Lipid Synthesis and Storage

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Fatty Acid Activation:

• Attachment of CoA by acyl CoA synthetase.

Lipid Digestion:

• Emulsification by bile in GI.

• Secretion of lipase, colipase, and cholesterol esterase by pancreas.

• Lipids absorbed and packaged in chylomicrons.

• Very little lipid loss in stool.

Fatty Acid Biosynthesis:

• Glucose is converted to fatty acid (palmitate) in liver.

• Then, sent to adipose for storage.

• Affected by insulin.

• Citrate shuttle transports acetyl CoA from mitochondria to cytoplasm.

Acetyl CoA Carboxylase:

• This is the rate limiting enzyme for fatty acid biosynthesis.

• Activates Acetyl CoA in cytoplasm.

• Requires: biotin, ATP, and CO2.

• Activated by: insulin and citrate.

Fatty Acid Synthase:

• AKA palmitate synthase.

• Palmitate is the only fatty acid that humans can synthesize de novo.

• Induced in liver after high-carbohydrate diet.

• Requires vitamin pantothenic acid.

Triglyceride Synthesis:

• Storage form of fatty acids.

• Formed by attaching 3 fatty acids to glycerol.

• Triglycerides packaged as VLDL and transported in blood.

Lipoprotein Metabolism:

• Triglycerides and cholesterol transported in blood as lipoproteins.

• Chylomicrons less than VLDL less than IDL less than LDL less than HDL.


• Caused due to LDL and HDL metabolism.

Vitamin E:

• Antioxidant in lipid phase.

• Prevents LDL oxidation.

• Prevents peroxidation of membrane lipids.

Hyperlipidemia or Hypertriglyceridemia:

• Excess lipid in blood.

Type I Hyperlipidemia or Hypertriglyceridemia:

• Due to deficiency of familial lipoprotein lipase, apoC-II; AR inheritance; increased triglyceride and chylomicrons; fatty liver, pancreatitis, pain after fatty meal.

Type II Hyperlipidemia or Hypertriglyceridemia:

• LDL receptor deficiency; familial hypercholesterolemia; AD inheritance; increased cholesterol, LDL; xanthomas of Achilles tendon.


• Low or absent apoB-100 and apoB-48.

• Very low serum triglycerides and cholesterol.

Cholesterol Metabolism:

• Metabolites are used in steroids, bile acids, Vitamin D, and cell membranes.

• HMG-CoA Reductase: converts HMG-CoA to mevalonate; activated by insulin; blocked by statin drugs.

Additional Readings:

Basic Biochemistry

1. Nucleic Acid Structure and Organization
2. DNA Replication and Repair
3. Transcription and RNA Processing
4. Genetic Code, Mutations, and Translation
5. Genetic Regulation
6. Recombinant DNA
7. Amino Acids, Proteins, Enzymes
8. Hormones
9. Vitamins
10. Energy Metabolism
11. Glycolysis and Pyruvate Dehydrogenase
12. Citric Acid Cycle and Oxidative Phosphorylation
13. Glycogen, Gluconeogenesis, and Hexose Monophosphate Shunt
14. Lipid Synthesis and Storage
15. Lipid Mobilization and Catabolism
16. Amino Acid Metabolism Disorders
17. Purine and Pyrimidine Metabolism
18. Electron Transport
19. Citric Acid Cycle and Glyoxylate Cycle
20. Glycolysis
21. Pyruvate Metabolism
22. Mitochondrial ATP formation
23. Gluconeogenesis
24. Glycogen Metabolism
25. Nitrogen Fixation (Metabolism) reactions, and Heme Metabolism
26. Amino Acid Metabolism
27. What is Medium Chain Acyl-CoA Dehydrogenase Deficiency (MCADD)?

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