Lipids 3 Objectives - Maltese

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Compare total energy reserves in lipids, protein and glycogen. Lipids > Protein > Glycogen > Glucose
Describe the difference between the energy storage capacity of fat and glycogen.
lipid energy storage is that they are anhydrous.
The key to high
1 gram of Glycogen produces 4 kcal, but 1 gram of Glycogen is complexed to 2 grams of water.
Therefore, 1 gram of wet glycogen = .33 grams of dry glycogen.
.33 gram x 4 kcal/g dry glycogen = 1.32 kcal/g wet glycogen
Lipids produce 9 kcal/gram
Describe the cells that are the major storage site for lipids.
Adipocytes contain a large lipid droplet
with the cytoplasm and organelles pushed up against the membrane.
Describe the structure of a triglyceride Glycerol backbone with 3 Fatty Acids connected through ester
linkages
Describe the pathway for digestion and transport of dietary TG's to adipocytes DIGESTION:
Triglycerides are emulsified by bile salts and digested by PANCREATIC LIPASES, to Fatty Acids and
MonoGlycerols. These then cross into cells where they are re-synthesized into Triglycerides.
TRANSPORT: Triglycerides associate with CHYLOMICRONS and VLDL's and are transported to Adipocytes.
Once they reach the the cells, LIPOPROTEIN LIPASE re-catabolizes them so that they can enter the
adipocyte and associate with the lipid droplet.
Note: Lipoprotein Lipase is stimulated by INSULIN.
What are the three enzymes involved in Fatty Acid mobilization?
TG --> DG + FA
ADIPOSE TRIGLYCERIDE LIPASE:
HORMONE-SENSITIVE LIPASE: DG --> MG + FA
MONOGLYCERIDE LIPASE: MG --> Glycerol + FA
Describe the regulation of TG mobilization.
7TM Receptor
1. Glucagon, Epinephrine or Norepinephrine bind to
2. G-Protein is activated and binds to Adenyl Cyclase
3. Adenyl Cyclase converts ATP to cAMP
4. cAMP activates Protein Kinase A
5. Protein Kinase A phosphorylates (activates) Perilipin and HS Lipase
a. Perlipin activates ATGL (by binding of a CoActivator). This catalyzes TAG --> DAG
b. HS Lipase catalyzes DAG --> MAG
c. MAG Lipase will automatically function
Describe Insulin's counter-effect on FA mobilization. Stimulates PHOSPHODIESTERASE (cAMP -->
ATP) and HS LIPASE PHOSPHATASE (HS Lipase-P --> HS-Lipase)
Describe the fate of glycerol released during glycolysis. GLYCEROL KINASE: Glycerol --> Glycerol 3Phosphate
Occurs in liver and kidneys
Glycerol 3-Phosphate --> DHAP --> Glyceraldehyde-3-Phosphate
G3P can proceed with Gluconeogenesis/TCA cycle depending on what is required in the body.
Give the two types of diabetes and the relationship between Obesity and Type II.
Type I
(Juvenile) - Pancreatic beta cells do not secrete insulin. As a result, glucose is not taken up and lipolysis
remains high.
Type II (Adult Onset) - Insulin is produced but its effects are blocked. As a result, glucose builds up,
causing more insulin to be released. Eventually, the pancreas becomes resistant to high glucose and
stops responding insulin.
Obesity causes adipocytes to release excessive fatty acids and proteins that interfere with insulin
binding.
List the 4 major steps in the formation of TG's from glycerol to Acyl-CoA.
1. Glycerol 3-P + AcylCoA --> Monoacyl-Glycerol-3P
This acyl group is typically SATURATED.
2. MAG-3P + AcylCoA --> DAG-3P + HS-CoA
This acyl group is typically UNSATURATED.
3. DAG-3P + H2O --> DAG + PO4
4. DAG + AcylCoA --> TAG + HS-CoA
Note: All AcylCoA are activated by AcylCoA Synthetase
What are the ketone bodies and where do they form. Also, why do the form there?
ACETOACETATE, BETA-HYDROXYBUTYRATE and ACETONE.
They form in the liver because there is no OAA available after beta-oxidation to accept the Acetyl-CoA (it
has all been consumed in Gluconeogenesis).
Recognize the reactions for the conversion of acetyl-CoA to Acetoacetate and beta-hydroxybutyrate.
KETOGENIC PATHWAY:
2 Acetyl Coa --> Acetoacetyl Coa + Acetyl Coa + H2O --> 3-Hydroxy-3MethylGlutarylCoA --> Acetoacetate
+ Acetyl CoA.
ACETOACETATE can undergo spontaneous decarboxylation to create ACETONE or can consume NADH to
create BETA-HYDROXYBUTYRATE.
Describe the reaction catalyzed by HMG-CoA Lyase.
3-HMG-CoA --> Acetoacetate + AcetylCoA
Rate-limiting for ketone body formation.
Explain how acetoacetate can be used as a source of energy in some tissues.
Acetoacetate + Succinyl CoA --> Acetoacetyl-CoA + Succinate.
Acetoacetyl-CoA + CoA --> 2 Acetyl Coa ----> TCA
The first reaction is catalyzed by SUCCINYL CoA TRANSFERASE.
Explain why the liver produces ketone bodies but does not use them as an energy source.
The liver does not have SUCCINYL CoA TRANSFERASE. As a result, Acetoacetate must be transported to
other tissues following ketone body formation.
Explain why ketone bodies are produced in untreated diabetics.
They are not getting glucose into the cell (no insulin) so they depend on lipolysis for energy production.
They also are using all Oxaloacetate for Gluconeogenesis. Bitch.
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