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At least 343 records · Page 19Linked to original sources
PubMed1987

Appetite and food preference in depression: effects of imipramine treatment.

A nutritional survey, the Pittsburgh Appetite Test (PAT), was developed to study potential changes in appetite and food preference reported by patients during a depressive episode and during antidepressant treatment. We examined a group of 50 depressed outpatients who were drug-free for 2 weeks prior to treatment with imipramine and psychotherapy for 4 months. A significant increase in the desire for "sweets" (carbohydrate--fat-rich foods) was observed during a depressive episode, compared to periods when patients recalled feeling well (retrospective data). During imipramine treatment, no further changes were observed in preference for either "sweets" or carbohydrates when compared to the medication-free period. Alterations in patient self-reports of appetite and body weight change were noted during imipramine treatment.

Adult↗
PubMed1993

Medial region of the amygdala: involvement in adrenal-steroid-induced salt appetite.

We report the following observations: first that cell body damage induced by ibotenic acid within the medial region of the amygdala resulted in the abolition of corticosterone-potentiated, aldosterone-induced salt appetite. Sodium depletion-induced salt appetite was not impaired by the lesion, nor was angiotensin-dependent salt appetite via captopril treatment. These results provide evidence that the medial region of the amygdala has a major role in the natriorexigenic effects of the adrenal steroids.

Aldosterone↗
PubMed1994

Role of the central nucleus of the amygdala and bed nucleus of the stria terminalis in experimentally-induced salt appetite.

The contributions of the central nucleus of the amygdala (CeA) and the bed nucleus of the stria terminalis (BST) to salt appetite were evaluated with two treatments which induce sodium chloride (NaCl) ingestion. Cumulative 3 h intakes of 2% NaCl after sodium depletion using furosemide, or subcutaneous (s.c.) injections of yohimbine (YOH), were measured in male, Sprague-Dawley rats both before and after electrolytic lesions of the CeA or the BST. Before surgery, sham-lesion and lesion groups drank equivalent amounts of 2% NaCl in response to furosemide depletion and YOH treatment. After surgery, rats with sham lesions increased their intakes of 2% NaCl following YOH while rats with CeA or BST lesions showed significant decreases. Rats with CeA or BST lesions also showed significant decreases in their intake of 2% NaCl after furosemide depletion, while intakes of the sham lesion groups remained unchanged. Lesions of either nucleus virtually eliminated 24 h need-free salt intake. Before and after surgery, all groups drank equivalent amounts of water in response to s.c. angiotensin II and to s.c. hypertonic saline, indicating the lesions specifically affected salt appetite. The results indicate that the CeA and the BST may be important sites for processing inputs mediating salt appetite.

Amygdala↗
PubMed1980

Geriatric nutrition: the role of taste and smell in appetite.

Proper nutrition is essential to the health of the oral tissues, and healthy tissues enhance prosthodontic treatment of the elderly. All dentists should be prepared to offer dietary advice to this expanding population. Taste and smell are essential to proper nutrition. In the elderly the peripheral sensory receptors decline, causing the appetite to wane. Taste and aroma are inextricably intertwined in determining the palatability and acceptance of food. For example, during an upper respiratory infection, the olfactory receptors are blocked. Food becomes tasteless; it loses both flavor and aroma and the appetite declines. As a result of aging, the taste buds on the tongue and the olfactory receptors in the roof of the nasal cavity regress. In addition, the gustatory and olfactory nuclei in the brain decline, causing a reduction in appetite and diet.

Aged↗
PubMed1984

The failure of ventricular sodium to control sodium appetite in the rat.

Dilution of CSF sodium by infusion of hyperosmotic mannitol into the cerebral ventricles of the rat does not evoke a salt appetite, nor does the addition of sodium to the CSF of the rat suppress the preexisting salt appetites produced by the hormones of sodium conservation or by adrenalectomy. CSF sodium concentration does not control sodium appetite in the rat. The proposal that it does so in sheep should not be generalized to other species without caution.

Adrenal Glands↗
PubMed1990

Thirst and sodium appetite in Dahl rats.

In confirmation of a previous study, rats of the Dahl S and R sublines exhibited no spontaneous preference for dilute NaCl solutions and an aversion for isotonic and hypertonic NaCl solutions when they were offered in a 2-bottle choice with water. A hysteresis effect was observed when choice was offered between water and a descending series of concentrations of NaCl solution compared with a preceding increasing series. In response to either chronic dietary administration of an angiotensin I converting enzyme inhibitor (ACEI) or acute sodium depletion, rats of the R subline developed a strong NaCl appetite, but the S subline did not. In contrast, rats of both sublines showed an NaCl appetite in response to a regimen of deoxycorticosterone acetate (DOCA). In acute drinking tests, rats of the S subline drank less water than those of the R subline in response to administration of either isoproterenol, ACEIs, or hypovolemia. Both R and S sublines drank similar amounts of water after SC administration of angiotensins I and II, and hypertonic NaCl. Compared with R rats, S rats had lower plasma renin activity in several of the above conditions, and their decreased thirst and sodium appetite appears to be a direct result of an underactive renin-angiotensin system.

Animals↗
PubMed1990

Umami and appetite: effects of monosodium glutamate on hunger and food intake in human subjects.

Subjects consumed soup (beef consomme) preloads of a fixed size containing different concentrations of monosodium L-glutamate (MSG). Effects on appetite following these preloads, and when no soup was consumed, were assessed in 3 studies. The soups supplemented with MSG were rated as more "pleasant," more "savoury" and more "satisfying" than soup with no added MSG. Compared with the no preload condition, consumption of the soups initially reduced appetitive motivational ratings and increased fullness ratings, but did not alter food intake in a test meal begun either 2 or 30 minutes later. This immediate inhibition of subjective motivation to eat was unaffected by MSG concentration. The failure of the soups to reduce subsequent food intake is presumably due to their low energy content (less than 10 kcal) and indicates that sensory stimulation alone is insufficient to reduce appetite. Indeed, the most important finding concerning MSG showed that motivation to eat recovered more rapidly following a lunchtime meal in which MSG-supplemented soup was served as the first course (compared both with the effect of unsupplemented soup and no preload). It is suggested tentatively that MSG through its stimulation of orosensory receptors and/or by improving the palatability of the soup may have influenced the metabolic disposal of nutrients consumed in the previous meal.

Adult↗
PubMed1992

Salt appetite induced by DOCA treatment or adrenalectomy in rats: analysis of ingestive behavior.

A detailed description of the increased intake of 0.5 M NaCl solution by rats after systemic treatment with desoxycorticosterone acetate (DOCA) or after adrenalectomy was obtained by measuring feeding and drinking activity every 6 s for 23 h. In both models of salt appetite, the induced increase in saline intake occurred mostly at night and in close temporal association with bouts of eating and water drinking rather than in isolation. Consequently, there was no significant change in the total number of ingestive episodes, despite the substantial increase in the number of saline bouts. Saline drinking was in small draughts that usually were preceded by food bouts and followed promptly by water bouts. These and other observations indicate that under standard maintenance conditions of ad lib access to food and fluids, adrenalectomy and DOCA treatment each produce a relatively weak stimulus of salt appetite, and large daily intakes accrue because the animals do not remain satiated and the appetite recurs repeatedly.

Adrenal Glands↗
PubMed1994

Physiological correlates of attenuated salt appetite in Fischer 344 rats.

Dietary NaCl deprivation stimulates a robust salt appetite in Wistar rats but has little influence on this behavior in rats of the Fischer 344 (F344) strain. To examine physiological substrates of attenuated salt appetite in F344 rats, several pertinent measures of renal function and fluid homeostasis were made in Wistar and F344 rats eating normal and NaCl-deplete diets. Physiological adjustments to NaCl deprivation were similar between the two strains; however, F344 rats showed smaller increases in plasma renin activity (PRA) than their Wistar counterparts. In addition, F344s decreased urinary sodium excretion more rapidly than Wistar rats in response to deprivation. The present studies also revealed several strain differences in baseline fluid and electrolyte regulation. Relative to the Wistar strain, F344 rats were characterized by high baseline PRA, increased arginine vasopressin (AVP) excretion, decreased urine volume, and diminished thirst. We propose that AVP and oxytocin activation may reduce salt preference and suppress the development of salt appetite in F344 rats.

Animals↗
PubMed1994

Serotoninergic modulation of sodium appetite in the rat.

There are two mechanisms leading to an enhancement of salt intake: one is induced by a sodium deficit and the other is need-free. The serotonin involvement in need-induced and/or need-free sodium appetite is interesting to consider because related drugs are already used against another cardiovascular risk factor, obesity. The effect of dexfenfluramine (1.5 or 3 mg/kg), an anorectic drug enhancing 5-HT transmission, and of metergoline (2 or 4 mg/kg), a 5-HT antagonist, was assessed in need-induced (depletion-induced), subsequent need-free, and spontaneous sodium appetite. Dexfenfluramine (3 mg/kg) decreased by 75% to 90% the depletion-induced intake of an aversive 3% NaCl solution, as well as the spontaneous intake of a less aversive 1.8% NaCl solution. Water intake was not diminished under these conditions. Metergoline significantly increased salt intake in need-free conditions in rats with either a history of three previous depletions or not. These results confirm the involvement of serotonin in sodium appetite and extend this involvement to both need-induced (natriorexis) and need-free (natriophilia) conditions. The metergoline experiments also suggest that 5-HT exerts a tonic inhibition on salt intake.

Animals↗
PubMed1996

Effects of beta-CCE on retention of aversively- and appetitively-motivated tasks in rats.

Beta-carboline-3-carboxylic acid ethyl ester (beta-CCE; 1.0 or 5.0 mg/kg, i.p.) or vehicle control was administered to male Sprague-Dawley rats immediately after training in an aversively- or appetitively-motivated task. Aversively-motivated training consisted of a one-trial step-though inhibitory (passive) avoidance task with a 0.6 mA, 1.0 s foot shock. Retention was tested 21 days after training. The 5.0 mg/kg dose of beta-CCE significantly enhanced retention performance in the inhibitory avoidance task compared to the vehicle control. For appetitive training, the animals learned a T-maze for water reward. Retention was tested 48 h later, and neither dose of beta-CCE was found to affect retention performance. These results suggest that beta-CCE, when administered immediately after training, may alter retention performance of an aversively-motivated task but not an appetitive task.

Animals↗
PubMed1982

The effects of chronic administration of naltrexone on appetite and water exchange in rats.

The effects of chronic administration of naltrexone (200 microgram/kg/hr) on appetitive behaviors and renal water and electrolyte excretions were studied in rats. Naltrexone reduced food and water intake, the renal excretions of water and electrolyte excretions were studied in rats. Naltrexone reduced food and water intake, the renal excretions of water and electrolytes, and osmolar clearance. No changes in plasma levels of electrolytes, plasma and urine Na+-K+ ratios, hematocrit ratio, plasma osmolality, the clearances of K+ and Na+, and the reabsorption of solute free water were found. The changes in appetite were compensated for by appropriate changes in renal excretions, resulting in no change in electrolyte balance or water exchange. These observations are discussed in relation to current theories of the role of endorphins in appetite control.

Animals↗
PubMed1991

Pharmacological approaches to appetite suppression.

It is relatively easy to demonstrate drug-induced anorexia in animals, but the significance of-such suppression of eating is often doubtful. Of the many agents shown to be 'active' in animals, only a very few are genuine appetite suppressants with clinical potential. Drugs that increase central 5-HT levels, or that activate peripherally acting peptides, are currently among the most promising candidates. John Blundell advocates a systems approach to the study of appetite control. Drug-induced changes in feeding should be interpreted according to a system which involves behaviour, peripheral physiology and brain neural pathways. Appetite involves more than alterations of food intake; the concept should take into account changes in hunger, food preferences, responses to taste and changes in macronutrient preferences.

Animals↗
PubMed1994

The involvement of nucleus accumbens dopamine in appetitive and aversive motivation.

In recent years, considerable emphasis has been placed upon the putative role of nucleus accumbens dopamine systems in appetitive motivation and positive reinforcement. However, considerable evidence indicates that brain dopamine in general, and nucleus accumbens dopamine in particular, is involved in aspects of aversive motivation. Administration of dopamine antagonists or localized interference with nucleus accumbens dopamine systems has been shown to disrupt active avoidance behavior. In addition, accumbens dopamine release and metabolism is activated by a wide variety of stressful conditions. A review of the literature indicates that there are substantial similarities between the characteristics of dopaminergic involvement in appetitive and aversive motivation. There is conflicting evidence about the role of dopamine in emotion, and little evidence to suggest that the profound and consistent changes in instrumental behavior produced by interference with DA systems are due to direct dopaminergic mediation of positive affective responses such as hedonia. It is suggested that nucleus accumbens dopamine is involved in aspects of sensorimotor functions that are involved in both appetitive and aversive motivation.

Animals↗
PubMed1990

Peripheral angiotensin II is not the cause of sodium appetite in the rat.

Activation of the renin-angiotensin system has been shown to arouse both water and sodium intake in the rat. The following experiments examine the contributions of the peripheral and central renin-angiotensin systems to the expression of sodium appetite in the adrenal-intact rat. Firstly, we find that, unlike intracerebroventricular angiotensin II, intravenous administration of the hormone at dipsogenic doses does not arouse sodium intake in the sodium replete rat when given alone or in combination with systemic mineralocorticoid pretreatment. Secondly, in the sodium depleted rat, we find that interference with central, but not peripheral, angiotensin II action suppresses sodium appetite. Together, these data confirm recent evidence which demonstrates that it is angiotensin II of cerebral origin, not angiotensin II of renal origin, that is necessary for the expression of sodium appetite.

Angiotensin II↗
PubMedDate not supplied

Dynorphin(1-13) impairs memory formation for aversive and appetitive learning in chicks.

The opioid peptide dynorphin(1-13) impairs memory formation in chicks (5). We examined whether this occurs for both aversively and appetitively motivated learning. Four-day-old chicks were injected with dynorphin(1-13) into the intermediate medial hyperstriatum ventrale and trained on either a peck avoidance (PA) or an appetitive discrimination (AD) task; 2-day-old chicks were trained on PA. In 2-day-old chicks, dynorphin was amnestic for PA at 0.01, 0.03, or 0.1 mM. In 4-day-old chicks, dynorphin impaired memory formation for PA at 0.1 mM, and for AD training at 0.03 mM. Thus, similar doses of dynorphin impair memory formation for both appetitive and aversive conditioning.

Animals↗
PubMed2006

Intravenous angiotensin and salt appetite in rats.

Circulating angiotensin II is crucial for the activation of salt appetite after sodium depletion. We tested if angiotensin (ANG) II infused intravenously at 50 ng/kg/min overnight (chronic) can mimic the rapid salt appetite similar to furosemide and overnight sodium depletion. In experiment 1, rats received chronic ANG II or vehicle infusions all night with access to water and chow but no saline solution. In the morning, the infusions continued, but half of the vehicle-infused group was switched to ANG II (acute). Thirty minutes after the switch, all rats received 10 mg/kg furosemide SC. One hour later they were provided water and 0.3 M NaCl to drink. Rats infused with vehicle or acute ANG drank little, but the chronic ANG group drank 11+/-1 ml of saline in 90 min. In experiment 2, the furosemide was omitted, and a group receiving a chronic infusion of phenylephrine at 6.25 microg/kg/min was included. The chronic ANG group drank 10+/-1 ml saline in 90 min, but the phenylephrine group, which also incurred a significant negative sodium balance overnight, drank little. Thus, an overnight infusion of ANG II is sufficient to mimic the robust expression of salt appetite as observed after furosemide and overnight sodium depletion.

Angiotensin II↗
PubMed2006

Influence of sweetened chewing gum on appetite, meal patterning and energy intake.

The concurrent increases of snacking and obesity suggest the possibility for some form of inter-meal oral stimulation with high satiety value to moderate rising obesity rates. This study explored the influence of sweetened chewing gum on appetitive ratings, meal patterning and food intake. Three test conditions were imposed after a fixed lunch preload: no gum chewing, gum chewing 2 h after lunch and gum chewing when hungry. Forty-seven participants, 29 males and 18 females, completed each treatment, one day a week for three weeks. Participants were fed lunch in a laboratory setting, and after being instructed on that day's test procedures, they were allowed to leave the laboratory. Throughout the remainder of the day, appetitive, mood and intake data were self-reported. The results indicate appetite ratings, meal patterning and food intake do not differ among the three treatment conditions. While these results did not support an effect of brief chewing of a sweetened gum, further exploration of variations of the sensory properties of gum and exposure patterns may still prove worthwhile.

Adolescent↗