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Exam 4 Biochemistry

Dr. B's LOs (19 lectures)

What are the the 6 different carbon sources for glucose synthesis in the liver and kidney? Alanine, Lactate, Pyruvate, Glycerol, alpha keto acids (non fed state) or Propinoic acid (fed state), and other monosaccharides (fed state)
When does gluconeogenisis start and in what tissue in most American's who are not suffering from starvation? Gluconeogenesis starts in the liver as soon as the liver starts responding to glucagon and after liver glycogen is gone, gluconeogenesis is the ONLY source of blood glucose.
What are the Alanine Cycle and the Cori Cycle and why are they so important? Lactic Acid production and alanine, which is used to transfer amino groups from muscle to liver for urea synthesis. Alanine and lactate can be used to synthesize glucose.
Energy cost of alanine cycle... 12 ATP
Energy cost of cori cycle... 6 ATP
Where does the energy needed for gluconeogenesis come from? The liver uses fatty acids in the fasting state to form ketone bodies. Burning fatty acids produces lots of ATP and it also produces lots of acetyl-CoA to make sure that the lactate and alanine that the liver is taking up get converted to glucose.
What are the two major amino acids in our blood and what are they used for? Glutamine is the number 1 amino acid in our blood and alanine is number 2 (in terms of concentration). (alanine forms pyruvate and glutamine forms alpha-ketogluterate).
How are amino acids used to synthesize glucose and which two amino acids can’t be used to synthesize glucose? Synthesize through gluconeogenisis and Leucine and Lysine.
Discuss the general process used for gluconeogenesis? (What are we reversing and where are we doing it?) A sort of reversal of glycolysis, from pyruvate back to glucose in just the mitochondria and cytoplasm of cells in the liver and kidney. Most steps are reversible but some you have to use completely different enzymes.
List the 3 steps (enzymes) in glycolysis that are not reversible. PEP -> pyruvate Glucose-6-PO4 -> Glucose F-1,6 BP -> F-6-PO4 Overall message, gluconeogenesis features enzymes that bypass irreversible KINASE steps
How is glucose released from the liver during gluconeogenesis? (enzyme used and the process used for the release of glucose). Glucose-6-Phosphatase; Remember that the liver is using Glucokinase (hexokinase IV).So this acts as the reversal of hexokinase and takes phosphate of G6P.
How is glucose transported to the membrane, does it need glut 2? Presence of G-6-phosphatase in ER of the liver and kidney cells makes gluconeogenesis possible. Muscle and brain DO NOT do gluconeogenesis. G-6-P is hydrolyzed as it passes into the ER. ER vesicles filled with glucose diffuse to the plasma membrane. No
Why does a deficiency of pyruvate kinase cause hemolytic anemia (RBC death)? Patients with a pyruvate kinase deficiency have 5-25% of normal activity. In RBCs, this restricts ATP formation needed for Na/K regulation using the ATP-dependent sodium pump. Because sodium can not be adequately pumped out of the cell, red blood cell s
what are the signs and symptoms of hemolytic anemia? Rapid breathing (tachypnea) and a rapid heart rate (tachycardia) occur because oxygen delivery to tissues is low due to the anemia. The heart has the highest requirement for oxygen. Fatigue, gallstones, enlarged spleen
how common is a gene defect in pyruvate kinase and how is this form of hemolytic anemia treated? supportive care: blood transfusions in times of physiological stress and symptomatic anemia,splenectomy-for severe anemia; bone marrow transplantation
What two enzymes are needed to reverse the pyruvate kinase reaction and which of these two enzymes is the rate-limiting step for gluconeogenesis? Pyruvate carboxylase and PEP carboxykinase. PEP carboxykinase is the rate-limiting enzyme for gluconeogenesis.
2. How does the liver process alanine and lactate to form the phosphoenolpyruvate that is needed for gluconeogenesis? Alanine transamination is required to convert alanine to pyruvate and lactate dehydrogenase is required to convert lactate to pyruvate. (5 total forms of LDH, HHHH, HHHM, HHMM, HMMM, MMMM)3 in liver.
why does ethanol inhibit gluconeogenesis in the liver? Ethanol drives up NADH levels in cytoplasm and this inhibits the conversion of malate  oxaloacetic acid.
Why does acetyl-CoA move carbon from pyruvate away from the TCA cycle and into gluconeogenesis? Not only does beta-oxidation of fatty acids provide lots of NADH and ATP to get citrate to leave mitochondria, it also provides lots of acetyl-CoA. The acetyl-CoA inhibits pyruvate dehydrogenase while stimulating pyruvate carboxylase.
List the 2 factors that regulate pyruvate carboxylase activity and the vitamin cofactor needed for this enzyme to work. Biotin is the vitamin needed for this enzyme to work. Regulation is from acetyl-CoA (stimulant) and ADP (inhibitor).
List the 2 factors involved in regulating phosphoenolpyruvate carboxykinase activity. Glucagon increases the formation of this enzyme and ADP inhibits formation of this enzyme.
6. What enzyme is used to reverse the phosphofructokinase-1 reaction, what tissues have this enzyme and what regulates this enzyme? 6. What enzyme is used to reverse the phosphofructokinase-1 reaction, what tissues have this enzyme and what regulates this enzyme?
How does fructose 2,6-bisphosphate help to prevent futile cycling? It stimulates phosphofructokinase-1 and inhibits fructose 1,6-bisphosphatase which helps prevent futile cycling in tissues that have both enzymes. It is used to supercharge GLYCOLYSIS and INHIBIT gluconeogenesis.
How does AMP help to prevent futile cycling? AMP inhibits fructose 1,6-bisphosphatase and stimulates phosphofructokinase-1 which helps prevent futile cycling in tissues that have both enzymes. AMP stimulates glycolysis and inhibits gluconeogenesis.
How does citrate help to prevent futile cycling? Citrate stimulates fructose 1,6-bisphosphate and inhibits phosphofructokinase-1. Stimulates gluconeogenesis and inhibits glycolysis.
What is the purpose for futile cycles (substrate cycles)? Futile cycles amplify metabolic signals and the roles of these cycles are to generate heat produced via the hydrolysis of ATP.
What is malignant hyperthermia, why does it occur, how often does it occur? Genetic defect where 1/15,000 children have a potentially fatal rise in body temperature when exposed to neutral anesthetics during surgery. Ryanodine receptor mutation. 3 x as much Calcium released.
how many people are at risk for this condition (malignant hyperthermia)? Rare event with genetic basis, 70 percent lethal if untreated: 1:50,000 risk in adults and 1:15,000 risk in children. Halothane, Isoflurane, and Desflurane are anesthetics that could cause disease in a susceptible patient.
how is susceptibility to this problem diagnosed and how is this problem treated? (malignant hyperthermia) early detection, d/c agents, hyperventilate, bicarb, IV dantrolene (2.5mg/kg), ice packs/cooling blankets, lasix/mannitol/fluids. ICU monitoring Susceptible patients—preop with IV dantrolene, keep away inhalational agents and succinylcholine.
Created by: vpack87



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