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- Which of the following regulatory mechanisms are used to regulate the enzyme activity of the pyruvate dehydrogenase complex (PDH)? 1) its activity is decreased by elevated levels of the products of the reaction via allosteric control 2) its activity can be modulated only through reversible covalent modification (phosphorylation/dephosphorylation) 3) insulin causes the complex to be phosphorylated, thus increases its activity 4) the complex is more active when dephosphorylated, a process triggered by insulin 5) the protein kinase that phosphorylates the PDH complex is sensitive to changes in the levels of ATP a) 2+3+5 b) 1+2+3 c) 1+3+5 d) 2+4+5The action of glucagon on liver cells leads to inhibition of pyruvate kinase. What is the most probable mechanism for this effect?E1 and E2 of the pyruvate dehydrogenase complex is coupled via: (d) Transfer of an acetyl group from TPP to lipoamide a and c b and d (a) Reductive decarboxylation of pyruvate coupled to oxidation of acetylation of lipoamide (c) Transfer of an acetyl group from lipoamide to TPP (b) Oxidative decarboxylation of pyruvate coupled to reduction of acetylation of lipoamide
- Explain the indirect effect that allosteric effectors have on pyruvate dehydrogenase activity through phosphorylation/dephosphorylation of components within the PDH-complex. 2. The proton-motive force is a measure of the potential energy generated across the mitochondrial inner membrane during electron transport. Explain the factors that constitute this potential energy, that will be converted to the chemical energy of ATP by the cell.Consider fructose-1,6-bisphosphatase (FBP) when responding to Parts A, B, and C. When writing your response, please put A, B, or C in front of the answer for each part. NOTE: Each part can be answered in 3-4 sentences.A. State the effect (inhibition OR activation) of insulin signaling on the activity of FBP. Explain why this effect makes sense and make sure you identify the pathway where FBP participates.B. In a type 2 diabetic liver cell, when the blood sugar level is high, will the activity of FBP be HIGHER, LOWER, or THE SAME AS the activity in a nondiabetic liver cell under the same conditions? Explain your reasoning.C. Now think about the insulin and glucagon signaling pathways that control activity of FBP. When a nondiabetic liver cell is exposed to low blood sugar, indicate one specific way the insulin or glucagon signaling pathway could be disrupted so that the activity of FBP is not controlled correctly. Then, explain the reasoning for your answer.phosphofructokinase is an allosteric enzyme that catalyzes the conversion of fructose 6-phosphate to fructose 1,6-bisphosphate and represents the key control point in mammalian glycolysis. The enzyme is a homotetramer that is inhibited by ATP binding, activated by AMP binding, negatively regulated by phosphorylation, and competitively inhibited by 2,5-anhydro-D-glucitol-1,6-diphosphate. (a) Would you expect a plot of the initial rate of fructose 1,6-bisphosphate formation as a function of substrate concentration to show a sigmoidal or hyperbolic curve? (b) How would each of the regulators above affect the dynamics of the T state to R state equilibrium of phosphofructokinase? Briefly explain your reasoning. (c) If it were possible to isolate phosphofructokinase monomers in an active form, how would you expect the kinetics in (a) to be affected? How would the rate of the reaction be affected by ATP, AMP, and 2,5-anhydro-D-glucitol-1,6-diphosphate? Briefly explain your answers.
- a. In the TCA cycle, which of the following combines with acetyl CoA to form a 6-carbon compound? i. oxaloacetate ii. thiamine iii. glucose iv. pyruvate b. The last step in glycolysis is the transfer of phosphoryl group from phosphoenolpyruvate to ADP catalyzed by pyruvate kinase. i. True ii. FalseExplain the indirect effect that allosteric effectors have on pyruvate dehydrogenase activity through phosphorylation/dephosphorylation of components within the PDH-complex.For each of the following proteins describe how the protein function would be altered (or not) in the following scenarios: A receptor tyrosine kinase that always dimerizes even in the absence of ligand 3-ketoacyl-CoA transferase (SCOT) that is expressed in the liver. CPT1 that doesn’t have a malonyl binding site 4. acylCoA dehydrogenase with complex V inhibited
- What is the metabolic significance of the following observations? (a) Only the liver form of pyruvate kinase is inhibited by alanine, and (b) only gluconeogenic tissues contain appreciable levels of glucose-6-phosphatase.Complete the following description of the mechanism of the pyruvate dehydrogenase complex by using words provided. Not all words will be used. Each word will be used only one time. 5 Three enzymes of the pyruvate dehydrogenase complex work together to catalyze the production of Acetyl CoA from Pyruvate. First, a 2-carbon unit composed of Carbons # Pyruvate are added to the co-enzyme and whereas Carbon # of leaves as CO» The C-2 unit together with the co-enzyme is called transferred to the 2nd co-enzyme 11 12 The C-2 unit is then which is initially in its state. The enzyme that catalyzes this step is From here, the C-2 unit is transferred to form a linkage with CoA-SH to generate Acetyl COA Oxidized Hydroxyethyl TPP Phosphodiester Reduced Hydroxypropiony! TPP Lipoamide E-1 NADH 3 Dihydrolipoyl dehydrogenase Thioester 2 HydroxyacetyITPp Dihydropipoyl Transacetylase Type the words in the correct order separated by commas. Example: 1, 3, E-1, Thioester, Lipoamide ...One consequence of ethanol addiction is fatty liver disease, an illness in which liver cells accumulate large amounts of triacylglycerols, the esters derived from glycerol and fatty acids. Ethanol is oxidized in the cytoplasm of liver cells by alcohol dehydrogenase and aldehyde dehydrogenase to yield acetate and 2 NADH. Acetate is then transported into the mitochondrion, where it is converted to acetyl-CoA and metabolized in the citric acid cycle. When alcohol is consumed in excessive quantities, the resulting high levels of NADH cause metabolic abnormalities, one of which is high levels of fatty acid synthesis. Fatty acid synthesis, also a cytoplasmic process, uses acetyl-CoA as a substrate and NADPH as a reducing agent. Speculate about how a high level of cytoplasmic NADH provides a source of NADPH for fatty acid synthesis.
