24-h Food Deprivation Research Articles

Angiotensin AT 1 and AT 2 receptors contribute to drinking elicited by eating in rats

A role for endogenous angiotensin II and its AT 1 and AT 2 receptor subtypes for mediating drinking elicited by eating was examined in adult male Sprague-Dawley rats. The ability of pharmacological antagonism of AT 1 and/or AT 2 receptors to abolish drinking elicited by exogenous angiotensin II was established first. The SC injection of the AT 1 antagonist losartan (DuP 753) was sufficient to abolish drinking elicited by SC angiotensin II. The ICV injection (through a surgically implanted chronic cannula) of losartan inhibited drinking elicited by ICV angiotensin II; the combined ICV injection of losartan plus the AT 2 antagonist PD123319 was sufficient to abolish drinking elicited by ICV angiotensin II. For rats drinking and eating after 24-h food deprivation, SC losartan plus PD123319 inhibited water to food ratio, but ICV losartan and/or PD123319 failed to inhibit food-related drinking. For nondeprived rats eating a small cracker, SC losartan and/or PD123319 attenuated water intake, but only ICV losartan produced statistically significant inhibition of drinking elicited by ingestion of cracker. The IG infusion (through a surgically implanted gastric catheter) of 2 ml 600 or 900 mOsm/kg NaCl, a treatment that is subthreshold for increase in systemic plasma osmolality at the initiation of drinking, elicited drinking that was attenuated by SC losartan and/or PD123319 and attenuated by ICV losartan only. The IG infusion of 2 ml 1800 mOsm/kg NaCl, a treatment that is above threshold for increase in systemic plasma osmolality at the initiation of drinking, elicited drinking that was not inhibited by SC or ICV losartan and/or PD123319. These results demonstrate that peripheral AT 1 and AT 2 and central AT 1 receptors for angiotensin II contribute to drinking elicited by eating and the gastrointestinal osmotic consequences of eating. These findings extend the evidence demonstrating a renal renin-angiotensin contribution to food-related drinking in rats.

Histamine H 3 receptors contribute to drinking elicited by eating in rats

A role for endogenous histamine and its H 3 receptor subtype for mediating drinking elicited by eating was examined in adult male Sprague-Dawley rats. The IP injection of the H 3 agonist R-α-methylhistamine (Ramh, 2.5 mg/kg) shortened the latency to initiate drinking and increased 1-h water intake in nondeprived rats freely eating pellets and drinking water. The ICV injection (through a surgically implanted chronic cannula) of 10 μg Ramh increased water intake; this Ramh-induced drinking was abolished by previous ICV injection of the H 3 antagonist thioperamide (Th, 60 μg). For rats drinking and eating after 24-h food deprivation, SC Th inhibited drinking behavior: for example, 10 mg/kg Th SC delayed the latency to initiate drinking and inhibited 1-h water intake without inhibition of food intake. In contrast, 60 μg Th ICV failed to inhibit food-related drinking in rats eating after food deprivation. For nondeprived rats eating a small cracker, 10 mg/kg Th SC delayed the latency to initiate drinking and abolished water intake without effect on eating, and 60 μg Th ICV had similar effects upon drinking elicited by ingestion of cracker. The IG infusion (through a surgically implanted gastric catheter) of 2 ml 600 or 900 mOsm/kg NaCl, a treatment that is subthreshold for increase in systemic plasma osmolality at the initiation of drinking, elicited drinking that was abolished by 10 mg/kg Th SC and attenuated by 60 μg Th ICV. The IG infusion of 2 ml 1800 mOsm/kg NaCl, a treatment that is above threshold for increase in systemic plasma osmolality, elicited drinking that was attenuated by 10 mg/kg SC or 60 μg Th ICV. These results demonstrate that peripheral and central H 3 receptors for histamine have a role in drinking elicited by eating and the postprandial gastrointestinal osmotic consequences of eating. These findings extend the evidence demonstrating a histaminergic contribution to food-related drinking in rats.

Reversal of dexfenfluramine-induced anorexia and c-Fos/c-Jun expression by lesion in the lateral parabrachial nucleus

The external subdivision of the lateral parabrachial nucleus (LPBE) shows strong Fos-like immunoreactivity (FLI) following anorectic doses of the indirect serotonin agonist dexfenfluramine (DFEN). In an effort to determine the contribution of the LPBE to DFEN-induced anorexia, bilateral ibotenate lesions were made in the LPBE, and the effects of the lesion on DFEN-induced anorexia and FLI as well as c-June-like immunoreactivity (JLI) were examined. It was found that LPBE lesion significantly attenuated DFEN anorexia: in a 1-h food intake test following 24-h food deprivation, DFEN (2 mg/kg) suppressed food intake by 60% in intact rats but only 34% in rats with LPBE lesions. In addition to this behavioral change, LPBE lesion completely abolished DFEN-induced FLI and JLI in the lateral subdivision of the central nucleus of the amygdala (CeL) and laterodorsal subdivision of the bed nucleus of stria terminalis (BSTLD), both of which showed strong FLI and JLI in intact rats. DFEN-induced FLI and JLI in other brain regions were not affected by LPBE lesion, including the ventromedial and lateral hypothalamus, caudate-putamen, and the nucleus of the solitary tract (NST). The parallel loss of DFEN-induced anorexia and FLI/JLI following LPBE lesion raises the novel possibility that LPBE-CeL/BSTLD pathway may be involved in DFEN anorexia.

Modulation of the satiety effect of cholecystokinin by estradiol

Data obtained from a wide variety of mammalian species indicate that feeding behavior can be influenced by changes in endogenous estrogens and by exogenous estrogenic treatments. The present experiment represents an initial investigation of the hypothesis that the suppression of food intake by estradiol is mediated by an enhancement of the satiety effect of cholecystokinin (CCK). Twenty-four female rats were ovariectomized and implanted either with a 5% estradiol silastic capsule or an empty capsule on the day of surgery. Three weeks later, animals received IP injections of CCK-octapeptide (5.0 or 10.0 μg/kg) or saline after 24-h food deprivation. Food and water intake were measured 60 min after treatment. Although CCK suppressed feeding in all subjects, the effects on food intake were greater in estradiol-treated females. CCK injections also reduced water intake, but there was no interaction between estradiol and CCK on drinking. These findings indicate that the inhibitory effect of CCK on food intake is enhanced in females treated with a physiological dose of estradiol, and suggest that the effects of estradiol on feeding behavior may be mediated by a potentiation of the satiety effect of CCK.

Development of tolerance to endogenous opiates activated by 24-h food deprivation

Four experiments assessed the effects of exposure to 24-h food deprivation on the tail-flick latency of rats exposed to a temperature stimulus. Confirming previous studies, Experiment 1 showed that food deprivation gave rise to analgesia, as indicated by increased tail-flick latencies, that was antagonized by naloxone. Experiment 2 found that analgesia was greatly reduced after five exposures to periods of 24-h food deprivation (alternating with 24-h free access to food), indicating the development of tolerance. Experiments 3 and 3a examined the development of tolerance to the analgesic effects of morphine following repeated morphine injections, saline injections, and exposure to 24-h food deprivation plus saline injections. The combined results of both experiments provided evidence that repeated exposures to either morphine or food deprivation, produced greater tolerance to morphine than did exposures to saline. That food deprivation was cross-tolerant with morphine indicated that tolerance to food deprivation-induced analgesia involved opioid mechanisms. The relevance of opioid tolerance to psychobiological models of feeding and to the development of an animal model of anorexia nervosa was discussed.

Senescence-accelerated mouse (SAM): Age-related reduced anxiety-like behavior in the SAM-P/8 strain

Age-related behavioral changes in the passive avoidance, food neophobia, elevated plus-maze, and water-lick conflict tests were studied using substrains of senescence-accelerated mouse (SAM-P/8 and SAM-R/1) at 2 to 20 months of age. SAM-P/8 mice exhibited a significant impairment of acquisition of passive avoidance compared with SAM-R/1 mice when they were trained repeatedly, and the acquired response in SAM-P/8 mice rapidly diminished in contrast to good retention in SAM-R/1 mice. SAM-P/8 mice showed an age-related decrease in the latency to eat novel food after a 24-h food deprivation as compared with SAM-R/1 mice at 2 to 12 months of age, despite no significant difference in latency to eat familiar food between the two strains. In the elevated plus-maze test, SAM-P/8 mice had apparent increases in the number of entries into open arms and time spent on open arms in comparison to SAM-R/1 mice at 4 through 12 months of age; this difference became obvious with aging, implying age-associated reduced anxiety in the SAM-P/8 strain. In addition, SAM-P/8 mice exhibited a significant increase in punished water drinking compared to SAM-R/1 mice in the water-lick conflict test, although unpunished water intake in SAM-P/u mice did not differ from that in the SAM-R/1 control. Aged SAM-R/1 mice, 20 months old, exhibited low anxiety-like behavior in the food neophobia and elevated plusmaze tests such as was seen in SAM-P/8 mice, when compared with young (4-month-old) SAM-R/1 mice. These results indicate that the SAM-P/8 strain shows age-related reduced anxiety-like behavior compared to the SAM-R/1 strain, which may be related to learning and memory impairment in the strain. It is suggested that the SAM-P/8 strain may be a useful animal model for studying emotional disorders and related memory impairments in dementia, which can be used at an early stage of age.

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.

Conditioned tolerance to the anorectic and corticosterone-elevating effects of nicotine

We have shown that tolerance to the behavioral effects of nicotine is partially dependent on conditioned environmental cues that predict drug delivery. The present research extends this finding to physiological effects of nicotine by assessing both the appetite-suppressing and adrenocortical-activating effects of nicotine, as measured by plasma corticosterone (CORT). In the first study, male rats on a 22-h food deprivation schedule were injected daily with 0.33 or 0.66 mg/kg (free base) of nicotine bitartrate or saline in a distinctive environment and tested for milk intake. Nicotine initially suppressed milk intake and tolerance developed over 10 days. Changing cues associated with drug administration partially reversed tolerance since injection of nicotine in a new environment reduced milk intake of tolerant animals. Similarly, animals who repeatedly received nicotine in one environment exhibited CORT levels lower than rats injected for the first time, and this tolerance also was partially reversed when administration occurred in the new environment. The second experiment indicated that the increased CORT of Experiment 1 was not a stress response associated with injecting animals in a different environment. These results indicate that tolerance to both behavioral and neuroendocrine effects of nicotine is influenced by conditioning.

Modulation of taste affect by hunger, caloric satiety, and sensory-specific satiety in the rat

Human judgements of the pleasure of sweetness have been reported to be modulated by caloric hunger, satiety, and sensory-specific satiety. This study examined both hedonic and aversive facial/somatic reactions to taste in the rat, in order to confirm the relation of hunger and satiety to taste affect, and to assess whether affective modulation depends upon the cognitive factors that mediate human self-interpretation of affect. In the first experiment, the affective reactions of rats to sweet, bittersweet, and water tastes were assessed in five states of caloric hunger or satiety. Caloric satiety reduced positive hedonic reactions below normal levels. Conversely, 48-h food deprivation (but not 24-h deprivation) increased hedonic reactivity. Hedonic enhancement by hunger was not restricted to sweet tastes, but also extended to the palatability of water. Only the hedonic reactions to taste were changed by hunger or satiety: taste aversion was not altered. The second experiment compared the magnitude of affective change during sensory-specific satiety and caloric satiety. Taste-reactivity elicited by sucrose solution or milk was assessed after satiating meals of each of those foods. Sensory-specific satiety further reduced hedonic reactions below the level achieved by caloric satiety alone. Both for caloric satiety and for sensory-specific satiety changes in affect were restricted to positive hedonic reactions: no increase in aversion accompanied the hedonic decrements. These results confirm that taste affect is modulated during caloric hunger, caloric satiety, and sensory-specific satiety. In addition they indicate that the modulation of taste affect by hunger and satiety is confined to the positive limb of the two dimensions (hedonic vs. aversive) of palatability.

Suprachiasmatic nuclei lesions eliminate light/dark variations in short-term feeding responses to deprivation or insulin treatment in rats

Short-term (1-h, 4-h and 12-h) and long-term (24-h) feeding responses to 24-h food deprivation (FD) or insulin treatment (IT) (8 mU/kg IP) were studied in male rats under a 12/12-h light/dark (L/D) cycle. The 24-h FD or the IT began either at onset (Dawn) or offset (Dusk) of the lights. In sham-operated rats (Shams) both protocols elicited greater short-term feeding responses at Dusk ( p<0.05 or less). In suprachiasmatic nuclei (SCN)-lesioned rats the L/D variations in short-term responses were absent. In both SCN and Shams the 24-h feeding responses did not depend on stimuli time-schedule. We conclude that the regulation of short-term (circadian), but not long-term, feeding responses to metabolic stimuli is dependent on SCN integrity in the rat.

Pregastric food-contingent stimulation elicits drinking in the absence of systemic dehydration in the rat

Adult male Sprague-Dawley rats surgically fitted with a stainless steel gastric cannula were prepared following 24-h food deprivation for sham feeding liquid diet with open gastric fistula. Sham feeding (pregastric food-contingent stimulation) of 5, 10, 20 or 40 ml of liquid diet elicited water intake that was not in proportion to volume of liquid diet sham fed. Rats sham feeding between 1 and 68 ml of sweetened milk showed no evidence of cellular or extracellular dehydration as measured by plasma osmolality and hematocrit, respectively. Subcutaneous injection of 100 mg/kg captopril, a dose sufficient to block conversion of angiotensin I to angiotensin II in brain and periphery, inhibited drinking elicited by sham feeding without effect on sham feeding. These results demonstrate that pregastric food-contingent stimulation elicits water intake that is not in proportion to amount of liquid diet sham fed and that occurs in the apparent absence of systemic dehydration. That such drinking could depend upon endogenous angiotensin II provokes consideration of a role for angiotensin II in the mediation of a pregastric (perhaps histaminergic) mechanism that initiates drinking in advance of postprandial dehydration.

Food deprivation alters liver glycogen metabolism and endocrine responses to hemorrhage

Liver glycogen content, blood glucose, insulin, glucagon, and epinephrine were determined during 1 h hemorrhagic hypotension at 60 mmHg and 23 h thereafter in fed and two groups of 24-h food-deprived rats receiving either no infusion or 30% glucose intravenously during hemorrhage. Liver glycogen content was reduced by greater than 90% after 24-h food deprivation. Fed and food-deprived rats given glucose developed similar and substantial elevations of blood glucose during hemorrhage, whereas changes in blood glucose were modest in food-deprived rats given no infusion. In fed rats, liver glycogen was reduced by 60% during the 1-h bleed, but within 2 h after hemorrhage repletion of liver glycogen content commenced. By 6 h, approximately 75% of the glycogen lost during hemorrhage had been restored, and 23 h after hemorrhage liver glycogen content was six times greater compared with nonbled controls. Although glycogen levels increased after hemorrhage in food-deprived animals, the increase was negligible compared with that found in fed rats. Infusion of glucose during hemorrhage or adrenergic blockade after hemorrhage did not alter glycogen repletion in food-deprived rats. Posthemorrhage fed animals had high levels of insulin, glucagon, and epinephrine during hemorrhage, whereas insulin levels remained low in food-deprived rats despite exogenously induced hyperglycemia. It is concluded that rapid and substantial glycogen repletion can occur even immediately poststress. The conditions seem to be related to the nutritional state at the time of the insult.

Changing environmental cues reduces tolerance to nicotine-induced anorexia.

Male rats on a 22-h food deprivation schedule were injected daily with a low dose of nicotine and allowed to drink sweetened milk for 10 min in a test cage in the colony room. Nicotine initially suppressed milk intake but complete tolerance developed within 10 days so that the amount of intake did not differ from saline controls. The role of temporal cues was tested on the next day by changing the timing of cues, and omitting others that normally preceded nicotine injection while keeping constant the physical environment within which injection and testing took place and the drug-test interval. Changing the timing of injection significantly suppressed milk intake. These results show that tolerance to the anorectic effects of a low dose of nicotine is partially dependent on the presence and timing of cues associated with tolerance acquisition.

Amino-Acid Metabolism Enzyme Activities in Rat White Adipose Tissue

The activities of alanine-, aspartate- and branched-chain amino-acid transaminases, glutamine synthetase, glutamate dehydrogenase and adenylate deaminase in white adipose tissue of adult male rats have been determined in animals submitted to 12-h cold exposure (4 degrees C) or to 24-h food deprivation. Starvation resulted in small changes in glutamate dehydrogenase and alanine transaminase when expressed per unit of protein weight, inducing an increase in branched-chain amino-acid transaminase and glutamine synthetase. Cold exposure showed the same effects as starvation with respect to glutamate dehydrogenase and alanine transaminase, but induced increases in glutamine synthetase and aspartate transaminase. It is concluded that starvation increases the handling of some amino acids by white adipose tissue and the detoxification of the ammonia thus evolved. The changes observed suggest a different pattern of amino-acid metabolism enzyme changes with either cold or starvation.

The anorectic effect of FG 7142, a partial inverse agonist at benzodiazepine recognition sites, is reversed by CGS 8216 and clonazepam but not by food deprivation

The benzodiazepine partial inverse agonist N′-methyl-β-carboline-3-carboxamide (FG 7142; 5.0 and 10.0 mg/kg, i.p.) produced a dose-dependent reduction in the consumption of a familiar, highly palatable diet by non-food-deprived male rats. At dose levels which exhibited no significant intrinsic effects, the benzodiazepine receptor antagonist 2-phenylpyrazolo-[4,3-c]-quinoline-3(5H)-one (CGS 8216; 1.25–5.0 mg/kg, i.p.) reversed the anorectic effect of FG 7142. When clonazepam and FG 7142 were given in combination, mutual cancelling of their opposite effects occurred. These results are consistent with an action of FG 7142 at benzodiazepine recognition sites to reduce the level of palatable food consumption, and imply that a bidirectional control of food intake via benzodiazepine recognition sites can be achieved. The anorectic effect of FG 7142 was not reversed by 24-h food deprivation, indicating a possible separation from the effects of hunger mechanisms.

Stress, Endogenous Opioids and Salt Intake

The effect of stress on NaCl intake was examined in mice given a choice of water and 1.5% NaCl to drink. Immobilization of mice for 15-min and 24-h food deprivation resulted in a 2.5- and 5-fold increases in NaCl intake, respectively, without affecting water intake. Naloxone treatment (0.01, 0.1 and 1.0 mg/kg) produced a dose-dependent decrease in the stress-induced NaCl intake, as did captopril treatment (5, 10 and 50 mg/kg). Intraventricular injection of angiotensin II in mice resulted in an increase in 1.5% NaCl intake, which was blocked by naloxone. Morphine (10 mg/kg) increased the preference of mice for a normally aversive 3.0% NaCl solution, but not for preferred, less concentrated, solutions of NaCl. The results suggest that both endogenous opioids and angiotensin II contribute to stress-induced NaCl intake, and that endogenous opioids may also mediate the increase in NaCl intake, observed with angiotensin II.

Effects of 24-hour starvation period on metabolic parameters of 20-day-old rats.

The effects of a 24-hour starvation period upon 20-day-old rat pups were studied both in animals kept in the presence of their starved dams and in their absence. The relative loss of body weight was more intense in the rats that received no milk, being however, severe in both groups. There was a significant maintenance of both plasma glucose levels and total amino acids, with differences in blood glucose compartmentation and a remarkable uniformity in the effects of starvation upon individual amino-acid concentrations. A significant increase in plasma urea was observed, higher in the rats kept in the presence of the dam. Ketone bodies increased with starvation but their final levels were lower than in adults. The general pattern of metabolic change observed suggests a situation, after 24-h food deprivation, similar to that of long term starvation in adults; with an active protein amino-acid catabolism but with a remarkable maintenance of circulating foodstuff levels.

Cholecystokinin-octapeptide effects on eating elicited by “external” versus “internal” cues in rats

Animals were pretrained using a paradigm that involved 3 weeks of restricted daily feeding. As a result of this experience, presentation of food-associated stimuli (“external cues”) to minimally (1-h) deprived (or even undeprived) rats is followed immediately by vigorous eating. This paradigm was used in order to test whether animals that are compelled to eat large meals despite being only minimally deprived do so because they are insensitive to endogenous cholecystokinin-octapeptide (CCK-8). CCK-8 is the active fragment of a polypeptide hormone and it is thought by some to be released after a meal and to serve as a short term satiety factor. Following minimal, or 24-h, food-deprivation, the effects of 0, 2, 4, or 8 μg/kg doses of CCK-8 were examined in these animals. Latency to contact food, meal initiation, time spent eating, meal size and a hoarding-like reaction were among the measures recorded. The major finding was that meal initiation was delayed dose-dependently in the minimally-deprived condition. Thus, animals eating apparently “by force of habit” were not insensitive to circulating CCK-8. Approach to food and hoarding-like behavior were virtually unaffected. In the 24-h food-deprivation condition, the pretrained animals were relatively resistant to the inhibitory effects of CCK-8 on eating. The effectiveness of CCK-8 appeared to be greatly enhanced by (and may even depend on) its summation with other satiety factors.

The metabolic effects of sodium dichloroacetate in experimental hepatitis in the rat [proceedings

Conference Article| October 01 1977 The Metabolic Effects of Sodium Dichloroacetate in Experimental Hepatitis in the Rat GUY A. H. JOHNSON; GUY A. H. JOHNSON 1University Chemical Pathology and Human Metabolism Unit, Level D, South Laboratory and Pathology Block, General Hospital, Southampton SO 94XY, U.K. Search for other works by this author on: This Site PubMed Google Scholar K. GEORGE M. M. ALBERTI K. GEORGE M. M. ALBERTI 2University Chemical Pathology and Human Metabolism Unit, Level D, South Laboratory and Pathology Block, General Hospital, Southampton SO 94XY, U.K. Search for other works by this author on: This Site PubMed Google Scholar Biochem Soc Trans (1977) 5 (5): 1387–1389. https://doi.org/10.1042/bst0051387 Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn MailTo Cite Icon Cite Get Permissions Citation GUY A. H. JOHNSON, K. GEORGE M. M. ALBERTI; The Metabolic Effects of Sodium Dichloroacetate in Experimental Hepatitis in the Rat. Biochem Soc Trans 1 October 1977; 5 (5): 1387–1389. doi: https://doi.org/10.1042/bst0051387 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsBiochemical Society Transactions Search Advanced Search This content is only available as a PDF. © 1977 Biochemical Society1977 Article PDF first page preview Close Modal You do not currently have access to this content.

Dorsomedial amygdala damage: A time-after-surgery assessment of feeding

The food consumption of Charles River male rats with dorsomedial amygdala lesions was compared with sham operates and normal controls on four tests spanning a 65-day postsurgery period. Following 24-h food deprivation (18- and 65-day postsurgery tests), lesioned animals ate significantly less than the other two groups (p <.01). Although 24-h food and water deprivation (35- and 50-day postsurgery tests) increased the absolute level of food consumption in all groups, the relative magnitude of the feeding deficit in lesioned animals remained approximately the same (p <.01). The results suggest that hypotheses which stress the “temporary deficit” nature of lesion effects do not adequately explain the changes in feeding following dorsomedial amygdala damage.