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At least 721 records · Page 40Linked to original sources
PubMed2000

Delayed onset of pulmonary hypertension associated with an appetite suppressant, mazindol: a case report.

The use of the appetite suppressant agents aminorex and fenfluramine derivatives has been reported as a risk factor for the development of pulmonary hypertension. A 29-year-old female developed pulmonary hypertension suspected to be due to an amphetamine-like appetite suppressant agent, mazindol ((+/-)-5-(p-chlorophenyl)-2,5-dihydro-3H-imidazo [2,1-a] isoindol-5-ol). She was admitted to Sapporo Medical University Hospital with dyspnea due to severe pulmonary hypertension. Twelve months prior to admission, she had taken mazindol continuously for a period of 10 weeks. As yet, her pulmonary hypertension has not completely improved. This is the first reported case of mazindol-associated pulmonary hypertension, which developed after a long latent interval, and it suggests that mazindol is also a risk factor for the development of pulmonary hypertension, making long-term follow-up necessary for patients taking this anorectic agent.

Adult↗
PubMed2006

Pork peptone stimulates cholecystokinin secretion from enteroendocrine cells and suppresses appetite in rats.

We found that soybean beta-conglycinin peptone (BconP) suppresses food intake through cholecystokinin (CCK) release from enteroendocrine cells in association with binding of the peptone to rat small intestinal brush border membrane (BBM). The aim of the present study was to find new appetite suppressing peptides. Peptones from chicken, pork, beef, beef liver, and egg white were examined for activities to bind with rat BBM, CCK-release from enteroendocrine cell line STC-1, and induce satiety in rats. Chicken and pork peptone (ChickP and PorkP) bound to BBM with highest ability as evaluated with a surface plasmon biosensor. PorkP and ChickP released CCK in higher amounts than BconP from STC-1 cells dose-dependently, with highest stimulation by PorkP. An orogastric preload of PorkP, but not ChickP, suppressed food intake similarly to BconP, dose-dependently. These results suggest that PorkP interacts directly with the small intestinal CCK cells to release CCK, and that it suppresses appetite in rats.

Animals↗
PubMed2005

Cholinergic modulation of appetite-related synapses in mouse lateral hypothalamic slice.

Nicotine administration reduces appetite and alters feeding patterns; a major deterrent to smoking cessation is hyperphagia and resultant weight gain. We demonstrate here that lateral hypothalamic (LH) circuits involving melanin-concentrating hormone (MCH) neurons are subject to cholinergic modulation that may be related to the effects of nicotine on appetite control. Cholinergic input to the perifornical LH area of the mouse is confirmed by examination of immunostaining for vesicular acetylcholine (ACh) transporter (VAT) in conjunction with antibodies to MCH and the vesicular GABA transporter (vGABAT). vAChT-positive neurons border the LH, and VAT-positive projections are detected throughout the perifornical area. MCH-positive dendrites appear studded with vGABAT-positive contacts, consistent with recordings of GABAergic inputs to LH/MCH neurons identified by their location, morphology, electrophysiological profile, and MCH expression. Activation of presynaptic nicotinic ACh receptors (nAChRs) enhances GABAergic transmission. GABAergic transmission is potentiated by (1) direct nicotine application, (2) increasing local ACh concentration, and (3) stimulation of cholinergic projections. Based on pharmacological studies and comparisons of wild-type versus alpha7 nAChR subunit mutant mice, we propose that alpha7*-nAChRs are required for the modulation of GABAergic inputs in LH. Prenatal exposure to nicotine elicits a persistent elevation of GABAergic transmission in the LH of postnatal pups. Furthermore, GABAergic inputs to LH of prenatal nicotine-exposed pups are insensitive to subsequent nicotine challenge. Our studies support the hypothesis that nicotine administration or elevated cholinergic tone enhance inhibition of perifonical LH/MCH neurons via activation of presynaptic alpha7*-nAChRs.

Acetylcholine↗
PubMed2004

Pharmacokinetics, safety, and endocrine and appetite effects of ghrelin administration in young healthy subjects.

OBJECTIVE: It has been demonstrated that ghrelin plays a major role in the regulation of GH secretion and food intake. These actions make ghrelin a strong candidate for the treatment of GH deficiency, anorexia and cachexia. However, only preliminary studies have been performed to assess ghrelin administration in humans. In this study, we have conducted a double-blind, randomized, placebo-controlled trial to investigate the pharmacokinetics, safety, and endocrine and appetite effects of ghrelin in young healthy volunteers. DESIGN: Eighteen male volunteers were randomly assigned into three groups of six subjects: low- and high-dose ghrelin groups, who received intravenous injections of 1 and 5 microg/kg ghrelin (acylated form) respectively, and a placebo group who were injected with mannitol instead of ghrelin. RESULTS: Acylated ghrelin disappeared more rapidly from plasma than total ghrelin, with elimination half life (t(1/2)) of 9-13 and 27-31 min respectively. The number of subjects that experienced adverse effects did not significantly differ among the three groups, and all adverse effects were transient and well tolerated. Both the low and high doses of ghrelin strongly stimulated GH release (peak plasma concentration (C(max,0-90 min)): 124.2+/-63.9 and 153.2+/-52.2 ng/ml for 1 and 5 microg/kg ghrelin respectively). Slight alterations of blood glucose and insulin levels after the injection were observed. Although not statistically significant, ghrelin administration tended to increase hunger sensation in a dose-dependent manner. CONCLUSIONS: These results suggest that ghrelin is safe, and that clinical trials may be started to assess the usefulness of ghrelin for the treatment of disorders related to GH secretion and appetite.

Adult↗
PubMed2005

Changes in autonomic control of heart associated with classical appetitive conditioning in rats.

The aim of this study was to examine the changes in autonomic control of the heart associated with classical appetitive conditioning in rats. We trained rats to learn that a movement into a test chamber was followed by delivery of reward (contextual conditioning) and performed power spectral analysis of heart rate variability from electrocardiograms recorded using the telemetry system. We investigated the sympathovagal balance of autonomic regulation of the heart in response to not only the conditioned stimulus (the movement into the test chamber), but also the unconditioned stimulus (reward), and compared the results of these two kinds of emotional states; it might be considered that "the reward-expecting state" is evoked by the conditioned stimulus and "the reward-receiving state" is evoked by the unconditioned stimulus in rats. The reward-expecting state resulted in a significant increase in both low frequency (LF) power and high frequency (HF) power with no change in heart rate (HR) and LF/HF ratio, indicating that both sympathetic and parasympathetic activity increased with no change in sympathovagal balance. The reward-receiving state resulted in a significant increase in HR and a significant decrease in LF power, HF power, and LF/HF ratio, indicating that both sympathetic and parasympathetic activity decreased with predominance in the parasympathetic activity. These results suggest that the method performed in our present study might be useful for distinguishing between two different emotional states evoked by classical appetitive conditioning in rats.

Animals↗
PubMed2004

Brain serotonin depletion enhances the sodium appetite induced by sodium depletion or beta-adrenergic stimulation.

We investigate the influence of brain serotonin depletion on the sodium appetite. Rats depleted of serotonin through the systemic administration of p-chlorophenylalanine (300 mg/kg, ip, for 2 days) showed an intense natriorexigenic response induced by sodium depletion (furosemide, 20 mg/kg, sc, 24 h before water and 1.8% NaCl presentation). Intake of 1.8% NaCl was always higher than that observed for the control group (12.9 +/- 1.4 and 21.4 +/- 3.0 mL vs 5.7 +/- 1.2 and 12.7 +/- 1.6 mL, 30 and 300 min after water and saline presentation). After 24 h, the natriorexigenic response continued to be significantly higher compared to control (33.6+/-5.1 vs 21.9+/-3.6 mL,P <0.05). Fourteen days after p-chlorophenylalanine administration, 1.8% NaCl intake did not differ from controls. Serotonin-depleted rats expressed an early natriorexigenic response after isoproterenol administration on the third day after the first injection of p-chlorophenylalanine. An increase in 1.8% NaCl intake was first observed at 120 min (1.9 +/- 0.2 vs 0.45 +/- 0.3 mL,P <0.05) and remained high up to the end of the 24-h observation period (17.3+/-3.2 vs 1.1+/-0.5 mL,P <0.05). After 7 and 14 days, the natriorexigenic response became comparable to that of control animals. Present results show that brain serotonin depletion exaggerates the sodium appetite induced by the paradigm of sodium depletion or after beta-adrenergic stimulation.

Adrenergic beta-Agonists↗
PubMed1980

Increased sodium appetite in adrenalectomized or hypophysectomized rats after intracranial injections of renin or angiotensin II.

Rats given free access to food, water and 2.7% NaCl and injected with either renin or angiotensin II into the preoptic area showed an immediate increase in water intake followed by an increase in intake of 2.7% NaCl. The rats continued to drink the hypertonic NaCl solution throughout the test session of 18 h. Intracranial injections of the dipsogen, carbachol, caused thirst but no sodium appetite. Bilateral adrenalectomy had no effect on either the initial water intake or the delayed intake of NaCl that was induced by intracranial injections of renin or angiotensin II. However, the increased water intake during the 18 h after the administration of renin was reduced to normal levels in adrenalectomized rats. Similar results were obtained with hypophysectomized rats. These results demonstrated that the delayed sodium appetite induced by renin or angiotensin II is not secondary to the stimulation of release of hormones from the pituitary gland or adrenal cortex.

Adrenalectomy↗
PubMed1985

The basis of superstitious behavior: chance contingency, stimulus substitution, or appetitive behavior?

This research examined three explanations for the "superstitious" behavior of pigeons under frequent fixed-time delivery of food: accidental response-reward contingency, stimulus substitution, and elicited species-typical appetitive behavior. The behavior observed in these studies consisted of occasional postfood locomotion away from the food hopper, and a predominant pattern of activity directed toward the hopper wall (wall-directed behavior), including approaching, stepping side to side, scratching with the feet, bumping with the breast, pendulum movements of the extended neck, and head bobbing, though not pecking. The consistency of these behavior patterns argued against explanation by accidental response contingencies, and the complexity of behavior was incompatible with the classic stimulus-substitution account. These studies also showed that: (1) response contingencies and prior stimulus experience can modify wall-directed behavior, but within definable limits; (2) pecking sometimes can be obtained in birds of specific strains, and by providing extended training; (3) placing the hopper in the floor at the center of a large chamber replaces wall-directed behavior with circling in a manner that resembles ground foraging for food. We conclude that superstitious behavior under periodic delivery of food probably develops from components of species-typical patterns of appetitive behavior related to feeding. These patterns are elicited by a combination of frequent food presentations and the supporting stimuli present in the environment.

Animals↗
PubMed1992

Immunization against cholecystokinin decreases appetite in lambs.

The effects of immunization against cholecystokinin (CCK) on feed intake, weight gain, and carcass characteristics were studied in sheep. Nine wether lambs at 10 wk of age were immunized with a conjugate of sulphated CCK octapeptide and human serum globulin or against human globulin alone. All CCK-immunized lambs produced antibodies, and the average titer 5 wk after the primary immunization was calculated to be sufficient to bind normal circulating levels of CCK. Mean daily feed intakes and BW were similar in the CCK-immunized and the control-immunized groups at the start of treatment, but after immunization, feed intake, appetite, and BW gain were decreased in the CCK-immunized animals. There was no effect on carcass composition or organ growth relative to body growth. It is concluded that the immunization procedure used in this study may have potentiated the actions of CCK rather than neutralizing its action as an appetite regulator.

Animals↗
PubMed2000

Separate systems for serotonin and leptin in appetite control.

Appetite control involves an integration of the drive signals arising form energy stores in the body with the satiety signals generated by periodic episodes of food consumption. Serotonin (5-hydroxytryptamine, 5-HT) has been implicated in the processes of within-meal satiation and postmeal satiety (5-HT1B and 5-HT2C postsynaptic receptors) which are concerned with the signals arising form the pattern of food intake. Central nervous system (CNS) 5-HT is sensitive to circulating levels of the precursor tryptophan, certain macronutrients and peripheral satiety factors such as cholecystokinin (CCK) and enterostatin. Hypothalamic 5-HT receptor systems inhibit neuropeptide Y (NPY), a potent stimulator of hunger and food intake. In contrast to the linking of 5-HT with the consequences of food ingestion, the hormone leptin (OB protein) is regarded as a signal linking adipose tissue status with a number of key CNS circuits. Leptin itself stimulates CNS leptin receptors (OB-r receptor) which link with pro-opiomelanocortin (POMC)/ MC-4 receptors. The effects of leptin may also be modulated by factors such as the corticotrophin-releasing factor (CRF), cocaine and amphetamine-regulated transcript (CART), orexins and galanin. Very little evidence exists to support any direct link between the actions of 5-HT and leptin, suggesting that they are separate systems. 5-HT is a part of an integrated network for short-acting satiety signals (episodic in nature), and leptin is a hormonal indicator of long-term (tonic) energy reserves. At a conceptual level, these may represent the distinction between 'satiety' and 'drive'. Interestingly, both 5-HT and leptin modulate the action of NPY, which may form a part of a common output pathway for the expression of appetite.

Animals↗
PubMed1997

Effects of amount and type of dietary fibre (soluble and insoluble) on short-term control of appetite.

Fibres which are soluble or insoluble in water have different physiochemical properties and may therefore be expected to exert different effects on post-ingestive satiety signals. This study compared the effects on short-term (24 h) appetite of two equienergetic high (22 g) fibre breakfasts, an equienergetic low fibre breakfast and a low energy, 'light' breakfast. Psyllium gum (the soluble fibre) and wheat bran (the insoluble fibre) were incorporated into breakfast cereals and consumed at breakfast by sixteen healthy, normal weight males after an overnight fast using a repeated measures, counterbalanced design. Ad libitum energy intake was assessed at a test snack 1.5 h after breakfast, later in the day using food boxes and the following day using food diaries. Motivation to eat and gastrointestinal sensations were tracked for the next 24 h. Hunger ratings showed a trend towards the subjects being less hungry and they consumed significantly less energy at snack time after the high insoluble than after the high soluble fibre breakfast cereal. The soluble fibre breakfast produced a greater suppression of snack intake than the light breakfast, but smaller suppression than the other breakfasts. Interestingly there was a trend toward reduced hunger and voluntary energy consumption following the soluble fibre compared with the insoluble fibre much later in the day (9.5-13.5 h after breakfast) although this was not significant. There was no significant effect of breakfast type on total day energy intake. The results suggest that different types of fibre modulate the timecourse of appetite control and may produce alterations in the experience of motivation and patterns of eating without necessarily effecting total energy intake.

Adolescent↗
PubMed1990

Metrifonate or praziquantel treatment improves physical fitness and appetite of Kenyan schoolboys with Schistosoma haematobium and hookworm infections.

We studied physical fitness, as determined by the Harvard Step Test (HST), and appetite, as measured by the consumption of a morning snack (maize meal porridge), in primary school boys infected with Schistosoma haematobium (100% baseline prevalence) and hookworm (94-100% prevalence) who received a single dose of metrifonate (MT, 10 mg/kg body weight) or praziquantel (PR, 40 mg/kg body weight), or a placebo (PL). Five weeks after treatment, HST scores and porridge intake increased significantly in the MT and PR groups, but the PL group did not change. At the second examination, the MT group showed a significant decrease in S. haematobium egg counts (mean = 180 vs. 14 eggs/10 ml adj, P less than 0.0002, 82% egg reduction in arithmetic means) as did the PR group (mean = 198 vs. 0.1 eggs/10 ml adj, P less than 0.0002, 99.9% reduction); the egg counts in the PL group did not change. The MT group also exhibited a significant decrease in hookworm egg counts (mean = 1,550 vs. 75 eggs per gram feces [epg], P less than 0.0005, 80% reduction). Treatment with either drug may allow improved physical fitness and appetite in areas where S. haematobium and protein-energy malnutrition are highly prevalent.

Adolescent↗
PubMed1999

Nicotine's effect on hypothalamic neurotransmitters and appetite regulation.

BACKGROUND: Tobacco smoking reduces appetite and body weight. Cessation of smoking leads to hyperphagia and weight gain. Food intake is a function of meal number (MN) and meal size (MZ) (i.e., Food intake = MN x MZ). The effect of nicotine on these feeding components and their relationships to dopamine and serotonin in the lateral hypothalamic area (LHA) were determined. METHODS: In Fischer-344 rats the effect of 7 days of systemic nicotine infusion on the feeding patterns was measured by rat eater meter and changes in serotonin (5HT) and dopamine (DA) in the LHA were measured by in vivo microdialysis. RESULTS: Nicotine infusion caused hypophagia through a significant decrease in MN with a smaller decrease in MZ, resulting in a body weight reduction. 5HT and DA concomitantly increased in LHA. Stopping nicotine resulted in hyperphagia by a significant increase in MZ. Body weight normalized. 5HT and DA in LHA decreased after nicotine was stopped. CONCLUSION: Nicotine's hypophagic effect was associated with increased 5HT and DA in LHA, whereas hyperphagia after nicotine cessation was accompanied by decreased concentrations of the neurotransmitters. These findings suggest that nicotine affects appetite regulation, in part by modulation of LHA-DA and 5HT.

Animals↗
PubMed1999

[Appetite suppressants and heart valve disorders].

Serotoninergic appetite-suppressant drugs, fenfluramine and dexfenfluramine, were withdrawn from the market in September 1997 on account of two major cardiopulmonary complications: primary pulmonary hypertension and valvular regurgitation. The valvular heart diseases involve mainly left-sided valves, and contrary to physiological valvular regurgitations, they appear mostly on the aortic valve. Prolonged exposure (> 3 months) appears to confer a higher risk of cardiac valve involvement. Pathological features are similar to carcinoid or ergot alkaloid-induced valve diseases, and suggest a common pathophysiological mechanism which would also explain pulmonary hypertension by the toxic effect of high levels of circulating serotonin. After the first reports documenting a dramatically high prevalence of valvular side effects (up to 33% according to the Food and Drug Administration), recent studies reported a lower prevalence and severity. The long-term outcome and the real incidence are unknown and require further research and epidemiological data. A clinical survey of the patients exposed to serotoninergic appetite-suppressants is necessary, to be repeated 6 to 8 months later in the absence of an initial cardiac murmur. Doppler echocardiographic examination should be performed after prolonged exposure (> 3 months) or a high dosage of these drugs, in circumstances such as the presence of cardiovascular symptoms, a cardiac murmur, or an uncertain cardiac examination because of weight of patients.

Adult↗
PubMedDate not supplied

Imbalanced protein and appetite.

Free amino acid concentration in the plasma of rats fed on different diets were compared. The diets contained 7 g protein/100 g furnished by: casein, or common corn, or opaque 2 corn, or eggalbumin, or gelatin. A protein free diet was also included. The results showed that imbalance of the protein diet influenced the appetite; whenever the NE/E aminoacid ratio increased, body development, appetite and plasma albumin decreased. An inverse correlation between the NE/E of free aminoacids of the plasma and voluntary intake was observed. The results also show that the plasma aminogram did not reflect the composition of the protein in the diet. The results obtained are discussed.

Animals↗
PubMed2000

Coincident activation of NMDA and dopamine D1 receptors within the nucleus accumbens core is required for appetitive instrumental learning.

The nucleus accumbens, a brain structure ideally situated to act as an interface between corticolimbic information-processing regions and motor output systems, is well known to subserve behaviors governed by natural reinforcers. In the accumbens core, glutamatergic input from its corticolimbic afferents and dopaminergic input from the ventral tegmental area converge onto common dendrites of the medium spiny neurons that populate the accumbens. We have previously found that blockade of NMDA receptors in the core with the antagonist 2-amino-5-phosphonopentanoic acid (AP-5; 5 nmol) abolishes acquisition but not performance of an appetitive instrumental learning task (Kelley et al., 1997). Because it is currently hypothesized that concurrent dopamine D(1) and glutamate receptor activation is required for long-term changes associated with plasticity, we wished to examine whether the dopamine system in the accumbens core modulates learning via NMDA receptors. Co-infusion of low doses of the D(1) receptor antagonist SCH-23390 (0.3 nmol) and AP-5 (0.5 nmol) into the accumbens core strongly impaired acquisition of instrumental learning (lever pressing for food), whereas when infused separately, these low doses had no effect. Infusion of the combined low doses had no effect on indices of feeding and motor activity, suggesting a specific effect on learning. We hypothesize that co-activation of NMDA and D(1) receptors in the nucleus accumbens core is a key process for acquisition of appetitive instrumental learning. Such an interaction is likely to promote intracellular events and gene regulation necessary for synaptic plasticity and is supported by a number of cellular models.

2-Amino-5-phosphonovalerate↗
PubMed2002

Critical time-window for NO-cGMP-dependent long-term memory formation after one-trial appetitive conditioning.

The nitric oxide (NO)-cGMP signaling pathway is implicated in an increasing number of experimental models of plasticity. Here, in a behavioral analysis using one-trial appetitive associative conditioning, we show that there is an obligatory requirement for this pathway in the formation of long-term memory (LTM). Moreover, we demonstrate that this requirement lasts for a critical period of approximately 5 hr after training. Specifically, we trained intact specimens of the snail Lymnaea stagnalis in a single conditioning trial using a conditioned stimulus, amyl-acetate, paired with a salient unconditioned stimulus, sucrose, for feeding. Long-term associative memory induced by a single associative trial was demonstrated at 24 hr and shown to last at least 14 d after training. Tests for LTM and its dependence on NO were performed routinely 24 hr after training. The critical period when NO was needed for memory formation was established by transiently depleting it from the animals at a series of time points after training by the injection of the NO-scavenger 2-phenyl-4,4,5,5-tetramethyl-imidazoline-1-oxyl 3-oxide (PTIO). By blocking the activity of NO synthase and soluble guanylyl cyclase enzymes after training, we provided further evidence that LTM formation depends on an intact NO-cGMP pathway. An electrophysiological correlate of LTM was also blocked by PTIO, showing that the dependence of LTM on NO is amenable to analysis at the cellular level in vitro. This represents the first demonstration that associative memory formation after single-trial appetitive classical conditioning is dependent on an intact NO-cGMP signaling pathway.

Animals↗
PubMed2002

Appetitive and aversive olfactory learning in humans studied using event-related functional magnetic resonance imaging.

We combined event-related functional magnetic resonance imaging (fMRI) with olfactory classical conditioning to differentiate the neural responses evoked during appetitive and aversive olfactory learning. Three neutral faces [the conditioned stimuli (CS+)] were repetitively paired with pleasant, neutral, or unpleasant odors [the unconditioned stimuli (UCS)] in a partial reinforcement schedule. A fourth face was never paired to odor [the nonconditioned stimulus (CS-)]. Learning-related neural activity, comparing unpaired (face only) CS+ stimuli with CS-, showed valence-independent activations in rostral and caudal orbitofrontal cortex (OFC). Medial OFC responded to the appetitive (app) CS+, whereas lateral OFC responded to the aversive (av) CS+. Within nucleus accumbens, neural responses showed divergent activation profiles that increased with time in response to the appCS+ but decreased in response to the avCS+. In posterior amygdala, responses were elicited by the appCS+, which habituated over time. In temporal piriform cortex, neural responses were evoked by the avCS+, which progressively increased with time. These results highlight regional and temporal dissociations during olfactory learning and imply that emotionally salient odors can engender cross-modal associative learning. Moreover, the findings suggest that the role of human primary (piriform) and secondary olfactory cortices transcends their function as mere intermediaries of chemosensory information processing.

Adult↗