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At least 19 recordsLinked to original sources
PubMed1991

Inhibition of hypothalamic thyrotropin-releasing hormone messenger ribonucleic acid during food deprivation.

Food deprivation in laboratory rats induces profound changes in the neuroendocrine system. We have investigated the hypothalamic and pituitary responses of the hypothalamo-pituitary thyroid axis to 48-h food deprivation in Sprague-Dawley rats. Peripheral T3 and hypophysial portal TRH were measured by RIA, and TSH beta, PRL, and pro-TRH mRNA were measured using in situ hybridization histochemistry. Peripheral total T3 was greatly reduced in food-deprived rats. Hypothalamic portal blood TRH levels declined significantly with time in control animals. The initial level of TRH in the portal blood of food-deprived rats was significantly reduced compared to that in controls, but did not fall further with time. In situ hybridization histochemistry revealed significantly lower pro-TRH mRNA in the paraventricular nucleus of food-deprived animals, while pro-TRH mRNA in the reticular nucleus remained unaltered. Furthermore, in the anterior pituitary, TSH beta mRNA decreased significantly in food-deprived animals, while PRL mRNA was unaltered. We conclude that the reduction in circulating T3 after food deprivation appears to be due primarily to decreased hypothalamic TRH synthesis and release.

Animals↗
PubMed1996

Relationships of consumer characteristics and food deprivation to food purchasing behavior.

A large part of domestic food intake may be determined by retail food purchase behavior, and it is commonly believed that this may be significantly influenced by the shopper's state of food deprivation. In the present study, 198 subjects recruited just prior to shopping at a large supermarket completed questionnaires eliciting information on demographic and situational variables, along with measures of time since last eating (TSLE), hunger, and dietary restraint. Upon leaving the store, subjects provided investigators with itemized receipts, having first identified all "unintended" purchases. There were no consistent main effects of TSLE, self-reported hunger, dietary restraint scores, or relative body weight on the number or cost of total, intended, and unintended food and nonfood purchases. However, there were significant interactions of weight status and measures of food deprivation upon measures of food purchasing. Although normal-weight subjects tended to increase their food purchases with food deprivation, the number and cost of food items fell markedly with extended food deprivation among overweight subjects. These effects were largely specific to food (i.e., generally not observed for nonfood purchases), but showed no consistent associations with unintended purchases or with particular foods or food groups. Higher dietary restraint and relative body weight were associated with lower reported hunger ratings, but not differences in mean TSLE, or other subject characteristics. These results run directly counter to common beliefs and recommendations for weight control and dieting, but support earlier work indicating that the food purchasing behaviors of normal-weight and overweight individuals are differently affected by food deprivation.

Adult↗
PubMed2001

A behavioral characterization of the effects of food deprivation on food and nonfood object interaction: an investigation of the information-gathering functions of exploratory behavior.

Previous research has shown that exploratory behavior serves not only to procure food, but also as a means of general information gathering. The purpose of this experiment was to investigate the function of exploratory behavior in rats by measuring behavior as they interacted with food and nonfood stimuli under different levels of food deprivation. Rats were food-deprived (0, 24, and 48 h), given free access to an open-field arena, and videotaped for a 20-min test session. The rats' behavior was assessed in a manner that isolated locomotor-, object-, and nonobject-related components. Deprivation did not affect locomotor activity levels; however, a decrease in rearing and propping against the test arena was shown. Rats distinguished between the food and nonfood objects because they attempted to ingest the food but not the nonfood object. Deprivation did result in increased contact with food objects; however, nonfood object interactions were maintained throughout the test session. These results suggest that exploratory behavior is separable from food seeking and functions in acquisition of information relating to multiple aspects of the environment.

Animals↗
PubMed1980

Naloxone reduces fluid intake: effects of water and food deprivation.

Food and fluid deprived and nondeprived male rats showed 36% and 46% decreases, respectively, in sucrose consumption 15-min after injection with 2 mg/kg of naloxone in one hr tests. The magnitude of this decrease was not correlated with an index of naloxone's ability to produce a sickness, as measured by the conditioned taste aversion test. Tests with animals scheduled to drink water in a 15-min daily session showed naloxone had similar effects in reducing water intake in 23-hr and 47-hr water deprived rats. Morphine, when self-administered, produced an increase in water intake during 6-hr sessions. The data support the idea that naloxone disrupts a component of normal regulation of ingestion.

Animals↗
PubMed2003

Acute food deprivation and chronic food restriction differentially affect hypothalamic NPY mRNA expression.

Although acute food deprivation and chronic food restriction both result in body weight loss, they produce different metabolic states. To evaluate how these two treatments affect hypothalamic peptide systems involved in energy homeostasis, we compared patterns of hypothalamic neuropeptide Y (NPY), agouti-related protein (AgRP), proopiomelanocotin (POMC), and leptin receptor gene expression in acutely food-deprived and chronically food-restricted rats. Both acute food deprivation and chronic food restriction reduced body weight and circulating leptin levels and resulted in increased arcuate NPY and decreased arcuate POMC gene expression. Arcuate AgRP mRNA levels were only elevated in acutely deprived rats. NPY gene expression was increased in the compact subregion of the dorsomedial hypothalamus (DMH) in response to chronic food restriction, but not in response to acute food deprivation. Leptin receptor expression was not affected by either treatment. Double in situ hybridization histochemistry revealed that, in contrast to the situation in the arcuate nucleus, NPY and leptin receptor mRNA-expressing neurons were not colocalized in the DMH. Together, these data suggest that arcuate and DMH NPY gene expression are differentially regulated. DMH NPY-expressing neurons do not appear to be under the direct control of leptin signaling.

Agouti-Related Protein↗
PubMed1982

Rapid acquisition of oral phencyclidine self-administration in food-deprived and food-satiated rhesus monkeys: concurrent phencyclidine and water choice.

Eight rhesus monkeys were trained to self-administer orally-delivered phencyclidine, with water concurrently available, under a fixed ratio (FR) schedule during daily 3-hr sessions. Liquid deliveries (0.55 ml) were contingent upon lip-contact responses on solenoid-operated drinking spouts. During the sessions, phencyclidine and water were available under FRs ranging from 1 to 16. Water was always available between sessions (FR 1), and food initially was available 24 hr/day. In Experiment 1 the monkeys initially were given access to water (FR 1) during the 3-hr sessions. Subsequently, phencyclidine (0.25 mg/ml) was substituted for water, and the monkeys were reduced to 85 percent of their free-feeding weights. The FR value was then increased from 1 to 8. Next, the monkeys received concurrent access to water from one spout and phencyclidine from the other (each under the FR 8 schedule), then the FR value was increased to 16 for both drug and water. Orally-delivered phencyclidine was rapidly demonstrated to function as a reinforcer (37.2 sessions) without using food to induce drinking. In Experiment 2 a similar procedure was used for another group of monkeys, except the monkeys remained food satiated throughout the acquisition phase. Phencyclidine was rapidly demonstrated to function as a reinforcer (25.9 sessions), although intakes were lower than in Experiment 1. After concurrent phencyclidine- and water-maintained performance stabilized at FR 16, the monkeys were food deprived, and phencyclidine intake increased to the levels reported in Experiment 1. Food deprivation greatly enhanced the reinforcing effect of phencyclidine and changed the temporal pattern of responding, but neither food deprivation nor food-induced drinking were necessary conditions to demonstrate the drug's reinforcing effects.

Animals↗
PubMed1995

Effects of neuropeptide Y, insulin, 2-deoxyglucose, and food deprivation on food-motivated behavior.

The current study demonstrates the ability of neuropeptide Y (NPY) to increase break points under a progressive ratio 1 (PR1) reinforcement schedule. An initial response resulted in delivery of a food reinforcer (45 mg pellet) under the PR1, and an additional response was required for each successive reinforcer. The break point, the number of responses emitted to obtain the last reinforcer, is considered a measure of reinforcing efficacy or motivational strength of the food reinforcer. NPY (0.3-10 micrograms) significantly increased break point to levels comparable to those produced by 36-48 h of food deprivation. Although insulin (3-8 U/kg) and 2-deoxyglucose (150-250 mg/kg) also increased food intake, neither increased break points to levels produced by NPY or food deprivation. These data suggest that NPY may change the value of food in ways that cannot be accounted for by changes in insulin, glucose levels or intracellular glucoprivation. These results emphasize that simply measuring the amount of freely available food eaten is not a fully adequate measure of the strength of the feeding behavior.

Animals↗
PubMed1983

The effects of food deprivation on beta-adrenergic responsiveness in male rats.

Male rats were deprived of food for varying lengths of time (0-96 h) and their responses to beta-adrenergic stimulation with isoproterenol were tested. Food deprivation for 48 or 96 h attenuated the increase in tail skin temperature normally seen following administration of isoproterenol. The degree of attenuation was dependent on the duration of the deprivation period. Rats deprived of food for 96 h and then refed for 48, 96, or 144 h showed a return of tail skin temperature response to near normal levels. The increase in heart rate observed following administration of isoproterenol was also attenuated following 48 or 96 h of food deprivation. Again, the degree of attenuation was dependent on the duration of the deprivation period. Food deprivation for 96 h led to a decrease in basal plasma levels of T3, T4, and glucose. The increase in plasma glucose following administration of isoproterenol was also attenuated following 96 h of food deprivation. In contrast to the thermal, cardiac, and glucose responses, the dipsogenic response to isoproterenol was increased following food deprivation. The attenuation in beta-adrenergic responses observed in the food-deprived rats might help explain the effects of food deprivation on cold tolerance.

Animals↗
PubMed1997

Food deprivation and food-delay effects on the development of adjunctive drinking.

Twelve rats were food-deprived to 90% or 70% of their free-feeding weights. Food pellets were then delivered every 60 s (Fixed Time 60-s schedule), and the development of adjunctive drinking was measured by the water consumed and the number of licks. For "master" rats, each lick was followed by 10-s delays in food delivery. Yoked control rats received food at the same time as their master rats and independently of their own behavior. At 70% deprivation, both master and control rats developed similar levels of schedule-induced licking, but the master rats drank less water. At 90% deprivation, master animals showed little drinking and licking, but the development of adjunctive drinking was not completely prevented. Drinking by yoked control rats did not differ as a function of deprivation level. In showing that lick-dependent delays in food delivery reduce the asymptotic development of adjunctive drinking as a function of the rats' level of food deprivation, these results support the view that environmental influences on schedule-induced drinking are modulated by motivational factors.

Animals↗
PubMed2001

Social dominance rank and accessory sex glands in wild adult male house mice born to food-deprived mothers.

Food deprivation after weaning often has greater effects on the reproduction of females than males. However, if animals are deprived prenatally (i.e., through deprivation of the mother during gestation), the reproduction of males may be more negatively impacted because it may decrease their ability to compete with other males and their attractiveness to females. We tested the predictions that adult sons of females that are food-deprived during gestation would tend to lose agonistic encounters with sons of well-nourished (control) females and would have smaller accessory sex glands as well. Sons of control mothers were more frequently dominant to sons of deprived mothers. They also had heavier vesicular-coagulating gland complexes and tended to have heavier preputial glands. However, among males that had not been tested for social dominance rank, there were no such differences in accessory gland weights. These data indicate that maternal food deprivation affects sons only if they engage in agonistic encounters. These effects may be due to a disruption of the organizational effects of testosterone that occur in neonatal male mice and they are likely to have a strong negative impact on the reproduction of the sons of deprived mothers.

Animals↗
PubMed1989

Evidence of increased gluconeogenesis during hemorrhage in fed and 24-hour food-deprived rats.

Food withdrawal 24 hr before hemorrhage has been shown to increase experimental post-hemorrhage mortality, and survival is associated with the degree of hyperglycemia. Lack of hyperglycemic response has been attributed to depleted glycogen reserves after 24-hr food withdrawal. To investigate the effect of short-term food deprivation on glucose metabolism during hemorrhagic stress, glucose production (rate of appearance, Ra), glucose uptake (rate of disappearance, Rd), glucose clearance, and glucose recycling were investigated in fed and 24-hr food-deprived rats under basal conditions, and during hemorrhagic hypotension using 3-H3-U-C14-glucose. During hemorrhage, blood glucose levels were higher in fed rats. Hemorrhage induced a decrease in glucose clearance irrespective of nutritional state in both 24-hr starved animals and rats in the postprandial state. Calculated glucose recycling increased in both groups after hemorrhage. The results indicate that hemorrhagic stress induces a rapid increase in gluconeogenesis, as reflected by increased glucose recycling.

Animals↗
PubMed2005

[Metabolic and endocrine effects of water and/or food deprivation in rats].

Metabolic and endocrine effects of water and/or food deprivation in rats. We aim at studying the effect of water deprivation, food deprivation and their combination for three days on adrenal cortex, pituitary-thyroid axis and vasopressinergic system activity in rats. Corticosterone level was determined by fluorimetric method. The levels of free thyroxine (FT4) and thyroid stimulating hormone (TSH) were determined by immunoenzymatic assay and vasopressin (AVP) level was determined by radio-immunoassay. In all three groups, basal levels of plasma corticosterone were increased. A thyroid dysfunction was shown after water deprivation, food deprivation and their combination reflected by a significant decrease in FT4 levels. Paradoxically, a significant decrease in TSH level was observed in food-deprived rats and in rats subjected to simultaneous food and water deprivation, while a slight and not significant decrease in TSH level was shown in water-deprived rats. A significant increase in plasma AVP level was observed after water deprivation and simultaneous water and food deprivation, while no change was found after food deprivation. The data indicated that water deprivation, food deprivation and their combination stimulated the adrenal cortex, thereby suggesting a stress state. On the other hand, it seems that nutritional stress modifies the pituitary-thyroid axis through mechanisms different from those of osmotic stress. Moreover, it seems that food deprivation partially prevented the stimulatory effect of water deprivation on vasopressinergic system.

Adrenal Cortex↗
PubMed1998

AP lesions block suppression of estrous behavior, but not estrous cyclicity, in food-deprived Syrian hamsters.

Food deprivation inhibits ovulatory cycles and estrous behavior in Syrian hamsters. Lesions of the area postrema (AP) prevented the suppression of estrous behavior in food-deprived hamsters, but they did not prevent the suppression of estrous cyclicity or the increase in running-wheel activity caused by food deprivation. Food deprivation or treatment with pharmacological inhibitors of glycolysis and fatty acid oxidation decreased estrogen-receptor immunoreactivity (ERIR) in the ventromedial hypothalamus (VMH), increased ERIR in the arcuate nucleus (Arc) and the posterior parvicellular paraventricular nucleus (PaPo), but had no effect on ERIR in the posterodorsal medial amygdala or the anterior parvicellular paraventricular nucleus. Lesions of the AP prevented the food deprivation-induced decrease in VMH ERIR and the increase in Arc ERIR, but they did not prevent the increase in ERIR in the PaPo. Thus, whatever physiological cues are produced by food deprivation, an intact AP is required for their transmission to the neural circuits controlling estrous behavior, VMH ERIR, and Arc ERIR. The AP is not essential for transmission of this information to the neural circuits controlling estrous cyclicity, running-wheel activity, or PaPo ERIR.

Amygdala↗
PubMedDate not supplied

Food deprivation and emotional reactions to food cues: implications for eating disorders.

Two studies examined emotional responding to food cues. In experiment 1, normal college students were assigned to 0-, 6- or 24-h of food deprivation prior to presentations of standard emotional and food-related pictures. Food deprivation had no impact on responses elicited by standard emotional pictures. However, subjective and psychophysiological reactions to food pictures were affected significantly by deprivation. Importantly, food-deprived subjects viewing food pictures showed an enhanced startle reflex and increased heart rate. Experiment 2 replicated the food deprivation effects from experiment 1, and examined participants reporting either a habitual pattern of restrained (anorexia-like) or binge (bulimia-like) eating. Food-deprived and binge eater groups showed startle potentiation to food cues, and rated these stimuli as more pleasant, relative to restrained eaters and control subjects. The results are interpreted from the perspective that startle modulation reflects activation of defensive or appetitive motivation. Implications of the data for understanding eating disorders are considered.

Adult↗