naloxone and Anorexia

There is an increasing body of evidence supporting the need for prophylactic management of the adverse events (AEs) associated with long-term opioid use in patients with chronic pain. Symptoms of bowel dysfunction, such as constipation, may have a significant impact on a patient's quality of life and willingness to continue opioid therapy, and therefore should be managed proactively to ensure that the patient can continue effective pain management. The fixed-dose combination (FDC) prolonged-release (PR) oxycodone/naloxone (OXN) may be an effective therapeutic approach to delivering analgesia, with a reduced risk for opioid-induced constipation.. The aim of this paper was to report the pharmacokinetic results from a single-dose study and a multiple-dose bioequivalence study of OXN versus separate formulations of oxycodone PR and naloxone PR administered concurrently in healthy subjects.. Both studies were open-label, randomized crossover studies in healthy adult male and female subjects. In the single-dose study, subjects were randomly assigned to 1 of 4 treatment groups: OXN FDC (44 x 10/55-mg, 2 x 20/110-mg, or 1 x 40/20-mg dose strength [each given at a total combined dose of 40/220 mg]) or oxycodone PR 40 mg + naloxone PR 20 mg given in separate formulations. In the multiple-dose study, 34 subjects were randomly assigned to 1 of 3 treatment groups: OXN FDC 40/20 mg, oxycodone PR 40 mg, or naloxone PR 20 mg. Treatments were considered bioequivalent if the 90% CIs for relative bioavailability calculations fell within a predetermined range of 80% to 125%. AEs were assessed by the investigator at each study visit.. The single-dose study included 28 subjects (22 men, 6 women; mean [SD] age, 32.3 [5.44] years; weight, 75.5 [9.3] kg; and body mass index [BMI], 24.2 [2.5] kg/mm(2)). The mean plasma oxycodone concentration-time curves for OXN and oxycodone PR + naloxone PR were similar. With oxycodone, the mean (SD) AUC(t) values with OXN 10/5, 20/10, and 40/20 mg and oxycodone PR + naloxone PR were 473.49 (72.16), 491.22 (82.18), 488.89 (91.04), and 502.28 (84.13) ng . h/mL, respectively; mean C(max) values were 34.91 (4.36), 35.73 (4.93), 34.46 (5.03), and 40.45 (4.71) ng/mL. For naloxone-3-glucuronide (the primary analyte of naloxone), the mean (SD) AUC(t) values with OXN 10/5, 20/10, and 40/20 mg and oxycodone PR + naloxone PR were 539.93 (142.24), 522.45 (128.57), 520.10 (133.18), and 523.37 (119.75) ng . h/mL, respectively; mean C(max) values were 62.01 (15.96), 63.62 (19.51), 61.95 (18.37), and 63.55 (16.75) ng/mL. There were no statistically significant differences between the treatments, and each of the treatment comparisons resulted in 90% CIs within the range for bioequivalence. The multiple-dose steady-state bioequivalence study included 34 subjects (28 men, 6 women; mean [SD] age, 36 [9.4] years; weight,78.9 [11.7] kg; and BMI, 24.6 [1.9] kg/m(2)). No significant differences were observed between the treatments, with the exception of naloxone-3-glucuronide C(min,ss) values. Mean C(min,ss) values of 22.6 and 24.0 ng/mL were obtained for the OXN combination and naloxone PR tablet, respectively. In the multiple-dose study, the most frequently reported AEs with OXN,oxycodone PR, and naloxone PR were headache (7%, 26%, and 17%, respectively), anorexia (10%, 16%, and 13%), and nausea (10%, 13%, and 7%).. The results from the single-dose study were consistent with the regulatory definition of bioequivalence of the FDCs and single components across the range of doses administered. The pharmacokinetic properties of the OXN FDC were similar to those of oxycodone PR + naloxone PR given as separate formulations, based on the regulatory definition. These findings were consistent with the results of the multiple-dose steady-state bioequivalence study. In this population of healthy volunteers, the pharmacokinetic properties of oxycodone apparently were not significantly influenced by administering oxycodone in a combination product, and the availability of naloxone-3-glucuronide from OXN was similar to that from the naloxone PR tablet. These findings suggest that the coadministration of oxycodone PR and naloxone PR in an FDC would not significantly affect the bioavailability of either of its constituents in these subjects.

Topics: Administration, Oral; Adult; Anorexia; Area Under Curve; Biological Availability; Cross-Over Studies; Delayed-Action Preparations; Dose-Response Relationship, Drug; Drug Combinations; Female; Half-Life; Headache; Humans; Male; Middle Aged; Naloxone; Narcotic Antagonists; Nausea; Oxycodone; Receptors, Opioid; Tablets; Therapeutic Equivalency

To determine whether aging is associated with a reduction in the opioid modulation of feeding, which may be important in the pathogenesis of the "anorexia of aging.". Three studies on separate days, in randomized order and double-blind fashion.. Clinical Human Research Laboratory, Department of Medicine, RAH, Adelaide, Australia.. Twelve older (5 male/7 female) (age 65-84) and 12 young (5 male/7 female) (age 20-26) healthy subjects.. Subjects received in double-blinded random order, intravenous bolus (10 minutes) and then continuous (140 minutes) infusions of saline (control), naloxone low dose (LD) (bolus 27 microg/kg; continuous 50 microg/kg/hr), or naloxone high dose (HD) (bolus 54.5 microg/kg; continuous 100 microg/kg/hr).. After 120 minutes, subjects were offered a buffet meal, and their energy intake was quantified. Hunger, fullness, nausea, and drowsiness were assessed using visual analogue scales.. The naloxone LD and HD infusions had no significant effect on ratings of hunger, fullness, or nausea, but increased drowsiness (P < .01) compared with the control infusion in both age groups. Older subjects ate less (P < .001) at the buffet meal than young subjects during all three infusions. Naloxone infusions reduced energy intake compared with control (P < .001), LD by 13.2 +/- 5.0% and HD by 10.7 +/- 5.0%, with no difference between the doses (P = .71). Overall, naloxone suppressed energy intake in both young and older subjects (P < .01). This suppression was slightly, but not significantly, greater in young than in older subjects (mean of LD and HD 16.4 +/- 4.9% vs 7.5 +/- 4.9%, P = .42), because of a trend to reduced suppression in older women.. We conclude that healthy older adults retain their sensitivity to the suppressive effects of naloxone on food intake. Possible gender differences in this sensitivity warrant further investigation. A decline in opioid activity is unlikely to contribute substantially to the physiological anorexia of aging observed in older people.

Topics: Adult; Aged; Aged, 80 and over; Anorexia; Appetite; Double-Blind Method; Eating; Endorphins; Energy Intake; Female; Humans; Male; Middle Aged; Naloxone

Exercise improves cardiovascular health, strengthens muscles and bones, stimulates neuroplasticity, and promotes feelings of well-being. However, when taken to extremes, exercise can develop into an addictive-like behavior. To assess the addictive potential of exercise, withdrawal symptoms following injections of 1.0 mg/kg naloxone were compared in active and inactive male and female rats. Active and inactive rats were given food for 1 hr or 24 hr/day. Additionally, a group of inactive rats was pair-fed the amount of food consumed on the previous day by food-restricted active rats. Rats fed for 1 hr/day decreased food intake and lost weight. Additionally, food-restricted active rats increased wheel running. There was a direct relationship between the intensity of running and the severity of withdrawal symptoms. Active food-restricted rats displayed the most withdrawal symptoms, followed by active rats given 24-hr access to food. Only minimal withdrawal symptoms were observed in inactive rats. These findings support the hypothesis that exercise-induced increases in endogenous opioid peptides act in a manner similar to chronic administration of opiate drugs.

Topics: Analysis of Variance; Animals; Anorexia; Body Weight; Disease Models, Animal; Feeding Behavior; Female; Male; Motor Activity; Naloxone; Narcotic Antagonists; Physical Conditioning, Animal; Rats; Rats, Long-Evans; Sex Characteristics; Substance Withdrawal Syndrome

Endogenous opioids have long been implicated in mechanisms of appetite control. A significant strand in the evidence base has been the hypophagic action of broad-spectrum opioid receptor antagonists (such as naloxone) in opiate-naïve animals. However, while much has been learned about sites of action, underlying receptor mechanisms and the role of taste hedonics, surprisingly little is known about the behavioural selectivity of naloxone-induced hypophagia. As such, two experiments employed detailed video analysis to profile the behavioural effects of naloxone (Experiment 1: 1.0-5.0 mg/kg; Experiment 2: 0.01-1.0 mg/kg) in non-deprived male rats during 1 h free-feeding tests with palatable mash. Results confirmed that, at doses > or =1.0 mg/kg, naloxone consistently suppresses food consumption and feeding behaviour but, congruent with its short biological half-life, had no carryover effects on post-treatment weight gain. Crucially, the anorectic doses of naloxone did not alter the time taken to find food or to commence feeding, the time spent feeding in the initial phase of testing, or the rate at which food was consumed. Furthermore, they neither interfered with non-ingestive components of the behavioural repertoire (e.g. locomotion, rearing) nor did they disrupt the normal structure of feeding behaviour (the behavioural satiety sequence, BSS). Rather, the principal effect of naloxone was to produce a shift to the left in (i.e. accelerate) the BSS. Findings are discussed in relation to the role of (mu) opioid receptor mechanisms in taste hedonics and the likelihood of a naloxone-induced reduction in the orosensory reward that would normally accompany/follow the ingestion of palatable food.

Topics: Analysis of Variance; Animals; Anorexia; Appetite Regulation; Dose-Response Relationship, Drug; Feeding Behavior; Food Preferences; Male; Naloxone; Narcotic Antagonists; Rats; Rats, Inbred Strains; Satiety Response; Statistics, Nonparametric; Taste

We recently reported that the 25 amino acid peptide xenin caused reduced feed intake when centrally injected in chicks. The present study was designed to explore possible mechanisms of the xenin-induced anorexigenic response in chicks. In Experiments 1 and 2, chicks were implanted with cannulas and xenin injections were made directly into the ventromedialis hypothalami (VMH). Chicks responded with reduced feed intake and increased c-Fos immunoreactivity at the VMH. In Experiment 3 chicks that received co-intracerebroventricular (ICV) injection of naloxone and a dose of xenin (100 pmol), that alone does not affect feed intake, had reduced feed intake. In Experiment 4, chicks responded to ICV xenin with reduced feed- but increased exploratory-pecking. Thus, we conclude that xenin may mediate its effect directly at the VMH and that the endogenous opioid system may counter anorexigenic effects of low xenin doses in chicks. Xenin also caused increased exploration of a novel environment, an effect that may be competitive with feeding. Taken together, these results suggest that xenin regulation of chick appetite is the result of several central and behavioral mechanisms acting in synergism.

Topics: Analgesics, Opioid; Animals; Anorexia; Appetite Regulation; Chickens; Eating; Feeding Behavior; Naloxone; Narcotic Antagonists; Neurotensin; Peptides; Proto-Oncogene Proteins c-fos; Receptors, Opioid

Intake of palatable solutions can enhance the anorectic potency of opioid antagonists. This experiment examined the relative contributions of orosensory experience and body weight gain to the enhanced anorectic potency of naloxone (0.125, 0.25, 0.5, and 1.0 mg/kg i.p.). Four groups of male hooded Lister rats (Charles River) were maintained on separate feeding regimes for 3 months. S-ADLIB rats were nondeprived with free access to lab chow and 20% (w/v) sucrose solution. S-RESTRICT rats received limited sucrose (50 ml/day) and chow (15 g/day) access, yoking their body weights to ADLIB rats receiving free access to lab chow only. RESTRICT rats received approx. 15 g of chow/day to maintain their body weights at 90% of the ADLIB rats. Fifteen-minute sucrose intake tests revealed marked differences between naloxone sensitivity of chronic sucrose drinkers and sucrose-naive groups. Intakes of S-ADLIB and S-RESTRICT were suppressed at all doses (max suppression >60%). In comparison to animals given sucrose, ADLIB and RESTRICT animals were significantly less sensitive (maximum suppression = 35%). Naloxone potency was independent of body weight differences. The data demonstrate that overconsumption of palatable ingesta, and not diet-induced weight gain, is sufficient to enhance antagonist potency. The study confirms that orosensory stimulation can induce plasticity in opioid systems, supporting an important role for opioids in intake regulation and general reward processes.

Topics: Animals; Anorexia; Body Weight; Diet; Dietary Sucrose; Dose-Response Relationship, Drug; Eating; Male; Naloxone; Narcotic Antagonists; Rats

Modulation of feeding behavior by neuropeptide Y (NPY) and opioids is well established, but the possibility that these neural influences provoke specific appetites, NPY for carbohydrate and opioids for fat, has also been considered. In other studies, intake of standard chow after NPY stimulation can be blocked by naloxone, indicating an interaction between these systems in the regulation of feeding. The present experiments examined the nature of NPY-opioid interactions in diet selection. Rats were administered NPY and naloxone concurrently, then chose between high-fat and high-carbohydrate diets. Subcutaneous administration of naloxone (0.01-0.3 mg/kg) potently reduced intake of the preferred diet, but not the nonpreferred diet. A similar pattern of selection was seen in a separate experiment where the same doses of naloxone were administered after 24-h food deprivation. These data support the idea that the opioid system mediates the "rewarding" aspects of feeding.

Topics: Animals; Anorexia; Dietary Carbohydrates; Dietary Fats; Eating; Food Deprivation; Food Preferences; Male; Naloxone; Neuropeptide Y; Rats; Rats, Sprague-Dawley

We studied the effect of the opioid receptor antagonist naloxone on intake of three isocaloric diets containing cornstarch, sucrose, or Polycose as the predominant carbohydrate in ad libitum-fed and food-restricted rats. A large body of evidence suggests that opioids affect palatability (reward)-rater than hunger (energy deficit)-driven food intake. We expected food intake to be driven by both energy needs and palatability in ad libitum-fed rats, whereas in food-restricted rats we expected intake to be driven by energy needs with a relatively small palatability component in the preferred sucrose and Polycose diet groups. In the ad libitum-fed rats, naloxone significantly reduced nocturnal intake of all three diets at doses of 0.3, 1.0, and 3.0 mg/kg. In contrast, naloxone failed to alter intake of the cornstarch diet in chronically food-restricted rats. However, naloxone decreased intake of the sucrose diet in food-restricted rats at doses of 0.3, 1.0, and 3.0 mg/kg and decreased intake of the Polycose diet at the 3 mg/kg dose. These data lend further support to the notion that opioids are involved in some other component of feeding than that induced by energy needs.

Topics: Animals; Anorexia; Diet; Eating; Food Deprivation; Food Preferences; Glucans; Male; Naloxone; Narcotic Antagonists; Rats; Rats, Sprague-Dawley; Starch; Sucrose; Taste; Time Factors

We measured neuropeptide Y (NPY) concentration in microdissected hypothalamic nuclei, by radioimmunoassay, and NPY mRNA in the hypothalamus in rats treated systemically with the nonspecific opioid antagonist, naloxone, to produce mild anorexia. Twenty rats were treated with daily SC injections of naloxone (7.5 mg/kg); 20 were treated with vehicle alone. Naloxone produced a 7% reduction in food intake (p < 0.01) and a reduction in weight gain (p < 0.002). Neuropeptide Y concentrations were increased specifically in the dorsomedial nucleus of the hypothalamus (DMN) in rats treated with naloxone (6.8 +/- 0.7 fmol/micrograms protein vs. 3.1 +/- 1.0 fmol/micrograms protein, p < 0.05, n = 10 per group). Total hypothalamic NPY mRNA was unchanged. Neuropeptide Y-opioid interactions may be important in the control of food intake.

Topics: Animals; Anorexia; Body Weight; Eating; Feedback; Hypothalamus, Middle; Insulin; Male; Naloxone; Neuropeptide Y; Opioid Peptides; Random Allocation; Rats; Rats, Wistar; RNA, Messenger

Opioid peptides have been implicated in reward-related components of eating, especially with fatty and sweetened foods. This study examined the effect of pre-exposure of rats to milk on the subsequent anorexic effect of naloxone in a separate daily mash intake test. Rats were given constant access to either skimmed or whole milk for 15 days, in addition to normal diet. A third (control) group received only the normal diet. Subsequently, all groups received 0, 0.125, 0.5 and 1.0 mg/kg naloxone prior to their daily mash intake test. Naloxone caused dose-dependent reductions in mash intake in all groups, but this effect was significantly greater in the group with whole milk than in controls, with the group with skimmed milk intermediate. Daily intakes of milk were similar with skimmed and whole milk, and milk intake in separate two-bottle choice tests provided no evidence for overall preferences for either solution. These results suggest that prior exposure to milk enhances opioid involvement in feeding, and possible mechanisms for this are discussed.

Topics: Animals; Anorexia; Body Weight; Dietary Fats; Drinking; Energy Intake; Male; Milk; Naloxone; Rats

The effects of body rotation in a horizontal plane and the opiate antagonist, naloxone, on the nociceptive responses and the feeding behavior of male mice were examined. In the first experiment the mice were rotated (70 rpm, schedule of 15 sec on; 5 sec off) for 60 minutes or exposed to sham rotation for the same duration. Midway through the rotation or sham procedure the mice were either injected with naloxone (1 mg/kg) or isotonic saline. At the end of the 60-minute treatment period the animals were placed on a warm surface (47.5 degrees C) and their latency to show a foot-licking response was measured. The rotation procedure produced a significant (p less than 0.01) increase in response latency in the saline-injected mice and the naloxone injections blocked this analgesic effect. This finding provides evidence for opioid involvement in the rotation-induced analgesia. In Experiment 2 mice on a food restriction schedule were rotated (70 rpm, 15 sec on; 5 sec off) or sham exposed for 60 minutes. Midway through this treatment period the mice were either injected with naloxone (1 mg/kg) or isotonic saline. Following the treatment period the mice were given access to food for 2 hours. The rotation procedure produced a significant (p less than 0.01) reduction in feeding (anorexia) in the first 30 minutes of food access for the saline-injected mice. Injections of naloxone significantly (p less than 0.05) enhanced the rotation-induced anorexia. These experiments demonstrate that rotation-induced analgesia in mice is blocked by the opiate antagonist, naloxone, whereas rotation-induced anorexia is not.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Analgesia; Animals; Anorexia; Feeding and Eating Disorders; Feeding Behavior; Male; Mice; Motion Sickness; Naloxone; Rotation

The most common sign of febrile diseases is anorexia, which develops at a time when adequate caloric and micronutrient availability may be critical. In order to study the relationship of fever and anorexia, feed intake in dwarf goats was studied under conditions of fever and antipyresis. Furthermore, experiments were done to establish whether a feed intake stimulant would override the anorexia during febrile conditions. Infection with Ehrlichia phagocytophila and i.v. injection of Escherichia coli endotoxin (0(111) B4, 0.1 microgram/kg body weight) both resulted in increased rectal temperatures and significant reductions in feed intake. Administration of the antipyretic drug flurbiprofen (1 mg/kg) to febrile animals inhibited the temperature responses, but food intake was still suppressed. Diazepam (0.06 mg/kg), a feed intake stimulant, did not override the anorexia associated with fever. Blocking the febrile response of E. coli LPS-injected goats with flurbiprofen plus diazepam or with flurbiprofen plus naloxone (0.1 mg/kg) did not antagonise their reduced feed intake either. The effects of these drugs and of endotoxin on rumen motility adds an interesting aspect to their activities in the CNS, since the CNS has been shown to regulate various aspects of forestomach motility, which in turn could alter feeding behaviour. Moreover, our findings are consistent with the hypothesis that the suppression of feed intake might depend on the release of interleukin-1.

Topics: Animals; Anorexia; Diazepam; Drug Therapy, Combination; Eating; Ehrlichia; Endotoxins; Escherichia coli; Escherichia coli Infections; Female; Fever; Flurbiprofen; Goats; Male; Naloxone; Propionates; Rickettsiaceae Infections

Uremia results in a decrease in food intake. In the present study we investigated whether opiates known to stimulate feeding would alter food intake in rats made uremic by 1 and 5/6 nephrectomy. Morphine increased food intake in sham nephrectomized rats, but failed to alter food intake in uremic animals and depressed the ingestion of rat chow in a group of weight restricted rats. Butorphanol tartrate increased feeding in sham and uremic animals but did not alter intake in the weight restricted group. Higher doses of butorphanol were needed to stimulate feeding in the uremic rats compared to the sham group, suggesting a relative resistance to opioid-induced feeding in the uremic rats. The opiate antagonist, naloxone, suppressed food intake in the uremic and sham groups more effectively than in the weight restricted rats. These data suggest that the opioid feeding system functions in a reduced fashion in uremic rats, but probably is not the sole factor involved in producing the anorexia associated with uremia.

Topics: Animals; Anorexia; Body Weight; Butorphanol; Endorphins; Feeding Behavior; Male; Morphinans; Morphine; Naloxone; Rats; Rats, Inbred Strains; Uremia

Anorexia is a major symptom of zinc deficiency, but the mechanism(s) for this anorexia are poorly defined. Recent studies have suggested an integral role for endogenous opiate peptides in appetite regulation. Dynorphin, a leucine-enkephalin containing opiate peptide, is a potent inducer of spontaneous feeding. In this study we showed that zinc deficient animals were relatively resistant to dynorphin-induced feeding. Measurement of dynorphin levels using a highly sensitive radioimmunoassay showed that zinc deficient animals had lower levels of dynorphin in the hypothalamus than did ad lib fed animals, with weight restricted animals having intermediate values. [3H]-naloxone binding was significantly increased to isolated brain membranes from zinc deficient animals using 1 nM unlabeled naloxone when compared to ad lib fed controls with the weight restricted animals again having intermediate values. These data suggest that abnormalities in endogenous opiate regulation of appetite may well play a role in the anorexia of zinc deficiency. The effects of zinc deficiency on endogenous opiate action appear to include alterations in receptor affinity, a post-receptor defect and alterations in the synthesis and/or release of dynorphin.

Topics: Animals; Anorexia; Brain; Dynorphins; Eating; Endorphins; Feeding and Eating Disorders; Humans; Hypothalamus; Male; Naloxone; Peptide Fragments; Radioimmunoassay; Rats; Rats, Inbred Strains; Zinc

Experiments were conducted to determine the anorexigenic effects of ventromedial (VMH) and lateral hypothalamic (LH) injections of the mu-opiate receptor antagonists, naloxone and naltrexone, on food-deprived (20 h) rats. Lever pressing to obtain food pellets was measured in groups of hungry, male Sprague-Dawley rats following VMH, LH or subcutaneous (SC) injections of saline, naloxone or naltrexone. VMH injections of either narcotic antagonist (5 and 10 micrograms/microliter) and LH injections of naloxone (5 and 10 micrograms/microliter) decreased the total 90-min food intake, compared to saline controls, due to suppressed feeding especially during the initial 30-min interval. Rats given SC injections of naloxone (10 mg/kg) also decreased their food intake compared to amounts eaten after SC saline was given. Decrements in food consumption relative to saline controls were similar following VMH or LH administration of naloxone. Moreover, the anorexia observed following VMH naloxone administration was similar to that found after VMH injections of equal doses of naltrexone.

Topics: Animals; Anorexia; Eating; Food Deprivation; Hypothalamic Area, Lateral; Injections; Male; Naloxone; Naltrexone; Rats; Rats, Inbred Strains; Ventromedial Hypothalamic Nucleus

In two experiments observational analyses have been made of eating and other behaviours following naloxone administration. Naloxone produced a clearly defined profile of behavioural changes. Although rats became became more inactive it was demonstrated that this was not responsible for the inhibition of food intake. The drug reduced the latency to approach food and to initiate eating bouts. In addition, naloxone hastened the termination of eating in the test period. Therefore naloxone simultaneously increases one aspect of motivation for food, yet also promotes the onset of satiation. This profile of naloxone's anorexic action is quite different to that of traditional anorexic drugs such as amphetamine of fenfluramine. This dual action of naloxone, disclosed by these studies, may account for certain curious features of naloxone's effect on food intake.

Topics: Animals; Anorexia; Eating; Feeding Behavior; Grooming; Male; Motor Activity; Naloxone; Rats; Rats, Inbred Strains

Topics: Adolescent; Adult; Anorexia; Body Weight; Feeding and Eating Disorders; Female; Humans; Male; Naloxone; Naltrexone

The long-lasting opiate antagonist, naltrexone (NTX), was examined for its effects on various types of consummatory behavior in male golden hamsters and rats. Rat, but not hamster, 24 hr food and water intakes were significantly decreased by four daily NTX (10.0 mg/kg) injections. Hamsters displayed a minimal night to day feeding ratio compared to rats. Hamsters increased food intake following insulin (50 U/kg) administration, but not after 24 hr food deprivation (FD) or 2-deoxy-D-glucose (2-DG; 800 mg/kg) injections. NTX (1.0 and 10 mg/kg) had no effect on feeding, but markedly attenuated hamster drinking induced by 48 hr water deprivation or hypertonic saline injection. Dexamethasone (DEX), a glucocorticoid which depletes pituitary beta-endorphin and produces anorexia in rats, had no effect on daily hamster intake. Since the normal feeding profile of the hamster is similar to that of naloxone and DEX-treated rats, hamsters appear to lack an opiate-sensitive feeding system. In contrast, stimulated drinking behavior of hamsters operates through an opiate-sensitive mechanism. Thus, there are marked species differences concerning the involvement of endogenous opioids in consummatory behavior.

Topics: Animals; Anorexia; Cricetinae; Deoxyglucose; Dexamethasone; Drinking; Eating; Feeding Behavior; Food Deprivation; Insulin; Male; Mesocricetus; Naloxone; Naltrexone; Rats; Rats, Inbred Strains