<p>Additional Study Questions for Fuel Metabolism Lectures</p><p>(1) Explain in detail why acetyl-CoA and pyruvate are at the “crossroads” of the major metabolic pathways.</p><p>(2) Explain the alternative fates of glucose-6-phosphate in the liver, depending on the glucose demand.</p><p>(3) Why does fasting result in an increase in liver concentrations of PEP carboxykinase and glucose-6-phosphatase.</p><p>(4) Explain why the sigmoidal kinetics behavior of glucokinase helps the liver to adjust its metabolic activities to the amount of available glucose.</p><p>(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?</p><p>(6) Summarize the roles of insulin, glucagons and epinephrine in regulating mammalian fuel metabolism.</p><p>(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).</p><p>(8) Explain the biochemical alterations induced by leptin that suggest its evolutionary advantage as a “thrifty gene” with regard to energy metabolism and storage.</p><p>(9) Explain the biochemical changes seen in obesity.</p><p>(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.</p><p>(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.</p><p>(12) Explain the proposed link between obesity and insulin resistance as described by Gerald Shulman in your text.</p>