7. In experimental laboratory, the effect of epinephrine on glycogen mctabolismin a muscle tissue sample of the mutant mice line was studied. After adding6.8. The Metabolism of Ethanol in the Liver307epinephrine to the investigated medium CAMP concentration in the cellsincreased, but glycogen phosphorylase was present only in dephosphorylated,inactive form. Give the enzyme defect most likely in the mutant mice muscles?To solve the problem, answer the questions:a) can these animals perform sudden, intense work, for example, to run awayfrom danger?b) can these animals do moderate physical activity?c) argue the answers by making a scheme of the hormone action on glycogenmetabolism in the muscles.

Epinephrine is also known as adrenaline which is a hormone that is also used as a medication…

Answered: 7. In experimental laboratory, the…

Biochemistry

9th Edition

ISBN:9781319114671

Author:Lubert Stryer, Jeremy M. Berg, John L. Tymoczko, Gregory J. Gatto Jr.

Publisher:Lubert Stryer, Jeremy M. Berg, John L. Tymoczko, Gregory J. Gatto Jr.

Chapter1: Biochemistry: An Evolving Science

Section: Chapter Questions

Problem 1P

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37.Assume that the phosphoryl group in the shown chemical (Phosphoenolpyruvate (PEP)) is labeled with 32P radioisotope. The radioisotope labeled chemical is then allowed to undergo gluconeogenesis in liver cells. Which of the phosphoryl groups in fructose-1,6-bisphosphate are labeled with radioisotope? (Assume that the only fate of the radioisotope chemical is to undergo gluconeogenesis in the liver)a. The phosphoryl group that is attached to the C-1 of fructoseb. The phosphoryl group that is attached to the C-6 of fructosec. Bothd. Neither a nor b
5. Based on your understanding of allosteric regulation and using terminology related to the allosteric (MWC) model, explain how the enzyme glycogen phosphorylase is affected by the binding of AMP and what affect this binding would have on the overall activity of the enzyme. Predict what would happen to the activity of the enzyme when glycogen phosphorylase is covalently modified and there are high levels of ATP in the cell.
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
(b) the activity of the malate-aspartate shuttle (MAS) system of isolated rat brain mitochondria suspended in an isotonic me- dium buffered to pH 7.4. Diagram A illustrates NADH fluo- rescence emission upon addition of Glutamate in the ab- sence and presence of Aspartate. Diagram B illustrates sim- ilarly NADH fluorescence emission upon addition of Gluta- mate in the presence of Aspartate followed by additions of submicromolar concentrations of Ca2+. As is well estab- lished, the MAS in brain, skeletal muscle, and cardiac mus- Diagrams A and B on the right show changes in Glu A Glu В -No Asp + 0 +0.12 -0.48 + 16 0.81 +1.8 ++ Asp 10 min 2 min cle mitochondria is activated by cytosolic concentrations of Ca2* < 3 µM. To simulate the cytosolic part of the MAS, the following reagents were added to the medium: 4 units/ml glutamate-oxaloacetate transaminase, 6 units/ml malate dehydrogenase, 66 µM NADH, 5 mM aspartate, 5 mM malate, 0.5 mM ADP, 200 nM ruthenium red (to block the mitochondrial…
4. a. Calculate the KM (Michaelis constant) and the vmax (the maximum initial rate) for both substrates (sphingosine and ATP). Show your work, and be careful about units. b. threo-dihydrosphingosine, a stereoisomer of sphingosine, is an inhibitor of sphingosine kinase. What kind of inhibitor (competitive, uncompetitive, noncompetitive) is threo-dihydrosphingosine? Citing information from the Lineweaver-Burke plots, explain how you can tell.
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2. The precise biochemical mechanisms underlying the rapid shutdown of glycolysis in skeletal muscle upon termination of muscle contraction have remained poorly understood for many decades. It is known that glycolytic flux declines after exercise even though Pi, ADP, and AMP remain high; however, while these adenosine-5'- nucleotides are allosteric activators of phosphofructokinase-1 (PFK-1), this enzyme remains of low ac- tivity despite their presence. The diagrams (A and B) on the right illustrate the increase in the concentrations of glycolytic in- termediates downstream of PFK-1 during exercise for 60 sec followed by the abrupt decline in their concentrations upon ces- sation of muscle contraction. Diagram C shows changes in the concentrations of phosphate metabolites pre- and post-exer- cise. A. Summed concentration of glycolytic intermediates down- stream of PFK-1 (F1,6P2 + DHAP + G3P + GAP + 1,3BPG + 3PG + 2PG + PEP; G3P, glycerol-3-phosphate). B: PFK-1 flux (grey) and the PGK +…
Many years later, in 1989, Wild, et al. revisited the idea of allosteric control of ATCase by CTP. They noted that CTP did indeed inhibit ATCase, but that the inhibition was always incomplete, even at high concentrations of CTP. They hypothesized that perhaps CTP did not act alone, but in combination with some other nucleotide. They tested the activity of ATCase in the presence of several nucleotide combinations. The results are shown in Table 3. a. What combination gives the most effective inhibition? b. What is the physiological significance of this combination? c. Revise Figure 1 to include this new information. d. Redraw Figure 2 to include this new information. How does the combination compare with the values for the nucleotides alone? Table 3: Relative specific activities for combinations of nucleotide effectors. A value greater than one indicates stimulation, a value less than one indicates inhibition. Nucleotide Effector ATP CTP GTP UTP ATP/CTP ATP/GTP ATP/UTP CTP/GTP CTP/UTP…

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