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Please explain the steps in this pathway on the picture.
![Regulation of PFK-2/FBPase-2
PFK-2
↑(F26BP]
(active)
он
Stimulates glycolysis,
inhibits gluconeogenesis
FBPase-2
(inactive)
-ATP
CAMP-
phospho-
protein
phosphatase
dependent
glucagon
(CAMP)
insulin -----
protein
kinase
H,0
ADP
PFK-2
V(F26BP)
(inactive)
0-P-0
Inhibits glycolysis,
stimulates gluconeogenesis
FBPase-2
(active)
Fig. 15-19, page 594](/v2/_next/image?url=https%3A%2F%2Fcontent.bartleby.com%2Fqna-images%2Fquestion%2F62f6355a-05e6-4234-9d59-a73a1309b418%2Fc124ff61-ab14-40b3-83be-0e5de2c2facd%2Fw69tw3d_processed.png&w=3840&q=75)
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- Stimulation of a certain Gs protein–coupled receptor activates protein kinase A (PKA). Predict the eff ect of PKA activation on the following substrates of PKA: (a) acetyl-CoA carboxylase, (b) glycogen synthase, (c) hormone-sensitive lipase, and (d) phosphorylase kinase.The epinephrine-mediated “amplificationcascade” of Figure 24.14 has six steps, all of which are catalyticwith one exception. This cascade leads to the activation of glycogenphosphorylase. This enzyme acts in turn on glycogen to yieldglucose-1-phosphate (G-1-P).(a) Which step is not catalytic?(b) If each catalytic step had a turnover (molecules of substrateacted on per molecule of enzyme) of 10, how many moleculesof G-1-P would result from one molecule of epinephrine?(c) What is the biochemical advantage of such a cascade?(d) How is the amplification cascade of this questionreversed?Researchers investigating the role of fat metabolism in diabetes generated PPAR peroxisome proliferator-activated receptor gamma (PPARγ) knockout mice. When fed a high fat diet, these mice did not gain extra adipose tissue or display significant weight gain. Explain why this is the case.
- Diabetes Type 1 and Type 2 Applying signal transduction mechanisms in the context of Type I and Type II Diabetes. Describe the mechanisms by which a cell receives a message and translates it into short-term or long-term effects. Including the role of phosphorylation and feedback inhibition.Under FASTING state, how do the hormonal changes bring about the effect to maintain glucose homeostasis in the body through the pathways of GLYCOLYSIS and GLUCONEOGENESIS; GLYCOGENOLYSIS and GLYCOGENESIS? (Please describe the signaling pathways in detail. )Explain what biochemical pathway/metabolic processes are affected in insulin resistance? How does this affect glycogen breakdown and gluconeogenesis.
- Compare the localization of GLUT4 with that of GLUT2 and GLUT3, and explain why these localizations are important in the response of muscle,adipose tissue, brain, and liver to insulinA cell where PKBPKB is always active has a mutation that results in the permanent activation of GSK3GSK3. Based on the information in Figure 2, predict the effect of this mutation on the activity of glycogen synthase. Justify your prediction.Phosphorylase kinase integrates signals from thecyclic-AMP-dependent and Ca2+-dependent signalingpathways that control glycogen breakdown in liver andmuscle cells (Figure Q15–4). Phosphorylase kinase is com-posed of four subunits. One is the protein kinase that cata-lyzes the addition of phosphate to glycogen phosphorylaseto activate it for glycogen breakdown. The other three sub-units are regulatory proteins that control the activity of thecatalytic subunit. Two contain sites for phosphorylation byPKA, which is activated by cyclic AMP. The remaining sub-unit is calmodulin, which binds Ca2+ when the cytosolicCa2+ concentration rises. The regulatory subunits controlthe equilibrium between the active and inactive confor-mations of the catalytic subunit, with each phosphate andCa2+ nudging the equilibrium toward the active confor-mation. How does this arrangement allow phosphorylasekinase to serve its role as an integrator protein for the mul-tiple pathways that stimulate glycogen…
- What would be the effect of the Glucagon initiated cascade on inhibition of ATP Synthase by IF1? Metabolic reprogramming in cancer cells correlates to an enhanced expression of IF1. What would be the effect on the TCA? Why might that lead to lactoacidosis?Mutations in glucokinase which lower the kcat for the enzyme or elevate the Km for glucose result in mild to moderate elevation of blood glucose. Explain how these mutations cause diabetes-like symptoms in patients.What is the physiologic significance of pyruvate dehydrogenase complex?What's the biochemical basis for the management of diabetes mellitus and contrast glucose homeostasis in neonates and adults.
