Biochemistry
9th Edition
ISBN: 9781319114671
Author: Lubert Stryer, Jeremy M. Berg, John L. Tymoczko, Gregory J. Gatto Jr.
Publisher: W. H. Freeman
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With respect to glycogen, what is the likely fate of excess glucose 6-phosphate in muscle?
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- Glucose 6-phosphatase deficiency is a glycogen storage disease referred to as von Gierke disease. Which of the following symptoms would you NOT expect to see in patients with this disease? (A) severe fasting hypoglycemia (B) excess adipose triglyceride storage and low circulating levels of fatty acids (C) hyperammonemia (D) liver enlargement resulting from excess liver glycogen storage (E) lactic acidosis (F) goutarrow_forwardIn the fasted state, FADH2 and NADH for oxidative phosphorylation are mainly provided by fatty acid oxidation. Explain how fatty acids are mobilised from adipose tissue by the action of glucagon.arrow_forwardWhy are the enzymes α-Amylase and α-glucosidase active in a patient with hyperglycemia or diabetes? How do they become activated?arrow_forward
- 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.arrow_forwardWhich of the following is the correct summary of the anaerobic breakdown of glucose in the skeletal muscle? Glucose + ADP + Pi ⟶ lactate + ATP Glucose + 2ADP + 2Pi ⟶ 2 lactate + 2ATP Glucose + 2ADP + 2Pi + 2NAD+ ⟶ 2 pyruvate + 2ATP + 2NADH + 2H+ Glucose + ADP + Pi ⟶ pyruvate + ATP Glucose + 2ADP + 2Pi ⟶ 2 pyruvate + 2ATParrow_forwardit is known that exercise is good for diabetics. explain how GLUT 4 transporters may be involved in this beneficial effect of exercise.arrow_forward
- Hexokinase deficiency (HKD) is a congenital disease that can disrupt intracellular glucose levels. Please provide an explanation of the diseases impact on intracellular glucose levels and the mechanism by which how GLUT1 regulates this disrupted glucose level.arrow_forwardA 16-year-old female is recently diagnosed with a deficiency of muscle glycogen phosphorylase. She and her family are concerned and ask the following questions. Based on what you know about skeletal muscle glycogenolysis and muscle metabolism, please respond to each question with a thoughtful answer that describes the metabolism in these various scenarios in language that your patient will understand, while also being sure to include the role of the relevant metabolic pathways, specific enzymes, and stimulus for their activity: I’m not sure I understand the issue. Can you explain how muscle glycogen is used normally during exercise? I really like to take long walks; will Istill be able to do this with my friends? As a result of this deficiency, will I need to get up at night to eat to maintain my blood glucose levels? Do I need to worry about producing excessive lactate during intense anaerobic exercise?arrow_forwardUnder 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. )arrow_forward
- Glycogen synthase in the liver is a target for phosphorylation by two protein kinases. What are these two protein kinases and how are they independently regulated by glucagon and insulin to regulate glycogen biosynthesis?arrow_forwardWhich of the following conditions is most likely to force a muscle cell to metabolize glucose anaerobically(fermentation) under normal oxygenation ? - Glyceraldehyde-3-phosphate dehydrogenase deficiency - Lactate dehydrogenase deficiency -Pyruvate kinase deficiency -Aldolase deficiency - Cytososic Glycerol-3-phosphate dehydrogenase deficiencyarrow_forwardWhat factors affect the rate of glycogen synthesis following depleting exercise, and what steps can we take to maximize glycogen restoration?arrow_forward
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