Patients with a form of early-onset diabetes were found to carry a variety of mutations reducing the function of theglucokinase (GK) enzyme. These patients are heterozygous for one of the mutations, and thus show only partialrather than complete loss of GK activity. Answer the following questions about these patients.How would blood sugar lovolc likoly bo affoctod in CK nautatie 3. Several of the mutant GK enzymes show a normal Vmax but reduced efficiency. What is a reasonable explanationfor this observation?a. These mutants have a reduced affinity for the glucose substrateb. These mutants have a reduced value for keatC. These mutants have a non-functional catalytic triadd. These are all reasonable explanations for this observation

Glucokinase is an isozyme of hexokinases. These enzyme functions mainly in the liver and converts…

3. Several of the mutant GK enzymes show a normal Vmax but reduced efficiency. What is a reasonable explanation for this observation? a. These mutants have a reduced affinity for the glucose substrate b. These mutants have a reduced value for kcat C. These mutants have a non-functional catalytic triad d. These are all reasonable explanations for this observation

3. Several of the mutant GK enzymes show a normal Vmax but reduced efficiency. What is a reasonable explanation for this observation? a. These mutants have a reduced affinity for the glucose substrate b. These mutants have a reduced value for kcat C. These mutants have a non-functional catalytic triad d. These are all reasonable explanations for this observation

Biochemistry

6th Edition

ISBN:9781305577206

Author:Reginald H. Garrett, Charles M. Grisham

Publisher:Reginald H. Garrett, Charles M. Grisham

Chapter18: Glycolysis

Section: Chapter Questions

Problem 20P: Understanding the Mechanism of Hemolytic Anemia Genetic defects in glycolytic enzymes can have...

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At body temperature, L-aspartate in proteins race-mizes to D-aspartate at an appreciable rate. Most pro-teins in the body have a very low level of D-aspartate, if itcan be detected at all. Elastin, however, has a fairly highlevel of D-aspartate. Moreover, the amount of D-aspartateincreases in direct proportion to the age of the person fromwhom the sample was taken. Why do you suppose thatmost proteins have little if any D-aspartate, while elastinhas levels of D-aspartate that increase steadily with age?
Patients with a form of early-onset diabetes were found to carry a variety of mutations reducing the function of the glucokinase (GK) enzyme. These patients are heterozygous for one of the mutations, and thus show only partial rather than complete loss of GK activity. Answer the following questions about these patients. 1. How would blood sugar levels likely be affected in GK-mutation patients? Briefly explain your choice (25 words or less) a. Higher than normal b. Normal C. Lower than normal d. Cannot predict based on the provided information
Suggest another mutation in glucose metabolism that causes symptoms similar to those of von Gierke disease.
The activity of the mammalian PDH complex is observed to decrease in mitochondria in thepresence of pyruvate when malonate is added to the preparation. How can the inhibition be relievedby addition of malate. Explain.
Tyrosinase enzyme activity is assayed by monitoring the oxidation of 3, 4-dihydroxyphenylalanine (dopa) to the red-colored dopachrome. Calculate the tyrosinase activity (U/mL) by using the experimental data given below
The enzyme serine hydroxymethy ltransferase (SHMT) catalyses the conversion of serine into glycine. The fo llowing table gives the initial rates, vo, for the SHMT-catalysed reaction of the substrate serine at var ious concentratio ns of serine, lSI.[S]/(mmol dm-3) 10 20 30 40vo(μmol dm-3 s-1) 1.63 2.94 4.10 4.95Use the data to determine the values of the MichaelisMenten constant, the maximum velocity of the reaction, and the maximum turnover number of the enzyme.
One treatment for hyperuricemia is administration of xanthine oxidase inhibitors like allopurinol. Discuss the mechanism and show an illustration how this drug able to alleviate symptoms of hyperuricemia.
Propionic acidemia has a relatively high prevalence in South Africa, among both black and white families. This fatal disease is often diagnosed by the elevated presence of propionyl carnitine, propionylglycine and methyl citrate in blood and urine. Discuss the metabolism involved and origin of these markers.
In the clinical case scenario provided, match the defective enzyme in Column A with the consequence of this enzyme defect in Column B. IND OAD DH Autopsy results from individual X showed normal levels of glucose and pyruvate, very low levels of NAD+ and very high levels of NADH. Their blood oxygen levels were normal, although the cause of death was given to be a lack of oxygen. Option A B C D Defective enzyme Phosphofructokinase Pyruvate dehydrogenase Cytochrome oxidase Lactate dehydrogenase write your answer here Consequence of this enzyme defect Impaired ATP production Impaired NAD production Impaired respiration Impaired oxygen I L OORD ORD OND DORO G
Leigh syndrome is characterized by psychomotor regression: that is, the progressive loss of mental andmovement abilities. Patients also suffer from lacticacidosis, a condition in which mitochondrial respiration is deficient, so their tissues metabolize glucoseanaerobically, leading to the buildup of lactate. Somepatients with Leigh syndrome have a mutation in themitochondrial gene MT-CO3, which encodes a subunit of the electron transport complex cytochromec oxidase. Other patients diagnosed with Leigh syndrome have a loss-of-function mutation in the nucleargene SURF1, which encodes a factor needed for theassembly of this same enzyme complex.a. How can the same symptoms result from mutationsin a mitochondrial gene and from mutations in anuclear gene?
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