Fasting and refeeding in the lactating dairy cow. 1. The recovery of milk yield and blood chemistry following a six-day fast.
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The amount of food eaten in a two hour trial by male Sprague Dawley rats was recorded after periods of food deprivation up to 42 hr in length. Rats ate 50-78% more when refed during the dark phase than when refed during the light phase. This occurred even when light fed animals were fasted for longer periods than the dark fed animals. Rats eat in a rhythmic pattern after deprivation. These data are in good agreement with data previously reported and extend it by increasing the number of observations, increasing the length of deprivation, and comparing different age groups.
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We studied [125I] insulin binding to circulating cells in patients with anorexia nervosa (eight females), in the basal cachectic state (seven patients) and after weight gain (eight patients) and compared the values to those obtained in 17 normal volunteers (eight females and nine males). Untreated patients showed increased insulin binding to receptors on erythrocytes (mean +/- S.E.M., 12.2 +/- 0.99 per cent of total); after weight gain, these increased levels returned to normal (6.8 +/- 0.42 vs 6.7 +/- 0.63 per cent of total). Increased binding was due to an increased number of receptors per cell, with little or no change in receptor affinity. In five patients (one untreated, four treated), results of [125I] insulin binding to erythrocytes correlated closely (r = 0.982) with results obtained with monocytes. We conclude that in patients with anorexia nervosa, insulin binding to receptors is altered and that the abnormality is corrected by restoration of normal food intake and body weight.
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The effect of undernutrition and subsequent rehabilitation on free and total alkaline ribonuclease activity (RNase) of cerebrum and liver was studied in 14- and 21-day-old rats. Free RNase activity was higher in both organs at 14 and 21 days of age. However, at day 21 the difference was statistically significant only in liver. Total RNase activity was not changed by undernutrition in cerebrum and was reduced in liver. Nutritional rehabilitation returned both free and total RNase activities to control levels in liver but had no apparent effect on cerebrum. The elevation of free RNase seems to be secondary to a reduced concentration of inhibitor protein and not to de novo synthesis of RNase.
The urine of sexually mature male rats contains a protein of hepatic origin, alpha2u-globulin, not found in the urine of immature or female rats; output of this protein is greatly reduced by fasting. We have examined the effects of feeding and of fasting for various lengths of time on urinary output and hepatic synthesis of alpha2u-globulin. Rats eating ad libitum showed diurnal rhythms of urinary alpha2u-globulin excretion reaching maxima between 2000 and 0800 hours, thus coinciding with the daily feeding period of the rat. Fasting for 12 hours extinguished this diurnal rhythm. When fasting was prolonged up to 36 hours, urinary excretion of alpha2u-globulin was reduced to very low levels. Hepatic synthesis of alpha2u-globulin under these nutritional conditions was investigated by incubating liver polyribosomes with [3H]leucine and a preparation of soluble enzymes for protein synthesis and separating the labeled alpha2u-globulin peptides by immunoprecipitation followed by electrophoresis on sodium dodecyl sulfate-polyacrylamide gels. By this technique, it was shown that only membrane-bound ribosomes in the livers of mature male rats make this protein. Semi-quantitative measurement suggested that the proportion of liver polyribosomes synthesizing alpha2u-globulin was unchanged after 12 hours of fasting, but was reduced after 24 and 36 hours of fasting. It is proposed that the diurnal rhythm in alpha2u-globulin output in the urine represents translational control of its synthesis in the liver, whereas the more extensive reduction with prolonged fasting is partly due to a selective reduction in transcription of the messenger RNA for this protein.
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The effects of fasting were examined on the rhythmic changes in the activities of maltase [EC 3.2.1.20] and leucine aminopeptidase [EC 3.4.11.1] in the small intestine of rats which has been kept under scheduled feeding conditions. Irrespective of whether the rats had been kept on a daytime or nighttime feeding schedule, the rhythms of maltase and leucine aminopeptidase persisted when the animals were starved. However, the amplitude of the leucine aminopeptidase rhythm began to decrease from the first day of fasting, while that of maltase did not. Conspicuous rhythms persisted for at least 2 days during fasting, but they gradually became vague and disappeared after 5 days. When rats were refed after fasting, the leucine aminopeptidase activity increased within a few hours, but the maltose activity did not. It is suggested that the rhythms of the digestive enzymes in the small intestine of rats are not a direct consequence of food intake, but are triggered off by the anticipatory mechanism which operates when rats expect to be fed. The rhythmic change of leucine aminopeptidase seemed to be intensified by food intake.
In man the first days of fasting are characterized by enhanced natriuresis despite an increase in aldosterone secretion. Therefore the possibility of a decreased renal tubular sensitivity to this hormone was considered. The response to aldosterone infused before a fast and again on day 4 of fasting was evaluated in 12 starving obese women in terms of urinary sodium, chloride and potassium excretion. The data were compared to those obtained from 20 untreated starving obese women. In addition, salivary flow and sodium output were measured before and after aldosterone infusion in 4 out of the 12 patients treated. The involvement of aldosterone in the mechanism of fasting natriuresis and glucose-induced sodium retention was evaluated by means of spironolactone treatment (Aldactone A; 300 mg/day p.o.) on days 6 to 8 of the fast, with an oral glucose load (100 g) on day 7. Aldosterone infused on day 4 of the fast caused on average only 40% of the antinatriuretic effect it achieved before the fast. On the other hand even before aldosterone infusion, salivary sodium output was markedly reduced during the fast to levels comparable to those observed after aldosterone treatment in the pre-fast period. Furthermore, spironolactone administration on day 6 of the fast was associated with a prompt and marked increase in natriuresis. These 3 sets of facts indicate a definite biological activity of aldosterone during the initial phase of fasting with factor(s) interfering at the renal level with the normal expression of the hormonal action on sodium balance. There was still a distinct antinatiuretic effect of glucose in the presence of spironolactone, but less pronounced than when glucose was administered alone. The well-documented hyperaldosteronism of a total fast may represent a compensatory mechanism to decrease sodium loss at the end of a week-long fast. In addition a marked sodium-retaining effect of glucose can be demonstrated after aldosterone action is blocked by spironolactone. This provides another indication that glucose stimulates sodium retention through mechanism(s) which do not involve aldosterone.
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