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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Glucose and fructose were studied in eight healthy volunteers who fasted twice for 4 days. Before and after the fasts each subject received a 4-hr glucose or fructose infusion providing 0.5 g/kg/hr. Glucose infusion during starvation resulted in a mean maximal plasma glucose rise of 401 +/- 21 mg/100 ml (+/- SEM) as compared to 119 +/- 10 mg/100 ml before starvation. Insulin/glucose ratios were lower than normal in fasted subjects. Fructose infusion during fasting produced a maximal plasma glucose rise of 91 +/- 9 mg/100 ml as opposed to 5+/-1 mg/100 ml before starvation. During fructose infusion in the fasted state, plasma fructose levels were higher than control and the rise in blood lactate and pyruvate was delayed, but finally lactate concentrations were above control values. The antiketotic effects of intravenous glucose and fructose were similar during fasting but fructose was significantly less potent in reducing free fatty acid levels. After starvation, urinary carbohydrate losses during glucose infusion were 5 times higher than those observed during fructose infusion. Thus, fructose utillization was less impaired during fasting than was glucose utilization, although fasting induced abnormalities in both glucose and fructose metabolism.
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PMID:Comparison of glucose and fructose tolerance before and after starvation. 90 56

Cerebral blood flow (CBF) was measured by means of Celabeled microspheres in infant (20-day-old) and adult (3-month-old) rats, anesthetised with Na-5-ethyl-5-(1-methylpropyl)2-thiobarbituric acid. Cerebral arteriovenous differences of acetoacetate, D-beta-hydroxybutyrate, glucose, lactate, and oxygen and brain DNA content were determined in other groups of similarly treated infant and adult animals fed or starved for 48 or 72 hr. The mean CBF values of 0.48+/-0.04 and 0.62+/-0.07 ml/(g X min), +/- SEM, in infant and adult animals, respectively, were not significantly different. CBF was unaffected by starvation. At any given arterial concentration the cerebral arteriovenous difference of acetoacetate was significantly higher in infant than adult rats. The same was true for D-beta-hydroxybutyrate at arterial concentrations above 1 mmol/liter. There was an approximately linear relationship between arterial concentration of acetoacetate and its cerebral arteriovenous difference in both infant and adult rats. A similar relationship was found for D-beta-hydroxybutyrate only in infant animals. In the fed state, the cerebral uptake of glucose and ketone bodies (micromoles per (mg DNA X min)) was not different in infant and adult rats. During starvation, cerebral uptake of ketone bodies expressed as micromoles per (mg DNA X min) was higher in infant than adult rats, indicating a higher rate of utilization of ketone bodies per cell in these animals. For glucose, no such difference was found in either fed or starved groups (Table 3). The average percentage of the total cerebral uptake of substrates (micromoles per min) accounted for by ketone bodies increased in both infant and adult rats during starvation. This percentage value was clearly higher in infant than adult rats during starvation. After 72 hr of starvation the values were 38.8% and 15.2% in infant and adult rats, respectively (Fig. 3). Calculated cerebral metabolic rate for oxygen (CMRO2), assuming complete oxidation of glucose and ketone bodies and expressed as micromoles per (mg DNA X min), was similar in fed and starved rats of both age groups (Table 3), indicating that ketone bodies serve as an alternative substrate for glucose during starvation. Calculated CMRO2 for glucose plus ketone bodies was similar to the measured CMRO2 in adult rats both in the fed and the starved groups. For infant rats, calculated CMRO2 for glucose plus ketone bodies was higher than measured CMRO2, indicating that in this age group a portion of substrate was used for synthesis or storage rather than for complete oxidation.
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PMID:The rate of cerebral utilization of glucose, ketone bodies, and oxygen: a comparative in vivo study of infant and adult rats. 98 May 50

The effect of 48-hour starvation on glucose metabolism was studied in six non-diabetic, normal weight men using a hyperinsulinemic (100 mU/min/m2) glucose clamp (3.5 mmol/L). The rate of glucose oxidation was calculated from measurements of respiratory gas exchange, after allowing for the oxidation of ketones and of protein. During the glucose clamp, the whole body glucose disposal rate decreased from 39.8 (SEM 4.6) mumol/kg/min in the fed state to 24.1 (2.1) mumol/kg/min in the starved state (P less than .01), consistent with insulin "resistance." The glucose oxidation rate decreased from 21.8 (1.3) to 3.9 (1.4) mumol/kg/min with starvation (P less than .001), but the nonoxidative glucose disposal rate was unchanged (18.0 [3.9] mumol/kg/min normally fed, and 20.2 [1.2] mumol/kg/min starved). With starvation, the rate of glucose uptake in the forearm during the glucose clamp was reduced from 59.4 to 15.4 mumol/min/L forearm (SE 5.6, P less than .01, ANOVA). There was a significant net increase in thermogenesis during the glucose clamp in the normally fed state (0.27 [0.08] kJ/min, P less than .01, ANOVA), but not following starvation (0.11 [0.09] kJ/min, NS, ANOVA). Therefore, starvation caused decreases in oxidative glucose disposal and in forearm glucose uptake; despite the whole body nonoxidative disposal rate of glucose being unchanged, the associated net thermogenic response was diminished.
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PMID:The effect of starvation on insulin-induced glucose disposal and thermogenesis in humans. 218 56

Urinary excretion of total carnitine in 48-h fasted rats dropped to 0.30 +/- 0.01 mumol/day from 2.23 +/- 0.4 mumol/day found in fed, control animals (mean +/- SEM). Despite this marked retention, the total carnitine content of the whole body remained constant, about 83 mumol, predicting a slow-down in biosynthesis. The conversion of butyrobetaine into carnitine takes place only in the liver in rats. 48 h of starvation caused a decrease in the liver butyrobetaine level from 11.6 +/- 1.19 nmol/g to 9.30 +/- 1.19 nmol/g, which in whole livers corresponds to a decrease from 138 nmol to 61.3 nmol. The conversion rate of butyrobetaine into carnitine was studied with radiolabelled butyrobetaine. 30 min after injection of [3H]butyrobetaine the carnitine pool in the liver of fasted rats was labelled to about the same extent as that in fed rats, but from a butyrobetaine pool with higher specific radioactivity. Therefore, the conversion rate of butyrobetaine into carnitine was reduced. The newly formed carnitine found in the whole body of fasted rats was estimated to be 59% of controls. We conclude that the biosynthesis of carnitine in fasted rats slows down, for which a decreased availability of butyrobetaine in the liver is responsible. Urinary excretion of butyrobetaine in the fasted group decreased to 74.1 nmol/day from the 222-nmol/day control value while the butyrobetaine content of whole body did not significantly decrease (2.85 mumol vs. 3.04 mumol). Urinary excretion of trimethyllysine was also depressed.
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PMID:Butyrobetaine availability in liver is a regulatory factor for carnitine biosynthesis in rat. Flux through butyrobetaine hydroxylase in fasting state. 251 27

Starvation for 24 h causes a striking fall in glutathione content from 3.19 +/- 0.27 to 1.88 +/- 0.14 (X +/- SEM) mumol/g tissue and of GGT activity from 31.75 +/- 4.17 to 19.49 +/- 3.13 (X +/- SEM) nmol/min/mg protein in the homogenate from whole mucosa of the upper small intestinal segments. This was associated with a significant increase in GSH-Px activity and the content of lipid peroxides (measured by the thiobarbituric assay). On semi-synthetic iron-supplemented diet the activities of GSH-T and GGT were significantly decreased as compared with crude diet. On semisynthetic iron-depleted diet GSH-T and GGT activities were further depressed, but this was accompanied with an additional depression of GSH, glutathione reductase (GSSG-R), and glutathione peroxidase (GSH-Px) activities and lipid peroxide concentrations. Food deprivation significantly lowers the mucosal GSH-content and could lead to a destabilization of this system presumably by increased oxidative stress. As compared to normal "crude" diet, semisynthetic diets and oral iron depletion have been shown to cause a depression of the intestinal GSH system. As a consequence of these effects, the resistance of the small intestinal mucosa toward exogeneous dietary toxins might be reduced.
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PMID:Glutathione and its related enzymes in the small intestinal mucosa of rats: effects of starvation and diet. 256 68

Ingestive behaviour of control and experimental rats following 96 hours of starvation was studied. The control animals were injected normal saline intraperitoneally (I.P.) whereas the experimental animals were injected I.P. with fresh plasma obtained from well fed rats. Having been presented with food 15 minutes after the injections, the food intake (Gms +/- SEM) of control animals for the first five hours after injection was 6.00 +/- 0.44, whereas, the intake in experimental animals for the same period was 0.55 +/- 0.05. The food intake was significantly suppressed for the next three days, attaining the normal values by the 4th day. Since all the rats were starved prior to injection, all of them increased in weight during the four days of study, but the increase seen in the experimental group was much subdued. Therefore the plasma factor, suppresses not only the food intake but also the gain in body weight.
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PMID:Ingestive behaviour of starved rats after single intraperitoneal injection of fresh plasma from well-fed rats. 262 Sep 71

Maintenance of vitamin A stores in the body is dependent on a number of basic metabolic processes. These processes, such as protein and carbohydrate metabolism, are disrupted in acute starvation, and, as a result, alterations in vitamin A status may result. We investigated this possibility in 8-week-old Sprague-Dawley male rats. The rats were starved for 24, 48, and 72 hr but had free access to water. At 24 hours of starvation, the plasma retinol concentration was depressed, but not significantly so. After 48 and 72 hours of starvation, however, the plasma retinol concentration decreased to less than half of the control values (61 +/- 4 vs 124 +/- 12 nmol/dl at 72 hours, mean +/- SEM, (p less than 0.005). The hepatic retinoid (retinyl esters + retinol) concentration (nmol/g liver) was increased at 24 and 48 hours of starvation compared to controls (p less than 0.05), and by 72 hours the concentration was 56% greater in starved rats than in fed controls (p less than 0.001). The total hepatic retinoid content (mumol/total liver) was decreased moderately at all periods of starvation compared to controls (p less than 0.05). In both starved and fed animals, the total hepatic content per 100 g body weight, a measure of total vitamin A reserves, was statistically the same. These results demonstrate that acute starvation in rats alters the vitamin A equilibrium between the plasma and hepatic stores without affecting the overall vitamin A reserves.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of acute starvation on vitamin A status in rats. 262 Dec 99

1. The effects of acute alterations in energy intake on the thermoregulatory responses to a cooling stimulus were studied in healthy, normal weight, young female subjects. On separate occasions, seven subjects were underfed for 7 days at 60 kJ day-1 kg-1 ideal body weight and six subjects were starved for 48 h. The cooling stimulus was provided by a coverall perfused with water at 16 degrees C. 2. After the application of the cooling stimulus, central body (auditory canal) temperature rose initially in both studies. After underfeeding, the magnitude of this rise in temperature was not significantly different from that seen in the normally fed state. After 48 h starvation, the rise in temperature on cooling was reduced from 0.30 (SEM 0.03) to 0.10 (0.04) degrees C (P less than 0.01). In two subjects in whom central body temperature had been maintained in the normally fed state, a fall occurred after starvation. 3. Underfeeding for 7 days did not affect thermogenesis or the degree of vasoconstriction in the forearm or hand in response to cooling. 4. After 48 h starvation, the thermogenic response to cooling was abolished and blood flow in the forearm remained higher than in the normally fed state. 5. In normal weight young females, thermoregulatory responses to a cooling stimulus were therefore substantially affected by 48 h starvation but not by 7 days underfeeding.
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PMID:Effects of underfeeding and of starvation on thermoregulatory responses to cooling in women. 280 91

Biliary cholesterol saturation indices (SI's) were measured in fasting duodenal bile from (i) obese and non-obese individuals with and without cholesterol gallstones, (ii) obese individuals undergoing weight reduction and (iii) obese gallstone patients receiving chenodeoxycholic acid (CDCA) therapy. Biliary lipid secretion rates were also measured in three obese subjects before and during 11 days starvation. The mean SI in fifteen non-obese controls (0.89 +/- SEM 0.06) was significantly lower than that in the twenty-four obese without (1.14 +/- 0.07; P less than 0.01), and in the twenty-nine non-obese with gallstones (1.30 +/- 0.05; P less than 0.001) while in sixteen obese gallstone patients, the mean SI of 1.55 +/- 0.06 was significantly higher than that seen in the other three groups (P less than 0.01-0.001). Although fifteen obese subjects lost 15% of their initial body weight during dieting, this did not change their SI's consistently. However in three obese individuals, total starvation did reduce the SI's and significantly lowered the biliary cholesterol secretion rate. Ten obese gallstone patients responded to 15.8 +/- 0.3 mg CDCA kg-1 day-1 by developing unsaturated fasting duodenal bile (SI 0.89 +/- 0.04). A further increase in CDCA dose to 19.0 +/- 0.7 mg kg-1 day-1, as a result of reducing body weight, was more effective in lowering SI's (0.75 +/- 0.06, range 0.51-1.0) than that achieved by increasing the dose to 18.9 +/- 0.46 mg kg-1 day-1 through more capsules per day (SI 0.89 +/- 0.03, range 0.67-1.25). These studies show that (i) biliary cholesterol SI's are greater when obesity and gallstones occur together than in either obesity or gallstones alone, and (ii) although weight loss in obese individuals does not consistently alter biliary cholesterol SI's, it may be beneficial in obese patients receiving CDCA therapy for gallstone dissolution.
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PMID:Effect of obesity and weight reduction on biliary cholesterol saturation and the response to chenodeoxycholic acid. 308 8

Brief starvation is accompanied by decreased circulating levels of most amino acids, which has been attributed to an increased splanchnic uptake of amino acids, primarily alanine, for gluconeogenesis. However, quantitative data on splanchnic exchange of amino acids and gluconeogenic precursors is lacking. Consequently, arterial concentrations and splanchnic exchange of whole blood amino acids, ketone bodies, glucose, and gluconeogenic precursors were measured in 16 prolonged fasted (60 to 64 hours) and 15 overnight fasted (12 to 14 hours) healthy, nonobese subjects. After the 60-hour fast net splanchnic glucose production decreased by 41% to 0.31 +/- 0.02 mumol/L (P less than .001), whereas the splanchnic uptake of gluconeogenic precursors increased and could account for the total glucose output. Net splanchnic uptake of taurine, threonine, serine, glycine, lysine, histidine, and arginine rose significantly in response to fasting (P less than .05 to .01) due to increased splanchnic fractional extraction. Although the splanchnic fractional extraction of alanine was augmented by 40% (P less than .001), net splanchnic uptake was not influenced by fasting. Total net splanchnic uptake of amino acids increased by 68%, from 231 +/- 44 mumol/min in the postabsorptive state to 388 +/- 63 mumol/min (mean +/- SEM) (P less than .05) in the 60-hour fasted state. However, only one half of this rise was accounted for by gluconeogenic amino acids.
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PMID:Splanchnic metabolism of amino acids in healthy subjects: effect of 60 hours of fasting. 319 1


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