Metabolism of Amino Acids
A vitamin B6 deficiency reduces the effectiveness of transaminase enzymes. Which amino acid is formed from transamination of a-ketoglutarate?
| A |
Glycine |
|
| B |
Glutamine |
|
| C |
Asparagine |
|
| D |
Glutamate |
A vitamin B6 deficiency reduces the effectiveness of transaminase enzymes. Which amino acid is formed from transamination of a-ketoglutarate?
| A |
Glycine |
|
| B |
Glutamine |
|
| C |
Asparagine |
|
| D |
Glutamate |
Glutamate is formed from a-ketoglutarate by the enzymes aspartate aminotransferase and alanine aminotransferase.
Transamination reaction is :
| A |
Net deamination with splitting of NI-b |
|
| B |
c and d both |
|
| C |
Transaminase enzyme & pyridoxial P01 binding is covalent |
|
| D |
Glutamate is formed |
Transamination reaction is :
| A |
Net deamination with splitting of NI-b |
|
| B |
c and d both |
|
| C |
Transaminase enzyme & pyridoxial P01 binding is covalent |
|
| D |
Glutamate is formed |
C i.e. Transaminase enzyme & pyridoxial PO4 binding is covalent; D i.e. Glutamate is formed
Co-enzyme used in transamination
| A |
NAD |
|
| B |
Biotin |
|
| C |
Pyridoxal phosphate |
|
| D |
Riboflavin |
Co-enzyme used in transamination
| A |
NAD |
|
| B |
Biotin |
|
| C |
Pyridoxal phosphate |
|
| D |
Riboflavin |
C i.e. Pyridoxal phosphate
– Pyridoxal phosphate (active B6) dependent conditions (in which it is used in treatment) are Homocystinuria, Oxaluria, Cystathioninuria and Xanthurenic acid uriaQ, Mn – “HOCX or Homo Ox Siton Zen”
– Homocystinuria is vitamin B6, B12 and folate. dependentQ
Maple syrup urine disease is d/t defective branched chain a-ketoacid dehydrogenase enzyme; and it may be a/ w thiamin (vitamin B1) deficiencyQ
Methylmalonyl acidttria is seen in vitamin B12 deficiencyQ.
Figlu (N- formimimino-glutamate) uria following a dose of histidine occurs in folate (folic acid) deficiency (Histidine load test). AICAR (amino imidazole carboxamide ribosyl 51-P) uria also occurs in folate deficiency.
Transamination of pyruvate and glutamic acid leads to the formation of
| A |
Oxaloacetate |
|
| B |
a-ketoglutarate |
|
| C |
Aspartate |
|
| D |
Malate |
Transamination of pyruvate and glutamic acid leads to the formation of
| A |
Oxaloacetate |
|
| B |
a-ketoglutarate |
|
| C |
Aspartate |
|
| D |
Malate |
Transamination of pyruvate and glutamic acid (or glutamate) 1/t formation of alanine and a-keto (oxo) glutarate.
Co-enzyme used in transamination ‑
| A |
NAD |
|
| B |
Biotin |
|
| C |
Pyridoxal phosphate |
|
| D |
Riboflavin |
Co-enzyme used in transamination ‑
| A |
NAD |
|
| B |
Biotin |
|
| C |
Pyridoxal phosphate |
|
| D |
Riboflavin |
Ans. is ‘c’ i.e., Pyridoxal phosphate
Pyridoxal phosphate (active form of vitamin B6) is the coenzyme for transamination reactions.
Transamination of alanine results in the formation of-
| A |
Pyruvate |
|
| B |
Oxaloacetate |
|
| C |
Aspartate |
|
| D |
Arginine |
Transamination of alanine results in the formation of-
| A |
Pyruvate |
|
| B |
Oxaloacetate |
|
| C |
Aspartate |
|
| D |
Arginine |
Coenzyme not required in formation of glutamate-
| A |
Thiamine pyrophosphate |
|
| B |
Pyridoxial phosphate |
|
| C |
Niacin |
|
| D |
None of the above |
Coenzyme not required in formation of glutamate-
| A |
Thiamine pyrophosphate |
|
| B |
Pyridoxial phosphate |
|
| C |
Niacin |
|
| D |
None of the above |
During transamination reaction glutamate is formed. Pyridoxial Phosphate acts as coenzyme.
True about transamination reaction are all except-
| A |
Transfer of alpha amino group from alpha amino acid to keto acid |
|
| B |
Alpha ketoglutarate is the most common receptor |
|
| C |
Threonine does not undergo transamination |
|
| D |
Biotin is required as a coenzyme. |
True about transamination reaction are all except-
| A |
Transfer of alpha amino group from alpha amino acid to keto acid |
|
| B |
Alpha ketoglutarate is the most common receptor |
|
| C |
Threonine does not undergo transamination |
|
| D |
Biotin is required as a coenzyme. |
Pyridoxial phosphate is a coenzyme in transamination reaction.
Glutamine in blood acts as-
| A |
NH3 transporter |
|
| B |
Toxic element |
|
| C |
Store energy |
|
| D |
Abnormal metabolite |
Glutamine in blood acts as-
| A |
NH3 transporter |
|
| B |
Toxic element |
|
| C |
Store energy |
|
| D |
Abnormal metabolite |
Glutamine is the major form of transport of ammonia
Ammonia is detoxified in brain to-
| A |
Uric acid |
|
| B |
GABA |
|
| C |
Urea |
|
| D |
Glutamine |
Ammonia is detoxified in brain to-
| A |
Uric acid |
|
| B |
GABA |
|
| C |
Urea |
|
| D |
Glutamine |
The brain is a rich source of glutamine synthase and predominantly detoxifies ammonia by synthesis of glutamate.
Which amino acid binds with NH4+ covalently and makes it non-toxic for transportation-
| A |
Serine |
|
| B |
Aspartate |
|
| C |
Glutamate |
|
| D |
Histidine |
Which amino acid binds with NH4+ covalently and makes it non-toxic for transportation-
| A |
Serine |
|
| B |
Aspartate |
|
| C |
Glutamate |
|
| D |
Histidine |
Co factors for glutamate dehydrogenase-
| A |
NAD |
|
| B |
FADH2 |
|
| C |
FMN |
|
| D |
FAD |
Co factors for glutamate dehydrogenase-
| A |
NAD |
|
| B |
FADH2 |
|
| C |
FMN |
|
| D |
FAD |
Hepatic L- glutamate dehydrogenase can use either NAD+ or NADP+.
Increased alanine during prolonged fasting represents-
| A |
Increased breakdown of muscle proteins |
|
| B |
Impaired renal function |
|
| C |
Decreased utilization of amino acid from Glucogenesis |
|
| D |
Leakage of amino acids from cells due to plasma membrane leakage |
Increased alanine during prolonged fasting represents-
| A |
Increased breakdown of muscle proteins |
|
| B |
Impaired renal function |
|
| C |
Decreased utilization of amino acid from Glucogenesis |
|
| D |
Leakage of amino acids from cells due to plasma membrane leakage |
During prolonged fasting there is increased gluconeogenesis. Alanine is provided by the muscle is one of the substrates for gluconeogenesis and is called Glucose Alanine cycle.
So plasma level of alanine increases in prolonged starvation.
Amino acid absorption is by-
| A |
Facilitated transport |
|
| B |
Passive transport |
|
| C |
Pinocytosis |
|
| D |
Active transport |
Amino acid absorption is by-
| A |
Facilitated transport |
|
| B |
Passive transport |
|
| C |
Pinocytosis |
|
| D |
Active transport |
Free amino acids are absorbed across the intestinal mucosa by sodium-dependent active transport. There are several different amino acid transporters, with specificity for the nature of the amino acid side-chain. Transporters of Amino Acids.
- For Neutral Amino Acids
- For Basic Amino acids and Cysteine
- For Imino Acids and Glycine
- For Acidic Amino Acids
- For Beta Amino Acids (Beta Alanine)
Meisters Cycle
- For absorption of Neutral Amino acids from Intestines, Kidney tubules and brain.
- The main role is played by Glutathione. (GSH)
- For transport of 1 amino acid and regeneration of GSH 3 ATPs are required.
