FIGURE 7 Quantitative turnover of substrates in a hypothetical person in the basal state after fasting for 24 hr (—1800 Calories). (From Cahill GF Jr. Starvation in man. N Engl J Med 1970;282:668-675.)

continues at a low but steady rate with carbon skeletons from amino acids providing substrate for gluconeogen-esis and the intermediates needed to maintain the tricarboxylic acid cycle. Glycerol liberated from triglycerides provides the other major substrate for gluco-neogenesis. Renal gluconeogenesis from glutamate accompanies production of ammonia stimulated by ketoacidosis. Virtually all other energy needs are met by oxidation of fatty acids and ketones until triglyceride reserves are depleted. In the terminal stages of starvation, proteins may become the only remaining substrate and are rapidly broken down to amino acids. Gluco-neogenesis briefly increases once again until cumulative protein loss precludes continued survival. Curiously, continued slow loss of protein during starvation of the extremely obese individual may result in death from protein depletion even before fat depots are depleted.

Figure 8 shows some representative values for hormone concentrations in blood in the transition from the fed to the fasting state. Values for cortisol remain unchanged or might even decrease somewhat until late in starvation. Concentrations of cortisol shown in the figure represent morning values and change with the time of day in a diurnal rhythmic pattern that is not altered by fasting (see Chapter 40). Even though its concentration does not increase during fasting, cortisol nevertheless is an essential component of the survival mechanism. In its absence, mechanisms for producing and sparing carbohydrates are virtually inoperative, and death from hypoglycemia is inevitable. The role of glucocorticoids in fasting is a good example of permissive action, in which a hormone maintains the instruments ofmetabolic adjustments so that other agents can manipulate those instruments effectively. Hypoglycemia or perhaps nonspecific stress may account for increased cortisol in the terminal stages of starvation.

The decrease in plasma concentrations of T3 are not indicative of decreased secretion of TSH or thyroid hormone, but rather reflect decreased conversion of plasma T4 to T3. At least during the first few days of fasting, T4 concentrations in plasma remain constant. The slight decline in T4 seen with more prolonged fasting probably reflects a decrease in plasma binding proteins. Recall that T3, which is formed mostly in extrathyroidal tissue, is the biologically active form of the hormone (see Chapter 39). Deiodination of thyrox-ine can lead to the formation of T3 or the inactive metabolite rT3. With starvation, the concentration of rT3 in plasma increases, suggesting that metabolism of thyroxine shifted from the formation of the active to the inactive metabolite. Some of this increase may also be accounted for by a somewhat slower rate of degradation of rT3. Decreased production of T3 results in an overall decrease in metabolic rate and can be viewed as an adaptive mechanism for conservation of metabolic fuels.

Secretion of GH follows a pulsatile pattern that is exaggerated during starvation (see Chapter 44). Fasting increases both the frequency of secretory pulses and their amplitude. The values for GH shown in Fig. 8 represent concentrations present in a mixed sample of blood that was continuously drawn at a very slow rate over a 24-hr period. The metabolic changes produced by an increase in GH secretion are similar to those that result from a decrease in insulin secretion. Growth hormone increases

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