycerol
- Addition of each fatty acid on a glycerol requires what kind of energy expenditure?
- Two high energy bonds (total of 6 ATP)
- T/F - In the fasted state, adipose release just enough FFA for metabolism.
- F - In the fasted state, adipose releases more FFA than is needed for metabolism.
- Describe the actions oof the liver with extra FFA in the fasted state. x 3
-
1. Liver RE-ESTERIFIES the fatty acids into triglycerides.
2. PACKAGES the lipid into lipid protein.
3. SECRETES it into bloodstream. - Repackaging FFA ensures what two things?
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1. Adequate energy supply
2. Homeostasis of serum lipids in blood - Describe the steps in fatty acid transport to mitochondria. x 4
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1. Formation of fatty acy-CoA.
2. Transfer to carnitine to form fatty acyl-carnitine
3. Facilitated diffusion via acyl-carnitine/carnitine transporter.
4. Transfer back to CoA inside mitochondria. - Where would you find Carnitine Acyltransferase I?
- On the cytoplasmic face of mitochondria.
- Where would you find Carnitine Acyltransferase II?
- Inside the mitochondria.
- What is the overall point in transferring fatty acid to mitochondria?
- To degrade the long fatty acyl-CoA in to Acetyl CoA. Then, feed Acetyl-CoA into the TCA and make ATP in ETC
- Usually, Beta oxidation of 1 saturated FFA molecule will produce how many Acetyl-CoA's?
- Eight
- Usually, Beta oxidation of 1 saturated FFA molecule will lead to how many CO2's?
- 16 CO2
- Usually, Beta oxidation of 1 saturated FFA molecule will lead to how many electrons?
- 64 e-
- What is the major point of beta oxidation?
- Fatty acids get cleaved to make Acetyl-CoA
- What is needed for beta oxidation of monoUNSATURATED fatty acid?
- An isomerase to convert the cis bond to trans.
- What is needed for beta oxidation of polyUNSATURATED fatty acid?
- Need a reductase and an isomerase.
- "When life gives you propionyl-CoA, make".....what?
- A TCA intermediate (Succinyl CoA)
- When do you get the three carbon molecule, propionyl CoA?
- It is the final product in odd-chain fatty acids.
- How does biotin play a role in odd chain FA beta oxidation?
- Takes propionyl-CoA and converts it a four carbon intermediate via carboxylation.
- Under low glucose levels, the brain uses what for food?
- ketones
- Which ketone is responsible for bad breath?
- acetone
- Ketones are produced from what molecule and where specifically?
-
Acetyl CoA
Hepatocyte mitochondria - Describe the general steps in ketone formation in the liver during a fasted state.
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1. Gluconeogenesis removes oxaloacetate from TCA.
2. Oxaloacetate removal SLOWS down TCA causing accumulation of acetyl-CoA.
3. Acetyl-CoA is then used to make ketones. - Loss of insulin in IDDM patients, is due to a loss of what and where?
- Beta cells in the pancreas.
- Accumulation of ketones in blood can lead to what?
- ketoacidosis
- Ketoacidosis can alter what?
-
Heme functions
Oxygen transport - What are the presentations of Carnitine deficiency? x 4
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1. Hypoketotic Hypoglycemic Encephalopathy.
2. Cardiomyopathy
3. Myopathy
4. GI Dysmotility - What parts are effected by Carnitine deficiency? x 3
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1. CNS
2. Skeletal muscle
3. Cardiac muscle - B12 Deficiency causes an accumulation of what molecules? x2
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Methylmalonyl-CoA
Homocyteine
5-MethylTHF - B12 deficiency can cause the same kind of anemia as what other disorders? x2
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1. Oroticaciduria I
2. Oroticaciduria II - Acyl CoA Dehydrogenase deficiency affects what enzymes? x3 from worst symptoms to least.
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1. VLCAD (Very Long Chain Acyl CoA Dehydrogenase)
2. MCAD (Medium Chain Acyl CoA Dehydrogenase)
3. SCAD (Short Chain Acyl CoA Dehydrogenase)