Biochemistry II Exam Solutions PDF

Okay, I will convert the image into a structured markdown format. # Biochemistry II Practice Go over exam 1 and find the correct answers from the textbook/lectures/notes. Read chapters 25, 29, 30, 31. **1.** 5pts The enzyme glycogen phosphorylase: a. breaks an α-1,4 glycolytic bond and adds phos...

Okay, I will convert the image into a structured markdown format. # Biochemistry II Practice Go over exam 1 and find the correct answers from the textbook/lectures/notes. Read chapters 25, 29, 30, 31. **1.** 5pts The enzyme glycogen phosphorylase: a. breaks an α-1,4 glycolytic bond and adds phosphate to carbon 6 of glucose b. Is a protein phosphatase that breaks an α-1,4 glycolytic bond and removes a terminal glucose c. breaks an α-1,4 glycolytic bond and transfers glucose-6-phosphate to the endoplasmic reticulum d. none of the above (The product is glucose 1-phosphate) e. both answers a and c are correct f. both a and b are correct ***What is the product of the action of glycogen phosphorylase?*** **2.** 5 pts In glycogenolysis, the presumed order of enzymatic glucose production is: a. glucoisomerase → Glucose-6-phosphorylase → glucose-6-phosphate → glucose b. glucose-6-mutase → Glucose-6-phosphorylase → glucose-1-phosphatase → glucose c. 4:4 transferase → α-1,6 glucosidase → glucose d. phosphoglucomutase → glucose-6-phosphatase → glucose e. none of the above f. both c and d are correct ***What two pathways produce glucose in glycogenolysis?*** **3.** 5 pts C1 of glucose is attached to glycogenin in a bond best described as: a. an other: R-O-C1 b. a glycosidic bond: C4-O-C1 c. a peptide C(O)-NH-C1 d. a thioether: R-S-C1 ***How is the first glucose molecule attached to glycogenin?*** **4.** 3 pts A deficiently in the enzyme glucose-6-phosphatase can lead to an enlarged liver, severe fasting hypoglycemia, acidosis, lipemia, and thrombocyte dysfunction. **5.** 5 pts In muscle during exercise, an increase in blood epinephrine, tissue AMP, $Ca^{2+}$-calmodulin, and cAMP would cause: a. glycogenesis ↑, glycogenolysis ↑, glycolysis ↑ b. glycogenesis ↑, glycogenolysis ↑, glycolysis ↓ c. glycogenesis ↓, glycogenolysis ↑, glycolysis ↓ d. glycogenesis ↓, glycogenolysis ↑, glycolysis ↑ e. glycogenesis ↓, glycogenolysis ↑, glycolysis ↓, and glucose is released to the bloodstream. f. both c and e are correct **6.** 5 pts In the fasted state: a. glycogen synthase is phosphorylated b. glycogen phosphorylase is dephosphorylated c. glycogen phosphorylase is phosphorylated d. glycogen synthase is dephosphorylated e. both a and c are correct f. both b and d are correct **7.** 5 pts Pyruvate carboxylase is activated by: a. β-oxidation of fatty acids b. lack of oxygen in the cytoplasm and an increase in $NAD^+$ c. lactate d. malate e. the build-up of citrate in the mitochondrial matrix **8.** oxaloacetate ***What is the product of β-oxidation of fatty acids?*** Acetyl CoA **9.** 5 pts Adipose tissue releases glycerol to the bloodstream where it is converted to DHAP in the liver. It does not use glycerol for synthesis of triacyl glycerides but rather glucose. It is then logical to assume that: a. adipocytes lack glycerol 3-phosphate dehydrogenase b. adipocytes contain glycerol kinase c. adipose tissue lacks glyceraldehyde 3-phosphate dehydrogenase. d. adipocytes lack glycerol 3-phosphate dehydrogenase *If adipocytes release glycerol and do not use it for fatty acid synthesis, which occurs in the liver mostly, would it be beneficial to phosphorylate it? If the liver takes up glycerol from the bloodstream, then it must be phosphorylated to trap it.* **10.** 5 pts Adipocytes (and all other cell types) must contain glycerol 3-phosphate dehydrogenase in order to (among other things): a. reduce FAD in the mitochondrial inner membrane and produce DHAP b. to oxidize NADH in the mitochondrial inner membrane and produce DHAP c. to convert DHAP to glyceraldehyde 3-phosphate d. to shuttle hydrogen atoms to the ETC *review mitochondrial glycerol 3-P dehydrogenase* **11.** 5 pts Citrate can inhibit the conversion of: a. DHAP to GA3P b. lactate to pyruvate c. glucose 6-phosphate to fructose 6-phosphate d. fructose 6-phosphate to fructose 1,6-bisphosphate e. DHAP to glycerol 3-phosphate *which glycolytic enzyme is inhibited by citrate?* **12.** 5 pts If citrate is transported from the mitochondrial matrix to the cytoplasm, it is likely that: IMAGE: Chemical reaction of Citrate inhibiting PFK-1 and Fructose 1,6-BP becoming Pyruvate Kinase **13.** IMAGE: High NADH, High ATP in Fed State creating Citrate and Pyruvate a. NADH/NAD+ ↑ b. FAD/FADH2↑ c. NADH/NAD+ ↓ d. NADP/NADPH ↑ *which ratio indicates high energy level in a hepatocyte? Excess citrate is transported when glucose levels are high and can also be directed to synthesis of fatty acids* **14.** 12 pts The presence of fructose 2,6-bisphosphate activates the glycolytic enzymes PFK-I and NA. The absence of fructose 2,6-bisphosphatase activates the enzyme fructose 1,6 bis phosphatase that converts fructose 1,6-bisphosphate to fructose 6 phosphate **15.** 5 pts If NADPH↓ and there is no need for ribose 5-phosphate, then: a. ribose 5-phosphate →→ glucose 6-phosphate b. fructose 6-phosphate + GA3P → erythrose 4P + xylulose 5P c. ribose 5-phosphate →→ glucose 1-phosphate d. fructose 6-phosphate + GA3P →→ pyruvate **16.** Review all modes of the pentose phosphate pathway See class notes. **17.** 5 pts Cellular consumption of NADPH and generation of $NADP^+$ in biosynthesis or in phagocytotic cells will activate the enzyme: a. Glucose 1-phosphate dehydrogenase b. Glucose 6-phosphate decarboxylase c. Glucose 6-phosphate dehydrogenase d. Glucose 6-phosphate diphosphatase *low levels of NADPH activates PPP* **18.** 5 pts Alanine aminotransferase: a. converts pyruvate + lactate to glutamate + α-ketoglutarate b. converts pyruvate + glutamate to alanine + α-ketoglutarate c. converts pyruvate + α-ketoglutarate to alanine + glutamate d. converts pyruvate + lactate to alanine + α-ketoglutarate IMAGE: L-Ketoacid + amino acid converting into amino acid + α-ketoacid **19.** 5 pts In the fasted state: a. pyruvate dehydrogenase is inactive, pyruvate carboxylase is active, and phosphoenol pyruvate carboxykinase is active b. pyruvate dehydrogenase is active, pyruvate carboxylase is active, and phosphoenol pyruvate carboxykinase is active c. pyruvate dehydrogenase is inactive, pyruvate carboxylase is inactive, and phosphoenol pyruvate carboxykinase is inactive d. pyruvate dehydrogenase is inactive, pyruvate carboxylase is inactive, and phosphoenol pyruvate carboxykinase is active *during gluconeogenesis, PDH is much less active. AcetylCoA is likely provided by fatty acid oxidation.* **20.** 9 pts In the fasted state, even chain fatty acids are completely converted to acetyl CoA and any remaining odd chain fatty acids are converted to propionyl CoA and enter the Krebs cycle as Succinyl Có A Check your notes **10.1.** 3 pts The glucose transporter GLUT 4 is expressed on skeletal and cardiac muscle and adipose tissue in response to insulin. *One GLUT type is expressed in response to insulin release* **21.** 5 pts Autocatalytic and enzymatic glycogen polymer chain elongation requires: a. UTP + glucose 4-phosphate → UDP-glucose + PP b. UDP + glucose 1-phosphate → UTP-glucose + PP c. UTP + glucose 1-phosphate → UDP-glucose + PP d. UDP + glucose 4-phosphate → UTP-glucose + PP **22.** Write all steps of gluconeogenesis including regulation See class notes. **23.** Show all steps of glycolysis starting from glucose including regulation. Write out the action of PFK-II/fructose 2,6 bisphosphatase in the fed and fasted state. See class notes **24.** Write out all steps of the Krebs cycle including regulation See class notes. ## Biochemistry II Exam 2 Nov.19 **1a.** (8 pts) Starting with a 5 carbon fatty acyl CoA, write the chemical structures resulting from the action of acyl CoA dehydrogenase, enoyl CoA hydratase, β-hydroxy acyl CoA dehydrogenase, and β-ketothiolase: 5 carbon fatty acyl CoA Product of acyl CoA dehydrogenase oxidation: Product of enoyl CoA hydratase hydration: Product of β-hydroxy acyl CoA dehydrogenase oxidation: Products of β-ketothiolase cleavage (2 products): One product of the β-ketothiolase cleavage above ultimately enters the Krebs cycle after conversion to succinyl CoA or acetyl-CoA. **1b.** (4 pts) Acyl CoA dehydrogenase carries its reducing equivalents as FADH2 which are delivered to ETF CoQ oxidoreductase in the electron transport chain. **1c.** (4 pts) β-hydroxy acyl CoA dehydrogenase carries its reducing equivalents as NADH which are delivered to NADH oxidoreductase in the electron transport chain. **25.** (6 pts) In the fasted state, glycerol released from adipocytes and taken up by the liver will first be converted to glycerol 3 phosphate by the enzyme glycerol Kinase and ultimately used to synthesize glycogen or Glucose 6-phosphate in the hepatocyte endoplasmic reticulum. **26.** (2 pts) In the Fed state, the precursor to molecules of glycerol for fatty acid synthesis in both adipocytes and hepatocytes is glucose **27.** (8 pts) In the Fed state, citrate is continuously produced by reciprocal regulation. An increase in acetyl CoA inhibits the enzyme pyruvate dehydrogenase and stimulates the enzyme pyruvate carboxylase. The reverse occurs when acetyl CoA concentration decreases due to reaction with oxaloacetate to form citrate. **28.** (4 pts) In the Fasted state, acetyl CoA is directed into ketogenesis, partly due to the reduction in the concentration of oxaloacetate, which either reacts with glutamate to form α-ketoglutarate and aspartate, or is reduced to malate (both products can be the starting point of gluconeogenesis). **29.** (6 pts) Acyl CoA carboxylase is inhibited by molecules of palmitoyl CoA and activated by molecules of citrate. Malonyl CoA inhibits carnitine palmitoyl transferase I so newly formed fatty acyl CoA cannot enter the mitochondrial matrix. **30.**(8 pts) In the Fed state, cytoplasmic malate is converted to pyruvate generating a molecule of NADPH and CO2 by the enzyme matic enzyme. **31.** (4 pts) In the Fed state, triacylglycerides are packaged with the protein Apo B100 (among others) and released to the bloodstream in fatty-protein clusters known as VLDL **32.** (2pts) The enzymes: Malic enzyme, glucose 6-phosphate dehydrogenase, and citrate lyase are synthesized in response to the hormone insulin **33.** (6pts) Mitochondrial glycerol 3-phosphate dehydrogenase oxidizes glycerol 3-phosphate to DHAP and concurrently reduces FAD to FADH2 **34.** (24 pts) Name the enzyme responsible for conversion of the Krebs cycle intermediates: a. oxaloacetate + acetyl CoA to citrate: citrate synthase b. citrate to isocitrate: acmitose c. isocitrate to α-ketoglutarate: isocitrate dehydrogenase d. a-ketoglutarate to succinyl CoA: α-ketoglutarate dehydrogenase e. succinyl CoA to succinate: succinate thiokinase or succinate synthetase f. succinate to fumarate: succinate dehydrogenase g. fumarate to malate: fumarate fumarase h. malate to oxaloacetate: malate dehydrogenase e. NADH is formed in reactions (letters) C D and H f. FADH2 if formed in reaction F **35.** (6pts) In the Fasted state, to spare glucose, cells of the CNS will convert D-β-hydroxybutyrate to acetoacetate by the enzyme D-β-hydroxybutyrate dehydrogenase. Succinyl CoA acetoacetate CoA transferase converts acetoacetate to acetoacetyl CoA. Thiolase converts acetoacetyl CoA to two molecules of acetyl CoA that enter the Krebs cycle.