Medical Biochemistry lecture notes
Week 1
Lecture 1
The only pathway that is not regulated is the fat storage.
Big three: glucose, pyruvate, acetyl CoA.
Many organs have their own tissue metabolism.
The brain cannot use fatty acids, so the liver uses amino acids (/proteins) to make glucose for the
brain.
Lecture 2
The muscle is not involved in regulating blood glucose levels, so it does not respond to glucagon (it
responds to exercise (EXAM QUESTION).
Blood glucose low: glucagon release (secreted by alpha pancreatic cells).
Blood glucose high: insulin release (secreted by beta pancreatic cells).
Only the liver releases glucose back into the bloodstream (G6Pase).
Lecture 3
Glucagon stimulates gluconeogenesis when glucose levels are low (starved). Glucagon also
stimulates phosphorylation.
3 carbon AA lead to pyruvate.
4 carbon AA lead to oxaloacetate (TCA cycle).
5 carbon AA lead to alfa-ketoglutarate (TCA).
Lysine and leucine are ketogenic amino acids and cannot be used in the gluconeogenesis pathway.
Transamination reaction is reversible.
During fasting period: alanine > pyruvate.
Acetyl-CoA can only go into the TCA cycle/ fatty acids, not reversible.
Lecture 4
Chylomicrons need to bypass the liver after uptake, via the lymph to the blood (because they need to
go to the fat tissue for storage for scarse times, also to the muscles to be used directly as an energy
source).
During fasting, adipose tissue can release fatty acids for energy or to create ketone bodies, transported
as FFA-Albumin complex.
Glucose is especially important for the brain: the brain has no beta-oxidation (since they cannot
absorb long chain fatty acids (because of myelin)).
Week 2
Lecture 1
Drugs inhibits enzymes.
The lower the KM, the higher the binding affinity of substrate for enzyme.
Competitive inhibitor: same V-max, different KM.
Non-competitive inhibitor: different V-max, same KM.
Allosteric activator: KM decreases, V-max stays the same.
Allosteric inhibitor: you need more substrate, KM increases.
Insulin promotes glycogen synthesis, inhibits glycogen phosphorylase (glucagon other way around).
Purines: Adenine, Guanine (need for synthesis: glutamine and aspartate).
Pyrimidines: Cytosine, Thymine (need for synthesis: aspartate, glycine, glutamine and FH4).
Nucleotide synthesis; you need ribose-5-phosphate from the PPP, and you need amino acids.
Methotrexate and 5-Fluorouracil are inhibitors in the generation of DNA and prevent tumors from
growing > chemotherapy indicative drugs.
Useful: video 3 slide with overview at the end.
Week 1
Lecture 1
The only pathway that is not regulated is the fat storage.
Big three: glucose, pyruvate, acetyl CoA.
Many organs have their own tissue metabolism.
The brain cannot use fatty acids, so the liver uses amino acids (/proteins) to make glucose for the
brain.
Lecture 2
The muscle is not involved in regulating blood glucose levels, so it does not respond to glucagon (it
responds to exercise (EXAM QUESTION).
Blood glucose low: glucagon release (secreted by alpha pancreatic cells).
Blood glucose high: insulin release (secreted by beta pancreatic cells).
Only the liver releases glucose back into the bloodstream (G6Pase).
Lecture 3
Glucagon stimulates gluconeogenesis when glucose levels are low (starved). Glucagon also
stimulates phosphorylation.
3 carbon AA lead to pyruvate.
4 carbon AA lead to oxaloacetate (TCA cycle).
5 carbon AA lead to alfa-ketoglutarate (TCA).
Lysine and leucine are ketogenic amino acids and cannot be used in the gluconeogenesis pathway.
Transamination reaction is reversible.
During fasting period: alanine > pyruvate.
Acetyl-CoA can only go into the TCA cycle/ fatty acids, not reversible.
Lecture 4
Chylomicrons need to bypass the liver after uptake, via the lymph to the blood (because they need to
go to the fat tissue for storage for scarse times, also to the muscles to be used directly as an energy
source).
During fasting, adipose tissue can release fatty acids for energy or to create ketone bodies, transported
as FFA-Albumin complex.
Glucose is especially important for the brain: the brain has no beta-oxidation (since they cannot
absorb long chain fatty acids (because of myelin)).
Week 2
Lecture 1
Drugs inhibits enzymes.
The lower the KM, the higher the binding affinity of substrate for enzyme.
Competitive inhibitor: same V-max, different KM.
Non-competitive inhibitor: different V-max, same KM.
Allosteric activator: KM decreases, V-max stays the same.
Allosteric inhibitor: you need more substrate, KM increases.
Insulin promotes glycogen synthesis, inhibits glycogen phosphorylase (glucagon other way around).
Purines: Adenine, Guanine (need for synthesis: glutamine and aspartate).
Pyrimidines: Cytosine, Thymine (need for synthesis: aspartate, glycine, glutamine and FH4).
Nucleotide synthesis; you need ribose-5-phosphate from the PPP, and you need amino acids.
Methotrexate and 5-Fluorouracil are inhibitors in the generation of DNA and prevent tumors from
growing > chemotherapy indicative drugs.
Useful: video 3 slide with overview at the end.
