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

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

Biology: The Dynamic Science (MindTap Course List)

4th Edition

ISBN:9781305389892

Author:Peter J. Russell, Paul E. Hertz, Beverly McMillan

Publisher:Peter J. Russell, Paul E. Hertz, Beverly McMillan

Chapter4: Cells

Section: Chapter Questions

Problem 1ITD

See similar textbooks

Similar questions

In relation to Carbamoyl Phosphate Synthetase enzyme, answer the following: A- What are the two isoforms of this enzyme, explain why there are two isoforms? B- What are the clinical manifestations associated with the deficiency of these two enzymes? C- Write down the biochemical reaction and the name of the metabolic pathway that these two isoforms are involved in, and how many ATP is utilized by these two isoforms?
TPCK and TLCK are irreversible inhibitors of serine proteases. One ofthese inhibits trypsin and the other chymotrypsin. Which is which? Explainyour reasoning. Suggest the effects of each of the following mutations on the physiologicalrole of chymotrypsinogen:(a) R15S(b) C1S(c) T147S
The clinical signs of two types of galactosemia—galactokinase deficiency or UDPglucose: galactose 1-phosphate uridylyltransferase deficiency—are markedly different. Although both forms cause gastrointestinal pain after drinking milk, transferase deficiency also causes liver, kidney, spleen, and brain malfunction, as well as mortality. With each kind of enzyme shortage, what products accumulate in the blood and tissues? Estimate the relative toxicity of these goods based on the information provided above.
. In Figure 6-11,a. in view of the position of HPA oxidase earlier in thepathway compared to that of HA oxidase, would youexpect people with tyrosinosis to show symptoms ofalkaptonuria?b. if a double mutant could be found, would you expecttyrosinosis to be epistatic to alkaptonuria?
Consider a hypothetical enzyme that is COMPLETELY deactivated when a Valine (Val) residue buried in the core of the enzyme is mutated to Glutamate (Glu). In one or two sentences max, explain the MOST LIKELY reason for this occurrence.
If glucagon binds to the liver cell, what is the expected regulation of the bifunctional enzyme phosphofructokinase-2/fructose-2,6-bisphosphatase and how would the levels of fructose-2,6-bisphosphate be impacted?
Which of the following is correct? A. The gene CYP21A2 is the one that codes for the formation of glucose-6 phosphate dehydrogenase B. Simple virilizing form of Congenital adrenal hyperplasia is the most sever form of this disorder C. Salt wasting type of congenita adrenal hyperplasia is the most severe form of this disorder. D. The gene CYP21A1 is the one that codes for the formation of galactokinase in type 2 galactosemia.
The brain is fueled almost exclusively by glucose. Using this fact, would it be a good idea to express glucose-1-phosphatase in muscle? What type of phenotype would be exhibited by a mouse expressing glucose-1-phosphatase in muscle?
What does this important observation imply about the relation between the amino acid sequence of insulin and its three-dimensional structure?
Briefly discuss why each of the three common forms of galactosemia involves impaired utilization of galactose. Which metabolic process is blocked in each condition?
The following diagram shows the biosynthesis of B12 coenzymes, starting with the vitamin. DMB is dimethylbenzimidazole. (a) What one additional substrate or cofactor is required by enzyme B?(b) Genetic deficiency in animals of enzyme C would result in excessiveurinary excretion of what compound?(c) Some forms of the condition described in (b) can be successfully treatedby injection of rather massive doses of vitamin B12. What kind ofgenetic alteration in the enzyme would be consistent with this result?(d) Genetic deficiency in animals of enzyme B will result in excessive urinaryexcretion of what amino acid?
The clinical symptoms of two forms of galactosemia—deficiency of galactokinase or of UDPglucose: galactose 1-phosphate uridylyltransferase—show radically different severity. Although both types produce gastric discomfort after milk ingestion, deficiency of the transferase also leads to liver, kidney, spleen, and brain dysfunction and eventual death. What products accumulate in the blood and tissues with each type of enzyme deficiency? Estimate the relative toxicities of these products from the above information.