Download Additional Study Questions for Fuel Metabolism Lectures

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Transcript
Additional Study Questions for Fuel Metabolism Lectures
(1) Explain in detail why acetyl-CoA and pyruvate are at the “crossroads” of the
major metabolic pathways.
(2) Explain the alternative fates of glucose-6-phosphate in the liver, depending on the
glucose demand.
(3) Why does fasting result in an increase in liver concentrations of PEP
carboxykinase and glucose-6-phosphatase.
(4) Explain why the sigmoidal kinetics behavior of glucokinase helps the liver to
adjust its metabolic activities to the amount of available glucose.
(5) After several days of starvation, the ability of the liver to metabolize acetyl-CoA
via the citric acid cycle is severely compromised. Why is this so?
(6) Summarize the roles of insulin, glucagons and epinephrine in regulating
mammalian fuel metabolism.
(7) Explain the way that the arcuate nucleus in the hypothalamus integrates the
hormonal signals presented by leptin, ghrelin, PYY3-36 and insulin. When
answering this question, state from which organs the peptides originate and their
specific effects on the NPY/AgRP and POMC/CART neurons. Also describe how
the neuropeptides secreted by these neurons affect food intake and energy
expenditure. (You do not have to consider “higher-level” interactions here, like
the interneuronal connections between NPY/AgRP and POMC/CART neurons, or
other neurons in the hypothalamus).
(8) Explain the biochemical alterations induced by leptin that suggest its evolutionary
advantage as a “thrifty gene” with regard to energy metabolism and storage.
(9) Explain the biochemical changes seen in obesity.
(10) Explain the biochemical changes seen in a person who is using the Atkins diet
and describe how the physical symptoms that we discussed in class arise from these
alterations.
(11 )Explain the biochemical changes seen in a person with diabetes and describe
how the physical symptoms that we discussed in class arise from these alterations.
(12) Explain the proposed link between obesity and insulin resistance as described by
Gerald Shulman in your text.