Studies of marked and persistent sodium retention in previously fasted and sodium-deprived obese subjects

To further delineate the effects of fasting and sodium deprivation on the handling of sodium when sodium intake is resumed, balance studies were performed on seven obese female subjects. All subjects underwent a period of total fasting, which continued for 27 to 29 days prior to resumption of sodium intake. Natriuresis in the first week of fasting and continued sodium chloride deprivation resulted in cumulative deficits of 383 ± 47 mEq (SEM) and 371 ± 41 mEq of sodium and chloride, respectively. Chloride space decreased from 21.2 ± 2.7 L to 18.7 ± 2.5 L, and aldosterone secretory rates (ASR) increased from 43 ± 13 μg 24 h to 597 ± 138 μg 24 h. Following resumption of sodium intake and simultaneous refeeding on low calorie diets in studies on four subjects (group I), cumulative sodium balances during the first seven days ranged from +586 mEq to +1,109 mEq; sodium retained/previously existing sodium deficit = 2.4, 3.2, 2.0, and 1.6 in the four subjects, respectively. Continued sodium retention resulted in cumulative sodium balances ranging from +670 mEq to +1,249 mEq at the end of 19 to 22 days in studies on three subjects. In the subjects whose cumulative sodium balance was +1,249 mEq, sodium retained/sodium deficit = 3.6. During the first five days of sodium intake and refeeding ASR decreased to 74 ± 26 μg 24 h. Sodium chloride administration without refeeding in studies on three subjects (group II) also resulted in retention of more than enough sodium to replenish previously existing sodium deficits. Cumulative sodium balances in two subjects who remained in positive sodium balance without resumption of caloric intake for 29 days were +820 mEq and +922 mEq, respectively. Subsequent refeeding, with only minor changes in sodium intake, resulted in additional sodium retention in all subjects. Cumulative sodium balances at the time of maximal sodium retention were similar to those observed in the studies on group I subjects. These studies identify two components to the sodium retention that occurs during refeeding and resumption of sodium intake after prolonged fasting and sodium deprivation, only one of which can be related to restoration of caloric intake. The magnitude and persistence of sodium retention are consistent with the possibility that "resetting" of sodium homeostatic mechanisms may also be a factor in sodium handling by previously fasted and sodium-deprived subjects.