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At least 145 records · Page 8Linked to original sources
PubMed1997

Na depletion-induced Na appetite of sheep is independent of brain angiotensin II.

Previous experiments indicated that the Na appetite of Na-deplete sheep is decreased by systemically administered captopril. The assumption that captopril does not readily cross the blood-brain barrier, lead to the conclusion that circulating ANG II acting in brain areas without a blood-brain barrier, i.e., circumventricular organs such as the subfornical organ or organum vasculosum of the lamina terminalis, contributes to Na appetite induced by Na depletion. The present experiments investigated the possibility that systemically administered captopril does, in fact, cross the blood-brain-barrier and thereby influence brain angiotensin II formation and that brain angiotensin II contributes to Na depletion-induced Na appetite of sheep. The results showed that systemically administered captopril blocked water intake caused by intracerebroventricular infusion of angiotensin I, and that Na depletion induced Na appetite was not decreased by intracerebroventricular infusion of various antagonists of the renin-angiotensin system. Thus, the results suggest that although captopril crosses the blood-brain-barrier and can influence the formation of brain angiotensin II, brain angiotensin II is not involved in the Na appetite of Na-deplete sheep.

Angiotensin II↗
PubMed1998

Increased appetite augments hypothalamic NPY Y1 receptor gene expression: effects of anorexigenic ciliary neurotropic factor.

Neuropeptide Y (NPY) is a potent endogenous appetite transducer but the NPY receptor subtype mediating the induction of appetite is unknown. Evaluation of hypothalamic NPY Y1 and Y5 receptor mRNA by RNase protection assay showed that appetite evoked either by fasting or food-restriction increased expression of Y1 mRNA. Suppression of appetite by the cytokine, ciliary neurotropic factor, blocked this increase in Y1 gene expression. In contrast Y5 mRNA levels were unchanged by these treatments. These findings suggest that NPY-induced stimulation of appetite requires signal transmission though Y1 receptor subtype in the hypothalamus.

Animals↗
PubMed2003

Agreement between weekly vs. daily assessment of appetite.

Hunger, satiation, and other aspects of appetite are frequently measured using end-anchored line ratings. This study investigated whether a single assessment of appetite, which covered the prior week, would yield the same results obtained by assessing appetite 3 days during the week. Participants were 51 women and 9 men (age mean 44.1, SD 9.8 years; BMI mean 38.0, SD 5.2 kg/m(2)) in a study evaluating the effectiveness of four weight control programs, three of which used sibutramine (15 mg/d). On three separate days of one week, participants rated appetite for that day. During a subsequent clinic visit, participants completed the same ratings in reference to the past week. The three daily values were averaged. All correlations between weekly and averaged daily values were strongly positive (r=0.63-0.80) and statistically significant (all p<0.001). All mean daily and weekly ratings fell within 3.3-7.2 mm of each other. Thus, good agreement was observed between the average daily assessments and one weekly assessment. The weekly assessment of appetite in the clinic appears to have several benefits, including uniformity of test administration and decreased burden on participants.

Adult↗
PubMed1988

Sodium appetite: species and strain differences and role of renin-angiotensin-aldosterone system.

The characteristics of the appetite for NaCl in humans differ in some aspects from those in other species. The mechanisms of appetite for NaCl have been studied in detail in two species, rats and sheep. We review the treatments known to induce an appetite for NaCl in rats, with special reference to differences among strains in their spontaneous preference for NaCl solution. The current view of the mechanism is critically appraised, with particular emphasis on the role of angiotensin II, mineralocorticoids, cerebroventricular sodium transport, and the relation between preference for NaCl and the concentration of sodium in saliva. The appetite for NaCl in rodents other than rats is considered next, and reveals that mice, hamsters and gerbils are reluctant to ingest NaCl either spontaneously or after treatment with several of the natriorexigenic stimuli that are effective in rats. The characteristics of the appetite for NaCl in non-rodent species, including sheep, rabbit, dog, and non-human primates, are then described. We discuss some of the possible differences in mechanism that might account for this behavioral diversity among species.

Animals↗
PubMed1987

Central inhibitory control of sodium appetite in rats: correlation with pituitary oxytocin secretion.

In the present experiments we examined neurohypophyseal hormone secretion in various models of sodium appetite in rats. Basal plasma levels of oxytocin were found to be low in sodium-deficient adrenalectomized rats and in intact animals treated daily with desoxycorticosterone acetate, both of which groups drank large amounts of NaCl solution, whereas basal plasma levels of arginine vasopressin were neither stimulated nor suppressed. Conversely, sodium appetite consistently was inhibited by treatments that stimulated pituitary oxytocin secretion. However, sodium appetite was not inhibited by administration of exogenous oxytocin, nor was it stimulated by administration of an oxytocin receptor antagonist. These and other results suggest that sodium appetite may be inhibited by activity in the supraoptic and/or paraventricular nuclei, the location of the neurons responsible for the synthesis of oxytocin, and can be stimulated only when activity in those neurons is reduced. Whatever the final neural pathway, our data support the hypothesis that the control of sodium appetite is governed by inhibitory as well as excitatory central mechanisms.

Adrenal Glands↗
PubMed1987

Salt appetite is enhanced by one prior episode of sodium depletion in the rat.

A single sodium depletion enhances the salt appetite that is expressed after a second and subsequent sodium depletions. The enhanced salt intake, as measured by a decrease in latency to drink and an increase in volume of 3% NaCl ingested, is not accounted for by an increased sodium loss. The enhanced salt intake occurs even when the interval between first and second depletion is as long as 4 months. The enhanced salt appetite does not depend on the drinking of salt after the animal's first sodium depletion and is specific for NaCl but not for KCl. Moreover, it can be produced without sodium depletion by the actions of the hormones aldosterone and angiotensin on the brain. These results suggest that angiotensin and aldosterone, which are released in response to sodium depletion, (a) increase renal sodium conservation, (b) evoke a salt appetite to restore the lost sodium, and (c) produce enduring changes in the brain that prepare it for more rapid and more vigorous expression of salt appetite in response to future sodium depletions. Thus the neural mechanisms that govern salt appetite are not only activated by the hormones of sodium conservation but appear also to be organized by them for a lifelong increase in avidity for salty substances.

Animals↗
PubMed1990

Amygdaloid complex lesions differentially affect retention of tasks using appetitive and aversive reinforcement.

The hypothesis that the amygdaloid complex (AC) is involved in the formation of stimulus-reward associations was examined. A series of experiments (1A-1C) directly compared the effects of lesions (produced by injection of the excitotoxin N-methyl-D-aspartic acid) on 1-trial appetitive and 1-trial aversive learning in rats. Experiments 1A and 1B, which used different degrees of reinforcement, revealed no effect of lesions on the appetitive task, whereas acquisition of the aversive task was significantly impaired. This impairment depended on the nature of the aversive reinforcement used: Impairment was seen when a highly aversive stimulus (footshock) was used but not when a less aversive stimulus (0.2% quinine solution) was used. Control experiments indicated that the effect of lesions was not due to reduced sensitivity to the foot-shock. In Experiment 2, a novel odor conditioning task examined further the effect of AC lesions on the acquisition of appetitive and aversive stimulus-reinforcement associations. As in Experiment 1, the AC lesions impaired learning of the aversive association but did not significantly influence the appetitive association. It is argued that, although the AC may be involved in some types of appetitively rewarded learning, the findings of a differential effect of AC lesions on aversively rewarded learning suggest a role in learning beyond the formation of stimulus-reinforcement associations.

Amygdala↗
PubMed1990

Salt appetite and lesions of the ventral part of the ventral median preoptic nucleus.

Angiotensin receptors in the most ventral part of the ventral median preoptic nucleus (VVMnPO) or organum vasculosum laminae terminalis appear to be important for salt appetite to angiotensin in rats. If so, then small lesions of this region should reduce salt appetite that is dependent on angiotensin. In separate experiments, the lesion greatly reduced salt appetite after treatments with chronic oral captopril or sodium depletion. On the other hand, the VVMnPO lesion actually enhanced salt appetite to deoxycorticosterone acetate. The lesion did not affect water intake to water deprivation, combined food-water deprivation, isoproterenol, or hypertonic saline, and basal plasma osmolality and sodium values were normal. These experiments suggest that VVMnPO lesions selectively affect angiotensin-induced salt appetite without producing the gross hydrational deficits that occur with larger lesions of the ventral forebrain.

Administration, Oral↗
PubMed1983

Thirst and sodium appetite after colloid treatment in rats: role of the renin-angiotensin-aldosterone system.

Recent experiments indicated that rats usually develop sodium appetite 5 hr after subcutaneous injection of polyethylene glycol (PEG) solution. However, sodium appetite appeared within 30 to 60 min if the rats had been maintained on sodium-deficient diet instead of Purina chow for 2-4 days previously. Elevated levels of aldosterone paralleled the appearance of NaCl consumption in both circumstances. In the present experiments, sodium appetite was no longer potentiated by pretreatment maintenance on sodium-deficient diet when the hypersecretion of aldosterone after PEG administration was prevented by prior hypophysectomy. Conversely, sodium appetite was enhanced in PEG-treated rats when angiotensin II (AII) was produced in unusually large amounts in the brain, owing to the systemic administration of captopril. This latter effect occurred even when drinking water was withheld and plasma sodium concentrations were markedly elevated. These and other findings raise the possibility that the normal secretion of aldosterone in rats after PEG treatment might permit physiological amounts of AII to be effective in stimulating sodium appetite. Such actions would complement the accepted physiological role of the renin-angiotension-aldosterone system in the maintenance of blood pressure and sodium balance.

Aldosterone↗
PubMed2001

Anandamide administration into the ventromedial hypothalamus stimulates appetite in rats.

This investigation reports the possible role of the endocannabinoid anandamide in modulating appetitive behaviour. Given that cannabinoids have been used clinically to stimulate appetite in HIV and cancer chemotherapy patients, there has been a renewed interest in the involvement of cannabinoids in appetite modulation. This is the first report on the administration of anandamide into the ventromedial hypothalamus. Pre-satiated rats received an intrahypothalamic injection of anandamide (50 ng x 0.5 microl(-1)) followed by measurement of food intake at 3 h post injection. Administration of anandamide induced significant hyperphagia. Pretreatment with the selective CB1 cannabinoid antagonist SR 141716 (30 microg x 0.5 microl(-1)), 30 min prior to anandamide injection resulted in an attenuation of the anandamide-induced hyperphagia (P<0.001). This study demonstrates that intrahypothalamic anandamide initiates appetite by stimulation of CB1 receptors, thus providing evidence on the involvement of hypothalamic endocannabinoids in appetite initiation.

Animals↗
PubMed2004

Relation between food intake and visual analogue scale ratings of appetite and other sensations in healthy older and young subjects.

OBJECTIVE: Visual analogue scales are widely used in appetite research, yet the validity of these scales to evaluate appetite and mood has not been assessed in older subjects. The aim of this study was to determine the relations between food intake and visual analogue scale (VAS) ratings of appetite and nonappetite sensations in healthy older and young subjects. DESIGN: Retrospective combined analysis of four single-blind, randomised, controlled appetite studies. SETTING: All studies were conducted in the University of Adelaide, Department of Medicine, Adelaide, Australia. SUBJECTS: A total of 45 healthy young men (n=24) and women (n=21) aged 18-35 y and 45 healthy older men (n=24) and women (n=21) aged 65-85 y were recruited by advertisement. INTERVENTIONS: Oral, intraduodenal or intravenous administration of treatments which suppressed food intake were compared to control. Up to 90 min after treatment, a test meal was offered and subjects ate freely for between 30 and 60 min. Perceptions were assessed by 100-mm visual analogue scales administered at regular intervals. RESULTS: Food intake at the test meal was positively related to perceptions of hunger, drowsiness, and calmness at both baseline and premeal (r>0.16, P<0.05), and inversely related to premeal ratings of fullness (r> 0.2, P<0.05) in both older and young subjects. Food intake was related to VAS ratings at least as strongly, if not more so, in older as in young subjects. CONCLUSIONS: These observations (i) confirm that food intake is related to perceptions of hunger and fullness as assessed by VAS in healthy older and young subjects, and (ii) suggest that sensations, not obviously associated with appetite, including 'drowsiness' and 'calmness', are also associated with food intake.

Adolescent↗
PubMed2002

Appetite suppression based on selective inhibition of NPY receptors.

AIM: The aim of this review is to critically assess available evidence that blockade of the actions of NPY at one of the five NPY receptor subtypes represents an attractive new drug discovery target for the development of an appetite suppressant drug. RESULTS: Blockade of the central actions of NPY using anti-NPY antibodies, antisense oligodeoxynucleotides against NPY and NPY receptor antagonists results in a decrease in food intake in energy-deprived animals. These results appear to show that endogenous NPY plays a role in the control of appetite. The fact that NPY receptors exist as at least five different subtypes raises the possibility that the actions of endogenous NPY on food intake can be adequately dissociated from other effects of the peptide. Current drug discovery has produced a number of highly selective NPY receptor antagonists which have been used to establish the NPY Y(1) receptor subtype as the most critical in regulating short-term food intake. However, additional studies are now needed to more clearly define the relative contribution of NPY acting through the NPY Y2 and NPY Y5 receptors in the complex sequence of physiological and behavioral events that underlie the long-term control of appetite. CONCLUSIONS: Blockade of the NPY receptor may produce appetite-suppressing drugs. However, it is too early to state with certainty whether a single subtype selective drug used alone or a combination of NPY receptor selective antagonists used in combination will be necessary to adequately influence appetite regulation.

Animals↗
PubMed2003

Effect of sensory perception of foods on appetite and food intake: a review of studies on humans.

OBJECTIVE: How much do the sensory properties of food influence the way people select their food and how much they eat? The objective of this paper is to review results from studies investigating the link between the sensory perception of food and human appetite regulation. CONTENT OF THE REVIEW: The influence of palatability on appetite and food intake in humans has been investigated in several studies. All reviewed studies have shown increased intake as palatability increased, whereas assessments of the effect of palatability using measures of subjective appetite sensations have shown diverging results, for example, subjects either feel more hungry and less full after a palatable meal compared to a less palatable meal, or they feel the opposite, or there is no difference. Whether palatability has an effect on appetite in the period following consumption of a test meal is unclear. Several studies have investigated which sensory properties of food are involved in sensory-specific satiety. Taste, smell, texture and appearance-specific satieties have been identified, whereas studies on the role of macronutrients and the energy content of the food in sensory-specific satiety have given equivocal results. Different studies have shown that macronutrients and energy content play a role in sensory-specific satiety or that macronutrients and energy content are not a factor in sensory-specific satiety. Sensory-specific satiety may have an important influence on the amount of food eaten. Studies have shown that increasing the food variety can increase food and energy intake and in the short to medium term alter energy balance. Further knowledge about the importance of flavour in appetite regulation is needed, for example, which flavour combinations improve satiety most, the possible connection between flavour intensity and satiety, the effect of persistence of chemesthetic sensation on palatability and satiety, and to what extent genetic variation in taste sensitivity and perception influences dietary habits and weight control.

Appetite↗
PubMed2006

Effects of peanut oil consumption on appetite and food choice.

OBJECTIVE: Peanut consumption may improve lipid profiles without promoting weight gain. Both properties have been attributed to their high-unsaturated fat content. Mono and polyunsaturated fatty acids reportedly hold stronger satiety value than saturated fats and may help appetite control. This study investigated the effects of chronic peanut oil consumption on appetite and food choice. RESEARCH METHODS AND PROCEDURES: A total of 129 healthy adults from three countries (Brazil, Ghana and US) were randomly assigned to one of four treatment arms: consumption of peanut oil, olive oil or safflower oil as 30% of individual resting energy expenditure (REE) for 8 weeks or no dietary intervention. Participants received no other dietary guidance. They completed appetite questionnaires eliciting information about hunger, fullness, desire to eat, and prospective consumption during all waking hours for 1 day at weeks 2 and 6 and for 1 or 3 days at weeks 0, 4 and 8. Diet records were completed at weeks 0, 4 and 8. RESULTS: No differences in appetitive ratings were observed over the 8-week trial. There were no significant treatment by time interactions. Total caloric intake was significantly higher at week 8 relative to baseline (F=10.08, P<0.05). The increases for each treatment were: peanut oil=197+/-114; olive oil=237+/-121; safflower oil=274+/-90; control=75+/-71. Free-feeding intake, an index of dietary compensation, was reduced significantly at weeks 4 and 8 compared to baseline (F=9.08, P<0.00). The declines (compensation scores) were (kcals): peanut oil=-208+/-105 (46%); olive oil=-235+/-105 (50%); safflower oil=-186+/-102 (44%). There were no significant differences across countries in appetite ratings. DISCUSSION: A prior intervention with whole peanuts reported a dietary compensation score of 66% over 8 weeks, this compares to a 46% compensation score observed with peanut oil. Our data suggests that the lipid fraction in peanuts elicits a weak effect on satiety.

Adult↗
PubMed2006

The effect of a medium-term activity- and diet-induced energy deficit on subjective appetite sensations in obese children.

OBJECTIVE: To assess the subjective appetite responses to an imposed activity- and diet-induced energy deficit during a residential intervention programme for obese children. DESIGN: A 6-week intervention of fixed, reduced dietary intake and 6 h/day of skill-based physical activity while resident in a weight loss camp. SUBJECTS: Thirty-eight obese (mean body mass index (BMI)=34.9 kg m(-2)) boys and girls (mean age 13.9+/-1.57). MEASUREMENTS: An electronic appetite rating system (EARS) was used to periodically measure subjective appetite sensations at the start (WK1) and at the end (WK6) of the camp. Subjective ratings of hunger and fullness were compared at the start and end of 6 weeks of an activity- and diet-induced-based weight loss intervention. RESULTS: At the end of the 6 weeks, the children had lost 8.4 kg in body mass. The diurnal profiles of subjective appetite sensations demonstrated clear oscillations in hunger and fullness. There was a significant increase in hunger (P<0.0001) and decrease in fullness (P<0.005) at the end (WK6) of the medium-term energy deficit. In WK6, morning ratings of hunger were higher than in WK1 (P<0.005) and the fixed energy evening meal induced a lower suppression of hunger (P<0.02). CONCLUSION: A programme of fixed, reduced-dietary intake combined with an activity and behavioural programme was successful at inducing a significant reduction in body mass in obese children. Subjective sensations of appetite were sensitive to a medium-term negative energy balance and weight loss. These data are essential as we continue to evolve methods of treatment for overweight and obese children.

Adolescent↗
PubMed2001

Effect of vanadium on insulin sensitivity and appetite.

Vanadium, a potent nonselective inhibitor of protein tyrosine phosphatases, has been shown to mimic many of the metabolic actions of insulin both in vivo and in vitro. The mechanism(s) of the effect of vanadium on the decrease in appetite and body weight in Zucker fa/fa rats, an insulin-resistant model, is still unclear. Because insulin may inhibit hypothalamic neuropeptide Y (NPY), which is known to be related to appetite, and increase leptin secretion in adipose tissue, we studied the possibility that the changes in appetite produced by vanadium may be linked to altered NPY levels in the hypothalamus. We also examined effects of vanadium on leptin. Zucker lean and fatty rats were chronically treated with bis(maltolato)oxovanadium(IV) (BMOV), an organic vanadium compound, in the drinking water. Plasma and adipose tissue leptin levels were measured by radioimmunoassay and immunoblotting, respectively. Hypothalamic NPY mRNA and peptide levels were measured using in situ hybridization and immunocytochemistry, respectively. BMOV treatment significantly reduced food intake, body fat, body weight, plasma insulin levels, and glucose levels in fatty Zucker rats. Fifteen minutes after insulin injection (5 U/kg, intravenous [IV]), circulating leptin levels (+100%) and adipose leptin levels (+60%) were elevated in BMOV-treated fatty rats, although these effects were not observed in untreated fatty rats. NPY mRNA levels in the arcuate nucleus (ARC) (-29%), NPY peptide levels in ARC (-31%), as well as in the paraventricular nucleus (PVN) (-37%) were decreased with BMOV treatment in these fatty rats. These data indicate that BMOV may increase insulin sensitivity in adipose tissue and decrease appetite and body fat by decreasing NPY levels in the hypothalamus. BMOV-induced reduction in appetite and weight gain along with normalized insulin levels in models of obesity, suggest its possible use as a therapeutic agent in obesity.

Adipose Tissue↗
PubMed1998

A population-based study of appetite-suppressant drugs and the risk of cardiac-valve regurgitation.

BACKGROUND: Recent case reports suggest that a combination of the appetite suppressants fenfluramine and phentermine is associated with an increased risk of cardiac-valve regurgitation. There are also reports of valvular disorders in persons taking fenfluramine or dexfenfluramine alone, particularly for more than three months. METHODS: We conducted a population-based follow-up study and a nested case-control analysis of 6532 subjects who received dexfenfluramine, 2371 who received fenfluramine, and 862 who received phentermine to assess the risk of a subsequent clinical diagnosis of a valvular disorder of uncertain origin. For comparison, we identified a group of 9281 obese subjects who had not taken appetite suppressants who were matched to the treated subjects for age, sex, and weight. All subjects were free of diagnosed cardiovascular disease at the start of follow-up. The average duration of follow-up for all subjects was about four years. RESULTS: There were 11 cases of newly diagnosed idiopathic valvular disorders, 5 after the use of dexfenfluramine and 6 after the use of fenfluramine. There were six cases of aortic regurgitation, two cases of mitral regurgitation, and three cases of combined aortic and mitral regurgitation. There were no cases of idiopathic cardiac-valve abnormalities among the subjects who had not taken appetite suppressants or among those who took only phentermine. The five-year cumulative incidence of idiopathic cardiac-valve disorders was 0 per 10,000 subjects among those who had not taken appetite suppressants (95 percent confidence interval, 0 to 15.4) and among those who took phentermine alone (95 percent confidence interval, 0 to 76.6), 7.1 per 10,000 subjects among those who took either fenfluramine or dexfenfluramine for less than four months (95 percent confidence interval, 3.6 to 17.8; P=0.02 for the comparison with subjects who had not taken appetite suppressants), and 35.0 per 10,000 subjects among those who received either of these medications for four or more months (95 percent confidence interval, 16.4 to 76.2; P<0.001). CONCLUSIONS: The use of fenfluramine or dexfenfluramine, particularly for four months or longer, is associated with an increased risk of newly diagnosed cardiac-valve disorders, particularly aortic regurgitation.

Adult↗
PubMed1993

Central oxytocin inhibition of salt appetite in rats: evidence for differential sensing of plasma sodium and osmolality.

Sodium chloride ingestion is stimulated during conditions of sodium deficiency to maintain body fluid and electrolyte balance. Recent studies have indicated that salt appetite in rats is often inversely related to peripheral and central secretion of the hormone oxytocin (OT). We studied the potential role of central OT on salt and water ingestion by treating rats intracerebroventricularly with OT conjugated to the A chain of the plant cytotoxin ricin (rAOT) to produce a chronic selective inactivation of brain cells containing OT-receptive elements. The rats treated with rAOT and control rats treated with the ricin A chain alone were given 5-hr two-bottle (water and 0.5 M NaCl) drinking tests 30 min after they were made hyperosmolar by injections of hypertonic (2M) mannitol solution, which elevated plasma osmolality but reduced plasma Na+ concentration. In the control rats only water intake was stimulated in response to the induced hyperosmolality, but in the rAOT-treated rats hypertonic mannitol caused a robust salt appetite as well as thirst. Analogous results were obtained in rats treated with two different OT-receptor antagonists prior to induction of hyperosmolality with mannitol. In contrast to these results, when hyperosmolality was induced by administration of equivalently hypertonic (1M) NaCl, which elevated both plasma osmolality and plasma Na+ concentration, only water intake but not salt intake was stimulated in both control and OT-receptor antagonist-treated rats. When salt appetite was stimulated by the physiological stimulus of polyethylene glycol-induced hypovolemia, hypertonic mannitol similarly inhibited salt ingestion in control animals but not in rAOT-treated rats, whereas hypertonic NaCl inhibited subsequent salt ingestion in both groups. These results suggest that salt appetite is regulated by both Na(+)- and osmolality-sensing mechanisms in rats. In addition, they indicate that central OT likely mediates a significant component of osmolality-related inhibition of salt appetite but does not appear to be essential for Na(+)-related inhibition of this important homeostatic behavior.

Animals↗