Hours Of Food Deprivation Research Articles

Overeating by Young Obesity‐prone and Lean Rats Caused by Tastes Associated With Low Energy Foods

Childhood obesity is a prominent health problem that may involve early learning about tastes and the energy content of foods. We tested the hypothesis that food tastes predictive of low energy content cause overeating in young animals. Juvenile and adolescent (4- and 8-week-old) male JCR:LA-cp lean (+/cp or +/+) and obesity-prone (cp/cp) rats were given sweet (saccharin) and salty (sodium chloride) gelatin cubes made with starch (high caloric) or no starch (low caloric) for 16 days of taste conditioning. After 10 hours of food deprivation, rats received pre-meals with flavors that had been paired or unpaired with high caloric content during taste conditioning, followed immediately by measurement of chow intake at regular meals. Our findings show that both lean (+/cp) and obesity-prone (cp/cp) juvenile rats ate more regular chow after a pre-meal with a flavor associated with low caloric value than after a similar pre-meal with a flavor predictive of high caloric content. This effect occurred with juvenile rats but not with adolescents. Data from our study indicate that the subversion of the relationship between taste and caloric content disrupts the normal physiological and behavioral energy balance of juvenile rats, resulting in overeating that is independent of genetic disposition for obesity.

Food deprivation induces adipose plasminogen activator inhibitor-1 (PAI-1) expression without accumulation of plasma PAI-1 in genetically obese and diabetic db/db mice

Relationships between energy intake and fibrinolytic functions have been documented in detail. We evaluated food deprivation (FD) as a means of modulating fibrinolytic activity in genetically obese and diabetic db/db mice and in their lean counterparts. Twelve hours of FD induced considerable gene expression of plasminogen activator inhibitor-1 (PAI-1) in both epididymal (3.8-fold, p < 0.05) and intestinal (2.4-fold, p < 0.05) adipose tissues without affecting plasma PAI-1 levels in db/db mice, whereas the FD did not affect these parameters in wild-type mice. Importantly, 24 hours of FD increased the plasma PAI-1 content in wild-type (1.9-fold, p < 0.01) but not in db/db mice, although adipose PAI-1 mRNA levels were significantly increased in db/db mice. The plasma PAI-1 content significantly correlated with hepatic PAI-1 mRNA levels in wild-type (r = 0.84, p < 0.01) and in db/db (r = 0.63, p < 0.01) mice. However, plasma PAI-1 did not correlate with adipose PAI-1 expression in db/db mice, although adipose tissue in general is thought to be the principal site of PAI-1 production in obesity. Hepatic PAI-1 expression was closely correlated with serum levels of free fatty acids in wild-type (r = 0.72, p < 0.01), but not in db/db mice. Adipose PAI-1 expression significantly correlated with serum corticosterone levels in both genotypes (wild-type, r = 0.52, p < 0.05; db/db, r = 0.51, p < 0.01), suggesting that adipose PAI-1 expression is up-regulated by fasting-induced glucocorticoids. The present findings suggested that fasting differentially affects fibrinolytic activity in obese and lean subjects and that PAI-1 expression in the liver as well as in adipose tissues comprises an important determinant of increased risk for cardiovascular disease in obesity.

Flavour-specific anticipatory hunger reinforced by either carbohydrate or protein

Recent evidence indicates that rats can learn to avoid aversive consequences of several hours of food deprivation by eating more of food having orosensory characteristics that predict a protracted fast. Two new studies tested if macronutrient composition of a flavoured meal before the reinforcing fast influences this acquisition of anticipatory hunger/satiety in a smooth-brained mammal. In one study, female Sprague-Dawley rats were trained for 11 cycles of 4 days with experimental meals of either carbohydrate or protein flavoured with either grape or cherry, with one odour followed by a 3-h fast and the other by 10 h of food deprivation. Both nutrient groups acquired anticipatory hunger. Then that learnt increase in meal size started to extinguish the hunger-avoidance response to the longer fast. The other study tested if this finding extended to experimental meals that combined carbohydrate and protein, and had vanilla or chicken flavours, to fasts of 4 and 12 h and to male rats as well as females within a training period of 6 cycles of 4 days. Evidence of anticipatory hunger early in training was clear only in the males. The combined results from the two experiments indicate that either carbohydrate or protein is sufficient for negative reinforcement of flavour-specific anticipatory hunger when the shorter fast lasts for 3 h. This food-discriminative anticipatory adjustment of meal size could be an automatically learnt part of hunger management for socially scheduled eating in human beings.

Linkage of Neuron Spike Activity in the Right and Left Amygdala in Food Motivation and Emotional Tension

Cross-correlation histograms were plotted to study the linkage of spike activity in simultaneously recorded neurons in the central nucleus of the right and left amygdala in rabbits in calm waking, after 24 hours of food deprivation, in satiation, and in emotional tension (on presentation of dogs). Histograms showed peaks displaced from zero in 50-67% of cases. In hunger, many cases (52%) showed pairs in which the first neuron to discharge was in the left amygdala, this being followed by a neuron in the right amygdala (peaks from 10-50 and 130-150 msec). Firing in the opposite order was seen more rarely (36%). On presentation of dogs, there was an increase in the number of cases showing a common input to neurons, along with an increase in the leading role of neurons in the right amygdala (57%), due to increases in inhibitory influences from this area on cells in the left amygdala. The interaction of amygdalar neurons in these states was in most cases at frequencies in the delta range (74%), mainly at 2-4 Hz.

Nutrition and hypothalamic neuropeptides in sheep: histochemical studies.

The identification and role of neuropeptides in the control of food intake and energy balance have been extensively studied in rodents, and for more than ten years, similar studies have been performed in sheep. As a photoperiodic ruminant, sheep are an interesting alternative animal model to rodents. In this review, we summarize the results obtained in sheep concerning the distribution of peptide-containing neurones in the hypothalamus and their central role in the control of food intake and energy balance, and compared them with relevant data from rodents. Even if the general organization and the role of hypothalamic neuropeptides are similar in sheep and rodents, numerous differences have been observed between these two species. In sheep, the magnocellular neurones of the paraventricular and supraoptic nuclei are characterized by the low density and the lack of galanin- and neuropeptide-Y-containing neurones, respectively. The sheep pituitary stalk presents neurones containing neuropeptides such as neuropeptide-Y or beta-endorphin, which are also found in the deep part of the infundibular nucleus. In this structure, several neuronal populations, including galanin, agouti-gene related peptide, somatostatin, are sensitive to energy balance variations, undernutrition or overfeeding, which may specifically modify neuropeptide levels in discrete neuronal subgroups. This feature is well illustrated by the number of neuropeptide-Y labelled neurones, that increases in the lateral part of the infundibular nucleus of undernourished ewes and decreases in the ventral part of overfed ewes. Conversely, after 24 hours of food deprivation, the number of neuropeptide-Y-immunolabelled neurones is unchanged in the sheep infundibular nucleus, whereas increased levels of this neuropeptide are described, in rats, by radioimmuno-assay. In conclusion, our review shows that peptide-containing neurone systems, involved in the regulation of food intake and energy balance in sheep, are generally similar to those observed in other species, but they present specific differences according to the physiological characteristics of the animal model.

Vasopressin-independent regulation of collecting duct aquaporin-2 in food deprivation

Humans and animals are frequently subjected to food deprivation or starvation. However, the adaptation of the kidney to this condition is not well understood. The purpose of these studies was to examine the effects of food deprivation on water handling by the kidney, the expression levels of collecting duct (CD) water channel aquaporin-2 (AQP2), and to determine the role of vasopressin in the adaptation of AQP2 to food deprivation. Sprague-Dawley (SD) and Brattleboro rats were placed in metabolic cages and deprived of food but had free access to water for 72 hours. Water balance and urine osmolality were measured daily. Kidney tissues were isolated and examined for the expression of AQP2 using semiquantitative immunoblotting and Northern hybridization. The circulating level of vasopressin and the mRNA expression levels of its precursor were determined by radioimmunoassay and Northern hybridization, respectively. In SD rats, the first 24 hours of food deprivation is associated with a significant polyuria and decreased urine osmolality (Uosm). This correlated with a significant down-regulation of AQP2 in the cortex and outer medulla. After 72 hours of food deprivation, Uosm increased above baseline, and urine volume dropped to a lower value. This was associated with a rebound increase in AQP2 expression in the cortex and OM and its up-regulation in the inner medulla. Interestingly, vasopressin mRNA expression and plasma levels were unchanged during food deprivation. Further, in homozygous Brattleboro rats, in which endogenous vasopressin is absent, food deprivation caused changes in urine volume, urine osmolality, and AQP2 expression, which are qualitatively similar to those observed in normal rats. Food deprivation impairs water handling by the kidney by causing dual changes in urine volume and urine osmolality. This effect is associated with parallel alterations in the expression of AQP2 and is independent of vasopressin activity. It is concluded that the increase in water reabsorption in the CD is an adaptive response of the kidney to a long period of food deprivation and is mediated via a vasopressin-independent mechanism.

Activation of the central nervous system in obese Zucker rats during food deprivation

This study was carried out to investigate the pattern of neuronal activations that occur in the obese fa/fa Zucker rat during food deprivation. The functional activation of neurons was estimated in lean and obese Zucker rats either fed ad libitum or food-deprived for 3, 6, 12, and 24 hours by assessing the expression of the immediate early gene c-fos. To identify the neurons instigating the activation of the hypothalamic-pituitary-adrenal axis in food-deprived obese rats, the retrograde tracer cholera toxin B subunit was injected in the parvocellular division of the paraventricular hypothalamic nucleus of obese rats and colocalized with c-fos mRNA during food deprivation. The expression of c-fos was barely detectable in food-deprived lean rats as well as in lean and obese animals fed ad libitum. However, 3 hours of food deprivation were sufficient to significantly induce c-fos in the paraventricular thalamic nucleus of obese rats. In addition, 6 and 12 hours of food deprivation resulted in the activation of regions that are similarly stimulated in "neurogenic" stresses. These regions include the parvocellular division of the paraventricular hypothalamic nucleus, the lateral septum, the basolateral amygdala, and some areas of the cortex. The highest number of neurons projecting to the parvocellular division of the paraventricular hypothalamic nucleus and revealing c-fos mRNA was, however, located in the paraventricular thalamic nucleus. In summary, the present results demonstrate in the obese fa/fa Zucker rats, that food deprivation leads to brain activations, which are in large part, similar to those induced by a "neurogenic" stress and that the paraventricular thalamic nucleus is involved in this response. These changes could contribute to the development of hyperphagia and obesity.

Determining the Value of Social Companionship to Captive Tufted Capuchin Monkeys (Cebus apella)

This study used a method similar to one introduced by Dawkins in 1990 to assess the magnitude of the psychological need for social companionship in pair-housed tufted capuchin monkeys (Cebus apella). This method permits classification of commodities as necessities or luxuries. The study directly compared the commodity of social companionship to the commodity of food, a known physiological necessity, in a series of preference tests following commodity deprivations. The majority of subjects chose their social companion over food at baseline and persisted in this preference even after several hours of food deprivation. In addition, subjects' preferences shifted from 1 commodity to the other with manipulation of social and food deprivation levels. Capuchin monkeys perceived social companionship as a necessity at a level similar to that of food.

Acute Elevation by Short-Term Dietary Restriction or Food Deprivation of Type I I-Compound Levels in Rat Liver DNA

Type I I-compounds are bulky endogenous DNA modifications detectable by 32P postlabeling that exhibit age, species, tissue, genotype, gender, and diet dependence. Their formation appears unrelated to oxidative stress. In fact, several lines of indirect evidence suggest that many type I I-compounds may represent normal functional DNA modifications. For example, long-term dietary restriction (DR), which retards the development of age-related diseases including cancer and extends median and maximum life spans, unexpectedly elicits significant increases rather than decreases in the levels of many I-compounds in different rodent tissues. Positive linear correlations have been observed between such levels and median life spans of the animals. In the present work we have investigated 1) whether elevation of I-compound levels does not depend on chronic DR, i.e., occurs after a short period of DR or fasting, and 2) whether I-compound levels return to control values after the animals are returned to unrestricted feeding after food deprivation. Female Fischer 344 rats (approx 140 g each) were randomized into three groups. Group 1 was fed a natural ingredient (Purina 5001) diet ad libitum (AL) throughout the study, Group 2 was switched to 60% of the AL amount (40% DR) at 0 hour, and Group 3 was given no food for up to 72 hours and then returned to AL feeding until the end of the experiment. Liver DNA of individual rats (n = 4) was isolated for I-compound analysis at 24, 72, and 240 hours. Restricted and food-deprived rats showed elevated levels of hepatic I-compounds, with fasting eliciting the highest levels. These effects were seen as early as the 24-hour time point. Refeeding after 72 hours of food deprivation restored the levels to control values, measured at 240 hours. Our observations are discussed in relation to carcinogenesis and tumor promotion. The almost instantaneous changes of endogenous DNA modifications showed their exquisite sensitivity to nutritional factors and provided strong new evidence for precise regulation of their formation and removal.

Can a glutamate-enriched diet counteract glutamine depletion in endotoxemic rats?

The study evaluated whether a glutamate-enriched diet would restore glutamine tissue pools and maintain tissue trophicity in endotoxemic rats. For this purpose, young male Sprague-Dawley rats received an intraperitoneal injection of lipopolysaccharide (LPS) from Escherichia coli at 3 mg/kg body weight. After 24 hours of food deprivation, the rats were enterally refed for 48 hours using Osmolite® enriched with glutamate at 4 g/kg/d (LPS-Glu group, n = 7) or glycine isonitrogenous to glutamate (LPS-Gly group, n = 7). A control group (healthy group, n = 7) had free access to a standard rodent diet. Tissue weights and protein contents were significantly lower in both LPS-treated groups than in the healthy group. No plasma or tissue accumulation of glutamate was observed except in the liver. Glutamine concentrations were increased in the jejunum, liver, and plasma in the LPS-Glu group versus the other two groups ( P < 0.05). Conversely, they were depleted in muscles of the endotoxemic groups versus the healthy group ( P < 0.05). Villus height was significantly greater in the LPS-Glu group than in the LPS-Gly group in the jejunum ( P < 0.05), but not in the ileum. In conclusion, a glutamate-enriched diet administered enterally to endotoxemic rats can counteract glutamine depletion in the splanchnic area but not in muscles. In addition, glutamate displayed a trophic effect restricted to the jejunum.

Miglitol (BAY m 1099) treatment of diabetic hypothalamic-dietary obese rats improves islet response to glucose.

The well-absorbed alpha-glucosidase inhibitor, miglitol (BAY m 1099), was included in the diets of hypothalamic-dietary obese diabetic rats to investigate its ability to improve glycemia and thereby reverse glucotoxic effects on islet secretory response. Female rats received bilateral electrolytic lesions of the ventromedial hypothalamus and were fed high-fat, sucrose-supplemented diets until hyperinsulinemia and hyperglycemia were observed after 3 hours of food deprivation (nonfed). Diabetic animals were assigned to miglitol-treated (40 mg/100 g of diet) or untreated groups for 3 weeks; pancreatic islets were isolated for incubation experiments. No differences in food intake, body weights, or nonfed plasma glucose or insulin levels were seen between treated and untreated diabetic rats. Islets isolated from untreated diabetic rats showed elevated basal insulin release and no insulin secretory response to an elevation in glucose concentration. In contrast, islets obtained from miglitol-treated rats showed more normal basal release and a significant insulin secretory response to glucose. Incubation of islets, obtained from normal control rats or untreated diabetic rats, in media containing miglitol at levels estimated to exist in plasma of treated rats had no effect on islet insulin secretory responses to glucose. Islet secretory response was improved despite continued hyperglycemia and severe insulin resistance. Miglitol treatment may improve islet sensitivity to glucose either through effects on islet metabolism requiring prolonged exposure or by improvement in postmeal glycemia, despite persistent hyperglycemia.

Manipulations of metabolic fuel availability alter estrous behavior and neural estrogen receptor immunoreactivity in Syrian hamsters.

Decreases in metabolic fuel utilization caused by food deprivation, diabetes, or treatment with metabolic inhibitors have been shown to suppress steroid-induced estrous behavior in ovariectomized Syrian hamsters. These same manipulations also caused a decrease in the number of detectable estrogen-receptor immunoreactive (ERIR) cells in the ventromedial hypothalamus (VMH) and the adjacent area lateral to it (VLH) in ovariectomized hamsters. Forty-eight hours of food deprivation or treatment with pharmacological blockers of glycolysis (2-deoxy-D-glucose) and fatty acid oxidation (methyl palmoxirate) decreased the number of detectable ERIR cells in the VMH/VLH. However, neither inhibitor given alone was sufficient to affect the number of detectable ERIR cells in the VMH/VLH, even when given in much higher doses. Therefore, the number of ERIR cells in the VMH/VLH, like steroid-induced estrous behavior, responds only to a combination of glucoprivation and lipoprivation and not to either alone. The effects of metabolic fuel restriction are not due to a general suppression of neural ERIR, because food deprivation or treatment with 2-deoxy-D-glucose and methyl palmoxirate actually increased the number of detectable ERIR cells in the medial preoptic area (mPOA) and had no effect in the nucleus of the solitary tract. Lesions destroying the area postrema (AP) prevented the decrease in ERIR cells in the VMH/VLH and the inhibition of estrous behavior caused by fuel restriction. However, AP lesions did not alter the effects of metabolic inhibitors on ERIR in the mPOA. On the other hand, subdiaphragmatic vagotomy abolished the effects of metabolic inhibitors on mPOA ERIR, but did not affect either lordosis or VMH/VLH ERIR. These results suggest that the suppression of estrous behavior induced by metabolic fuel restriction is at least in part due to a decrease in the number of ERIR neurons in the VMH/VLH. In addition, the estrogen-sensitive neurons in the VMH/VLH and mPOA receive metabolic cues via different neural pathways. The AP, but not vagus nerves, is required for ERIR neurons in the VMH/VLH to detect fuel availability; the vagus nerves, but not the AP, are necessary for estrogen-binding neurons in the mPOA to detect visceral information.

Concentrations of amino acids in plasma and whole blood in response to food deprivation and refeeding in healthy two-day-old foals

Summary Concentrations of amino acids in plasma and whole blood in response to 10 hours of food deprivation were determined in healthy 2-day-old foals (n = 8) and were compared with control values in foals of the same age (n = 8) allowed free access to suckle. In addition, response of concentrations of amino acids in plasma to 15 minutes of free-access suckling was determined at the end of the 10-hour period in both groups. Response of 13 amino acids in plasma of food-deprived foals was significantly (P &lt; 0.05) different, compared with that in control foals. Concentrations of 3 amino acids (alanine, glycine, and phenylalanine) in plasma increased significantly (P &lt; 0.05), whereas concentrations of 7 amino acids (asparagine, citrulline, histidine, ornithine, proline, tryptophan, and tyrosine) in plasma decreased significantly (P &lt; 0.05) during food deprivation. Response of concentrations of 2 amino acids (glycine and histidine) in whole blood was significantly (P &lt; 0.05) different from that in plasma of food-deprived vs control foals. Refeeding of food-deprived foals resulted in significantly (P &lt; 0.05) different responses for concentrations of all but 2 amino acids (cystine and taurine) in plasma, compared with responses in controls. Changes in concentrations of amino acids in plasma and whole blood of foals in response to food deprivation are similar to those in foals with septicemia and in children with grade 1 or 2 kwashiorkor. The significantly different response of food-deprived foals to refeeding may be attributable to increased protein intake or altered physiologic state.

Kinetic analysis of D-xylose absorption after its intragastric administration to mares deprived of food

Summary Multicompartmental analysis was applied to study the kinetics of D-xylose distribution after its intragastric administration to healthy mares deprived of food for 12, 36, 72, and 96 hours. Disposition of D-xylose was described by a 5-compartment model. Maximal plasma D-xylose concentration was similar for 12 and 36 hours of food deprivation and was greater (P = 0.0001) than the values for 72 and 96 hours. Peak concentration of D-xylose appeared progressively later as food deprivation proceeded (P = 0.0001). Fractional rate of transfer (k1,6) was less after 96 hours of food deprivation, compared with 12 hours (P = 0.0001), and percentage of D-xylose absorbed was reduced (P = 0.0441) after food deprivation. Fractional rate of transfer (k6,5), representing gastric emptying, tended to progressively decrease with food deprivation. Results indicated that formal kinetic analysis can be applied to D-xylose absorption kinetics in horses. Reduction in the extent of D-xylose absorption after food deprivation may be partly caused by decreased rate of D-xylose absorption across the small intestinal mucosa, but other factors, such as gastric emptying and nonabsorptive losses, may also be involved.

Physiological responses to social status and housing conditions in male mice subject to food competition tests

Abstract Seventy eight male mice were individually housed at weaning. After 14 days of isolation, the males were allocated to 13 permanent groups of three mice (Triads), 13 permanent groups of two mice (Couples) and 13 mice remaining in isolation for 21 days. Four 10‐min observation periods, each preceded by 24 hours of food deprivation, were carried out in a neutral cage. In one of the shorter walls of this cage a plastic tube was connected to the cage. A pellet of food was firmly attached to the inner surface of the tube and the behaviour of the mice was recorded on a videotape. Twenty‐four hours after finishing the last observation, the mice were killed and selected organs cleaned and weighed. Relative organ weight differences between dominant and subordinate males showed similar tendencies in both Triads and Couples. Dominants had heavier testes, thymuses, intact and squeezed seminal vesicles, squeezed preputial and prostates and lighter adrenals than subordinates. However, Triads and Couples showed d...

Effect of food deprivation and refeeding on rat organ temperatures.

Small thermocouple sensors were surgically implanted in the liver, kidney, hind leg muscle, interscapular brown adipose tissue, small and large intestines, dorso-lumbar internal side of the skin, periovaric adipose tissue and the lower aorta of Wistar rats. The aortic temperature was taken as core temperature. The sensors allowed continuous long-term monitoring of the temperatures of these organs. A period of 18 hours of food deprivation resulted in an overall decrease of mean core and organ temperature, brown adipose tissue temperature dropping to values lower than those of the aorta in the fed state. Liver, kidney and small intestine maintained higher temperatures than the aorta both in fed and starved states. Refeeding overshot the core temperature with increases in most organs versus both the fed and food-deprived situations. The results are concordant with an active role of brown adipose tissue in dietary induced thermogenesis. Three days of food deprivation did not alter the basic circadian rhythm of core temperatures in the rat kept at 22 degrees C, whereas it did modulate both nightly maximum and diurnal minimum temperatures to much lower settings than either in the fed or refed situations. The rat adapts to starvation by decreasing core and organ temperatures and widening the amplitude of the daily temperature cycle.

Effects of a 24‐hour fast on cigarette smoking in humans

The effects of 24 hours of food deprivation on cigarette consumption, smoke exposure and mood were studied in seven research volunteers. A within-subjects design was used in which subjects smoked low-yield (0.1 mg nicotine) and high-yield (0.7-1.1 mg nicotine) cigarettes in both a fed and a fasting state. Each of the four experimental conditions--FED/LOW-YIELD, FED/HIGH-YIELD, FAST/LOW-YIELD, FAST/HIGH-YIELD--was enacted twice according to a randomized block design. Cigarette consumption was measured during the 24-h period before experimental sessions. The session included a 60-min smoking period, in which number of puffs per cigarette, number of cigarettes smoked, carbon monoxide (CO) exposure and mood were assessed. Although cigarette consumption during the 24 h prior to sessions did not vary as a function of feeding condition, CO levels at the end of this 24-h time period were slightly, but significantly, higher in the FAST condition (mean CO level: 30.3 ppm) than in the FED condition (mean CO level: 28.1 ppm). During the laboratory session, amount of smoking and CO exposure were similar across feeding conditions. Interactions between feeding condition and dose were obtained on several mood measures that reflected sedation and arousal: in the high-yield condition, subjects were more sedated after fasting, whereas in the low-yield condition, they reported being less sedated after fasting. We conclude that fasting does not alter cigarette consumption but may increase smoke exposure during ad libitum smoking, perhaps via a change in some aspect of smoking behaviour not measured in the present study (e.g. puff volume).

Comparison of anorectic drugs in rats trained to discriminate between satiation and deprivation

Eight male rats were trained to discriminate between the internal states produced by food deprivation of 3 hours (satiation) and that produced by food deprivation of 27 hours duration (deprivation). One lever, in a two-lever operant chamber, had to be pressed to receive reinforcement in the satiation state, whereas pressing the other lever was required when the rat was in the deprivation state. Once the rats were trained, increasing the number of hours of food deprivation, from 1 to 48 hours, resulted in more deprivation-appropriate lever responses in the two-lever operant task. Administration of doses of fenfluramine (0.5–1.5 mg.kg), its active metabolite norfenfluramine (0.25–1.0 mg/kg) or d -amphetamine (0.5–1.5 mg/kg) produced a dose-responsive decrease in deprivation-appropriate responses when each drug/dose was injected (i.p.) 15 min prior to deprivation (27 hours) testing. Norfenfluramine was 1.5 times more potent than fenfluramine which was 1.5 times more potent than amphetamine.

Effects of food deprivation on subjective responses to d-amphetamine in humans

The effects of 24 hours of food deprivation on the subjective response to 10 mg oral d-amphetamine were studied in 12 healthy normal volunteers. A within-subjects design was used in which subjects ingested amphetamine and placebo capsules in both a fed and a fasting state. Each of the four experimental conditions—FED/DRUG, FED/PLACEBO, FAST/DRUG, FAST/PLACEBO—was enacted twice according to a randomized block design. Three subjective effects questionnaires, the Profile of Mood States, the Addiction Research Center Inventory, and the Visual Analogue Scale, were completed prior to and 1, 3 and 6 hr after the early morning capsule ingestion. Typical elevations in such subjective effects as elation and vigor were obtained after amphetamine ingestion in both feeding conditions, but fasting neither potentiated nor attenuated the drug response. Subjects at the end of the session, however, were more likely in the FAST/DRUG condition than in the FED/DRUG condition to label the capsule they had ingested at the beginning of the session as a stimulant.

A water deprivation test for the differentiation of polyuric disorders in birds

A water deprivation test was developed for the differentiation of polyuric disorders in birds using the racing pigeon as a model. For a period of 3 days of food and water deprivation, urine and plasma osmolalities and body weight of 40 clinically healthy racing pigeons were monitored. Reference values for urine osmolality after 40 hours of food deprivation were 79 to 480 mOsmol/kg. After 64 hours of food deprivation and 24 hours of water deprivation these values were 450 to 875 mOsmol/kg. No significant rise in urine osmolality was seen after the first 24 hours of water deprivation. It is concluded that an urine osmolality greater than 450 mOsmol/kg is indicative of a normal concentrating capacity of the kidney in the pigeon. Data from the literature suggest that these values can be applied to other avian species.