When the O, supply from blood fails to meet the demand of O,-consuming cells, oxygen deprivation (hypoxia) occurs. This is common, for example, in exercising muscle. It has been recognized for over 100 years that O,- deprived cells show increased conversion of glucose to lactate, known as the Pasteur effect. Activation of the Pasteur effect during hypoxia is mediated by hypoxia-inducible factor-1 (HIF-1). HIF-1 is a transcription factor that upregulates the expression of several glycolytic enzymes that support the increased glycolytic ATP production as mitochondria become starved for 0. At the same time glycolysis is increasing, the rate of mitochondrial respiration decreases. New rescarch reveals that in addition to upregulat- ing enzymes in the glycolytic pathway, HIF-1 also induces the expression of cytoplasmic lactate dehydrogenase (LDH) and mitochondrial pyruvate dehydrogenase kinase (PDK). (a) Explain why glucose consumption must increase in hypoxic tissues to provide the same amount of ATP that could be produced from glucose in normoxic (normal O, levels) tissues. (b) How would increasing LDH expression increase the rate of glycolysis? (c) How would increasing PDK expression decrease the rate of mitochon- drial respiration?
When the O, supply from blood fails to meet the demand of O,-consuming cells, oxygen deprivation (hypoxia) occurs. This is common, for example, in exercising muscle. It has been recognized for over 100 years that O,- deprived cells show increased conversion of glucose to lactate, known as the Pasteur effect. Activation of the Pasteur effect during hypoxia is mediated by hypoxia-inducible factor-1 (HIF-1). HIF-1 is a transcription factor that upregulates the expression of several glycolytic enzymes that support the increased glycolytic ATP production as mitochondria become starved for 0. At the same time glycolysis is increasing, the rate of mitochondrial respiration decreases. New rescarch reveals that in addition to upregulat- ing enzymes in the glycolytic pathway, HIF-1 also induces the expression of cytoplasmic lactate dehydrogenase (LDH) and mitochondrial pyruvate dehydrogenase kinase (PDK). (a) Explain why glucose consumption must increase in hypoxic tissues to provide the same amount of ATP that could be produced from glucose in normoxic (normal O, levels) tissues. (b) How would increasing LDH expression increase the rate of glycolysis? (c) How would increasing PDK expression decrease the rate of mitochon- drial respiration?
Human Anatomy & Physiology (11th Edition)
11th Edition
ISBN:9780134580999
Author:Elaine N. Marieb, Katja N. Hoehn
Publisher:Elaine N. Marieb, Katja N. Hoehn
Chapter1: The Human Body: An Orientation
Section: Chapter Questions
Problem 1RQ: The correct sequence of levels forming the structural hierarchy is A. (a) organ, organ system,...
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Transcribed Image Text:When the O, supply from blood fails to meet the demand of O,-consuming
cells, oxygen deprivation (hypoxia) occurs. This is common, for example,
in exercising muscle. It has been recognized for over 100 years that O,-
deprived cells show increased conversion of glucose to lactate, known as the
Pasteur effect. Activation of the Pasteur effect during hypoxia is mediated
by hypoxia-inducible factor-1 (HIF-1). HIF-1 is a transcription factor that
upregulates the expression of several glycolytic enzymes that support the
increased glycolytic ATP production as mitochondria become starved for
0. At the same time glycolysis is increasing, the rate of mitochondrial
respiration decreases. New rescarch reveals that in addition to upregulat-
ing enzymes in the glycolytic pathway, HIF-1 also induces the expression
of cytoplasmic lactate dehydrogenase (LDH) and mitochondrial pyruvate
dehydrogenase kinase (PDK).
(a) Explain why glucose consumption must increase in hypoxic tissues to
provide the same amount of ATP that could be produced from glucose in
normoxic (normal O, levels) tissues.
(b) How would increasing LDH expression increase the rate of glycolysis?
(c) How would increasing PDK expression decrease the rate of mitochon-
drial respiration?
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