Between your evening meal and breakfast, your blood glucose drops and your liver becomes a net producer rather than aconsumer of glucose.Which statements describe the hormone-stimulated process that triggers glucose production by the liver?The increase in (CAMP] causes protein kinase A to phosphorylate pyruvate kinase, thus inhibiting glycolysis in muscletissue to promote gluconeogenesis in the liver.The decrease in [fructose 2,6-bisphosphate] stimulates FBPase-1, the key enzyme in gluconeogenesis.Epinephrine stimulates an enzyme cascade involving hepatic protein kinase A (PKA) and phosphorylase b kinase,which eventually leads to glycogen breakdown in the liver.O The rapid decrease in blood glucose levels triggers glucagon release by the pancreas.Glucagon stimulates CAMP-dependent phosphorylation of PFK-2/FBPase-2, which decreases[fructose 2,6-bisphosphate].The decrease in [fructose 2,6-bisphosphate] stimulates PFK-1, the key enzyme in gluconeogenesis. Pyruvate kinase catalyzes the transfer of a phosphoryl group from phosphoenolpyruvate to ADP in the last step ofglycolysis, forming pyruvate in the process. Vertebrates have several isozymes of pyruvate kinase, which can beallosterically inhibited by compounds including ATP and acetyl-CoA. What is an effect of CAMP-dependent protein kinase(PKA) inactivation of the liver isozyme but not the muscle isozyme?Glycogen synthesis is promoted in the liver as an energy store.O Glycolysis is inhibited in the liver, but not muscle, when blood sugar is low.Under stress (fight-or-flight) conditions, the liver can use glycolysis to break down glucose.Phosphate from the dephosphorylation of the liver isozyme is used to generate ATP and provide energy for movement.

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Biochemistry

9th Edition

ISBN:9781319114671

Author:Lubert Stryer, Jeremy M. Berg, John L. Tymoczko, Gregory J. Gatto Jr.

Publisher:Lubert Stryer, Jeremy M. Berg, John L. Tymoczko, Gregory J. Gatto Jr.

Chapter1: Biochemistry: An Evolving Science

Section: Chapter Questions

Problem 1P

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Why would LDH be up- or down-regulated depending on location of cancer cells? Anaerobic cancer cells enhance rates of ATP production and rely on pyruvate to lactate conversion. LDH5 expressed can vary in favoring pyruvate for conversion to lactate (anaerobic metabolism). Aerobic compartments in newly formed fibrobasts and vessels use lactate to convert to pyruvate for oxidative phosphorylation and favor lactate conversion to pyruvate by LDH1 (aerobic metabolism). Lactate dehydrogenase is upregulated in both cancer cells and supporting stroma and vessels, thus only LDH5 is upregulated showing enhanced expression levels and thus presence at the plasma membrane to increase levels of lactate for export, LDH1 levels are always consistent. LDH1 is upregulated in response to the export of lactate by MCT1, while LDH5 is down-regulated Neither LDH1 or LDH5 are both consistently expressed, regardless of oxygen levels
Why does epinephrine stimulate glycolysis? I know why epinephrine stimulates glycogenolysis which is to release glucose stores. But epinephrine stimulating glycolysis seems counterintuitive as it would synthesize less glucose and more pyruvate?
Many diabetics do not respond to insulin because of a deficiency of insulin receptors on their cells. How does this aff ect (a) the levels of circulating glucose immediately after a meal and (b) the rate of glycogen synthesis in muscle?
The main enzyme of glycogen degradation is [Select] is low, this enzyme is activated by [Select] [Select] When blood glucose in response to the hormone
vny can acetone sometimes be detected in the breath of patients with type 1 diabetes? A. Glucagon signaling is faulty, leading to an excess of oxaloacetate, which enables acetyl-CoA to enter the citric acid cycle, therefore resulting in the production of ketone bodies including acetone OB. Insulin signaling is faulty, so excess malonyl-CoA is generated, which leads to excess acetyl-CoA from beta oxidation Oc. None of the other answers is correct OD. Insulin signaling is correct, but excess acetyl-CoA is generated anyway, leading to the production of ketone bodies including acetone O E. Insulin signaling is faulty, fatty acids are catabolized to acetyl- COA despite high blood glucose, and excess acetyl-CoA is converted to ketone bodies,
Gluconeogenesis occurs in liver and kidney. Which is of the following enzyme are important for gluconeogenesis are expressed exclusively in these tissues? Select one: a. Glucose-6-phosphatase b. Fructose-1,6-Bisphosphatase c. Phosphoenolpyruvate carboxykinase d. Pyruvate carboxylase
Glucose can be made from oxaloacetate during gluconeogenesis, but if oxaloacetate concentrations are decreased,what other substance can be used to make glucose? How might this contribute to increased fat loss?
Which of the following glycolytic enzymes catalyzes the conversion of fructose-1,6-bisphosphate into the two product molecules dihydroxyacetone phosphate, and glyceraldehyde-3-phosphate? phosphoglycerate kinase pyruvate kinase malate dehydrogenase aldolase phosphofructokinase
Which of the following statements is true for the shown reactions? Deficiency of oxaloacetate stimulates the formation of X and y Insulin signaling stimulates the formation of X and Y Both A and B Neither A nor B
Glucagon The function of glucagon is in promoting energy release and inhibiting energy storage in response to low circulating glucose levels, which are largely controlled by insulin [24]. Besides its role in blood–glucose regulation, patients treated with glucagon receptor an tagonists (GRA) often suffer from dyslipidemia, fatty liver and weight gain, suggesting that glucagon play an important role in lipid metabolism [25]. Glucagon acts mainly on the hepatocytes which possess the highest level of glucagon receptors. Following mecha nisms may be involved during this process: (1) At the molecular level, following glucagon binding to its receptor on the hepatocyte, cAMP will be activated and accumulated, which in turn activates cAMP-response element-binding protein (CREB). As a result, the tran scription of carnitine acyl transferase (CPT-1) increases, which converts fatty acids into acylcarnitine and activates β-oxidation-increasing fatty acid catabolism [26]. In addition,…
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Which changes would be expected in a normal human after a meal rich in carbohydrates (select all that apply)? O increased secretion of the pancreatic hormone, insulin O increased glucose uptake in myocytes via glucose transporters increased activity of glucose 6-phosphatase in hepatocytes O increased activity of the liver enzyme, glucokinase O increased activity of GSK-3 in both myocytes and hepatocytes

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