1. ATP and Phosphocreatine as Sources of Energy for Muscle During muscle contraction, the concentration of phosphocreatine in skeletal muscle drops while the concentration of ATP remains fairly constant. However, in a classic experiment, Robert Davies found that if he first treated muscle with 1-fluoro-2,4-dinitrobenzene (p. 97), the concentration of ATP declined rapidly while the concentration of phosphocreatine remained unchanged during a series of contractions. Suggest an explanation.
2. Metabolism of Glutamate in the Brain Brain tissue takes up glutamate from the blood, transforms it into gluta-mine, then releases it into the blood. What is accomplished by this metabolic conversion? How does it take place? The amount of glutamine produced in the brain can actually exceed the amount of glutamate entering from the blood. How does this extra glutamine arise? (Hint: You may want to review amino acid catabolism in Chapter 18; recall that NH4 is very toxic to the brain.)
Glycerol 3-phosphate is required for the biosynthesis of tria-cylglycerols. Adipocytes, specialized for the synthesis and degradation of triacylglycerols, cannot use glycerol directly, because they lack glycerol kinase, which catalyzes the reaction
Glycerol + ATP-> glycerol 3-phosphate + ADP
How does adipose tissue obtain the glycerol 3-phosphate necessary for triacylglycerol synthesis?
4. Oxygen Consumption during Exercise A sedentary adult consumes about 0.05 L of O2 in 10 seconds. A sprinter, running a 100 m race, consumes about 1 L of O2 in 10 seconds. After finishing the race, the sprinter continues to breathe at an elevated (but declining) rate for some minutes, consuming an extra 4 L of O2 above the amount consumed by the sedentary individual.
(a) Why does the need for O2 increase dramatically during the sprint?
(b) Why does the demand for O2 remain high after the sprint is completed?
5. Thiamine Deficiency and Brain Function Individuals with thiamine deficiency show some characteristic neurological signs and symptoms, including loss of reflexes, anxiety, and mental confusion. Why might thiamine deficiency be manifested by changes in brain function?
6. Potency of Hormones Under normal conditions, the human adrenal medulla secretes epinephrine (C9H13NO3) at a rate sufficient to maintain a concentration of 10"10 m in circulating blood. To appreciate what that concentration means, calculate the diameter of a round swimming pool, with a water depth of 2.0 m, that would be needed to dissolve 1.0 g (about 1 teaspoon) of epinephrine to a concentration equal to that in blood.
7. Regulation of Hormone Levels in the Blood The half-life of most hormones in the blood is relatively short. For example, when radioactively labeled insulin is injected into an animal, half of the labeled hormone disappears from the blood within 30 min.
(a) What is the importance of the relatively rapid inac-tivation of circulating hormones?
(b) In view of this rapid inactivation, how is the level of circulating hormone kept constant under normal conditions?
(c) In what ways can the organism make rapid changes in the level of a circulating hormone?
8. Water-Soluble versus Lipid-Soluble Hormones On the basis of their physical properties, hormones fall into one of two categories: those that are very soluble in water but relatively insoluble in lipids (e.g., epinephrine) and those that are relatively insoluble in water but highly soluble in lipids
(e.g., steroid hormones). In their role as regulators of cellular activity, most water-soluble hormones do not enter their target cells. The lipid-soluble hormones, by contrast, do enter their target cells and ultimately act in the nucleus. What is the correlation between solubility, the location of receptors, and the mode of action of these two classes of hormones?
9. Metabolic Differences between Muscle and Liver in a "Fight or Flight" Situation During a "fight or flight" situation, the release of epinephrine promotes glycogen breakdown in the liver, heart, and skeletal muscle. The end product of glycogen breakdown in the liver is glucose; the end product in skeletal muscle is pyruvate.
(a) What is the reason for the different products of glycogen breakdown in the two tissues?
(b) What is the advantage to an organism that must fight or flee of these specific glycogen breakdown routes?
10. Excessive Amounts of Insulin Secretion: Hyperin-sulinism Certain malignant tumors of the pancreas cause excessive production of insulin by the 3 cells. Affected individuals exhibit shaking and trembling, weakness and fatigue, sweating, and hunger.
(a) What is the effect of hyperinsulinism on the metabolism of carbohydrates, amino acids, and lipids by the liver?
(b) What are the causes of the observed symptoms? Suggest why this condition, if prolonged, leads to brain damage.
Thyroid hormones are intimately involved in regulating the basal metabolic rate. Liver tissue of animals given excess thy-roxine shows an increased rate of O2 consumption and increased heat output (thermogenesis), but the ATP concentration in the tissue is normal. Different explanations have been offered for the thermogenic effect of thyroxine. One is that excess thryroxine causes uncoupling of oxidative phos-phorylation in mitochondria. How could such an effect account for the observations? Another explanation suggests that the thermogenesis is due to an increased rate of ATP utilization by the thyroxine-stimulated tissue. Is this a reasonable explanation? Why?
13. Sources of Glucose during Starvation The typical human adult uses about 160 g of glucose per day, 120 g of which is used by the brain. The available reserve of glucose (~20 g of circulating glucose and ~190 g of glycogen) is adequate for about one day. After the reserve has been depleted during starvation, how would the body obtain more glucose?
14. Parabiotic ob/ob mice By careful surgery, researchers can connect the circulatory systems of two mice so that the same blood circulates through both animals. In these parabiotic mice, products released into the blood by one animal reach the other animal via the shared circulation. Both animals are free to eat independently. If an ob/ob mouse (both copies of the OB gene are defective) and a normal OB/OB mouse (two good copies of the OB gene) were made parabiotic, what would happen to the weight of each mouse?
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