Amino Acid Metabolism (original) (raw)
Amino Acid Metabolism
Digestion of Dietary Protein:
Stomach:� HCl (denature) and Pepsin
Pancreas:� Trypsin (carbonyl of arg and lys);Chymotrypsin (carbonyl of Trp,Tyr, Phe, Met, Leu); Elastase (carbonyl of Ala,Gly Ser); CarboxypeptidaseA (amine side of Ala, Ile, Leu, Val); Carboxypeptidase B (amine side of Arg,lys)
Small Intestine:� aminopeptidase(cleaves N-terminal residue of oligopeptides)
Nitrogen Removal from Amino Acids:� make ammonia or aspartateto feed urea cycle.
Aminotransferase:�������������� a-amino acid + a-ketoglutarate � a-keto acid + glutamate
����������������������������������������� Glutamate + Oxaloacetate � Aspartate+ a-ketoglutarate
����������������������������������������� Cofactor:pyridoxal phosphate/pyridoxaminephosphate
����������������������������������������� High serum AST and ALT indicate liver damage.
Oxidative Deamination:������ Glutamate dehydrogenase(mitochondria)
����� Glutamate + NAD+ (NADP+) � a-ketoglutarate+NADH (NADPH) + NH3
����� Allosteric Regulators:�ATP/GTP inhibit; ADP/GDP activate
Urea Cycle (liver):
Mitochondrial reactions:
Carbamoylphosphate synthetase I:
CO2 + NH4 + 2 ATP �� carbamoyl phosphate���������������� (rate limiting)
Ornithine transcarbamoylase:
L-ornithine+ carbamoyl phosphate � L-citrulline+ Pi
Cytosol reactions:
L-citrulline+ L-Aspartate + ATP � Argininosuccinate+ AMP + PPi �(argininosuccinate synthase)
Argininosuccinate � Fumarate + L-Arginine� (argininosuccinate lyase)
L-Arginine �Urea + L-ornithine (arginase)
Overall:
Aspartate+ NH3 + CO2 + 3 ATP � Urea + fumarate + 2 ADP + AMP + 2 Pi + PPi + 3 H2O
Urea is transported to kidneys for excretion
Metabolism of ammonia:
Sources:� amino acids, glutamine (glutaminase), bacteria in intestine, from amines (catecholamine degradation), purine and pyrimidine catabolism
Transport of ammonia:� urea and glutamine
Hyperammononemia:� ammonia intoxication - tremors, slurring of speech, and blurring of vision, coma/death.�Cause by cirrhosis of the liver or genetic deficiencies
Catabolism of Amino Acids
Ketogenic:� formation of ketonebodies (leucine and lysine, exclusively)
Glucogenic:� intermediates of citric acid cycle (see figure 22.3)
Essential vs. non-essential:�PVT TIM HALL
Cofactors to remember:�SAM, Biotin, Folic Acid (carriers of one-carbon units)
Biosynthesis of nonessential amino acids:
TCA cycle member + amino acid � a-keto acid + nonessential amino acid
Phenylalanine hydroxylase:
Phenylalanine + O2 + coenzyme tetrahydrobiopterin� � tyrosine + H2O + dihydrobiopterin
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Metabolic defects in amino acid metabolism:
PKU = hyperphenylalaninemiacaused by deficiency in phenylalanine hydroxylase or deficiency in coenzyme tetrahydrobiopterin.� No tyrosine, no catecholamines
Conversion of Amino Acids to Specialized Products
Amino acids are precursors for porphyrins, neurotransmitters, hormones, purines, and pyrimidines
Porphyrins:� biosynthesis of heme, important in coordinating iron.
Glycine +succinyl CoA � d-aminolevulinicacid (ALA)���� [d-aminolevulinic synthase]
Regulation by negative feedback (hemin)
Increased ALA synthase production via activation of P450s
d-aminolevulinic � porphobilinogen���������� (d-aminolevulinic acid dehydrase, inhibited by lead)
Porphyrias:� defects in hemesynthesis.� Erythropoietic or hepatic.
Degradation of Heme:� Occurs in liver and spleen.� Heme is converted to biliruben (requires NADPH).� Transported in blood via bilirubinalbumin complex to liver where it is conjugated and then excreted with bile.
Jaundice:� yellow skin and sclerae cause by deposition of bilirubin.� Hemolytic, obstructive, or hepatocellularjaundice.
Creatine:� derivative Creatine phosphophate can donate phosphate group to ADP to form ATP in muscles.� Synthesized from arginine and glycine precursors.� Used as indicator of Kidney function.
Histamine:� Synthesized from Histadine, used as neurotransmitter.� Powerful vasodilator.
Serotonin:�Neurotransmitter synthesized from tryptophan.
Catecholamines:� Synthesized from tyrosine.
Melanin:� Also synthesized from tyrosine.