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PubMedDate not supplied

Repeated thermal therapy diminishes appetite loss and subjective complaints in mildly depressed patients.

OBJECTIVE: We observed that repeated thermal therapy improved appetite loss and general well-being in patients with chronic heart failure. The purpose of this study is to clarify the effects of repeated thermal therapy in mildly depressed patients with appetite loss and subjective complaints. METHODS: Twenty-eight mildly depressed inpatients with general fatigue, appetite loss, and somatic and mental complaints were randomly assigned to thermal therapy group (n = 14) or nonthermal therapy group (n = 14). Patients in the thermal therapy group were treated with 60 degrees C far-infrared ray dry sauna for 15 minutes and were then kept at bed rest with a blanket for 30 minutes once a day, 5 days a week for a total of 20 sessions in 4 weeks. RESULTS: Four weeks after admission, somatic complaints, hunger, and relaxation scores significantly improved (p < .001, p < .0001, p < .0001, respectively) and mental complaints slightly improved (p = .054) in the thermal therapy group compared with the nonthermal therapy group. Furthermore, the plasma ghrelin concentrations and daily caloric intake in the thermal therapy group significantly increased compared with the nonthermal therapy group (p < .05). CONCLUSIONS: These findings suggest that repeated thermal therapy may be useful for mildly depressed patients with appetite loss and subjective complaints.

Adult↗
PubMed1984

Involvement of the renin-angiotensin system in captopril-induced sodium appetite in the rat.

The angiotensin converting enzyme inhibitor, captopril, given to rats in their drinking water (about 40 mg/day) for 6 days caused an increase in intake of hypertonic NaCl solution which began 1-2 days after the captopril was started and reached a plateau after 4-5 days. Twice-daily subcutaneous injections of captopril (15 mg per injection) elicited a sodium appetite similar in pattern to that seen with oral administration. The rats remained in sodium and fluid balance during oral captopril treatment and the haematocrit did not alter. Captopril infused directly into the ventricles (12 micrograms/h), or captopril reaching the brain from the periphery across a leaky blood-brain barrier, suppressed the sodium appetite which normally follows oral captopril. Continuous intravenous infusion of captopril at rates high enough to block angiotensin converting enzyme in the brain (25, 50 or 500 mg/day) did not cause sodium appetite. As soon as the rate was reduced to a low value (5 mg/day), NaCl intake increased. In conclusion, moderate levels of circulating captopril which do not cross the blood-brain barrier in sufficient amounts to block cerebral angiotensin converting enzyme, result in an increase in circulating angiotensin I which stimulates sodium appetite when it is converted to angiotension II in the brain.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2000

Hindbrain serotonin and the rapid induction of sodium appetite.

Both systemically administered furosemide and isoproterenol produce water intake (i.e., thirst). Curiously, however, in light of the endocrine and hemodynamic effects produced by these treatments, they are remarkably ineffective in eliciting intake of hypertonic saline solutions (i.e., operationally defined as sodium appetite). Recent work indicates that bilateral injections of the serotonin receptor antagonist methysergide into the lateral parabrachial nuclei (LPBN) markedly enhance a preexisting sodium appetite. The present studies establish that a de novo sodium appetite can be induced with LPBN-methysergide treatment under experimental conditions in which only water is typically ingested. The effects of bilateral LPBN injections of methysergide were studied on the intake of water and 0. 3 M NaCl following acute (beginning 1 h after treatment) diuretic (furosemide)-induced sodium and water depletion and following subcutaneous isoproterenol treatment. With vehicle injected into the LPBN, furosemide treatment and isoproterenol injection both caused water drinking but essentially no intake of hypertonic saline. In contrast, bilateral treatment of the LPBN with methysergide induced the intake of 0.3 M NaCl after subcutaneous furosemide and isoproterenol. Water intake induced by subcutaneous furosemide or isoproterenol was not changed by LPBN-methysergide injections. The results indicate that blockade of LPBN-serotonin receptors produces a marked intake of hypertonic NaCl (i.e., a de novo sodium appetite) after furosemide treatment as well as subcutaneous isoproterenol.

Administration, Oral↗
PubMed1987

Remote effects of aversive contingencies: Disruption of appetitive behavior by adjacent avoidance sessions.

Disruption of ongoing appetitive behavior before and after daily avoidance sessions was examined. After baselines of appetitive responding were established under a fixed-interval 180-s schedule of food presentation, 4 rats were exposed to 40-min sessions of the appetitive schedule just prior to 100-min sessions of electric shock postponement, while another 4 rats received the 40-min appetitive sessions just following daily sessions of shock postponement. In all 8 subjects, fixed-interval response rates decreased relative to baseline levels, the effect being somewhat more pronounced when the avoidance sessions immediately followed. The disruption of fixed-interval responding was only partially reversed when avoidance sessions were discontinued. During the initial exposure to the avoidance sessions, patterns of responding under the fixed-interval schedule were differentially sensitive to disruption, with high baseline response rates generally more disturbed than low rates. These disruptions were not systematically related to changes in reinforcement frequency, which remained fairly high and invariant across all conditions of the experiment; they were also not systematically related to the response rates or to the shock rates of the adjacent avoidance sessions. The results, while qualitatively resembling patterns of conditioned suppression as typically studied, occurred on a greatly expanded time scale. As disruption of behavior extending over time, the present data suggest that some forms of conditioned suppression are perhaps best viewed within a larger temporal context.

Journal Article↗
PubMed1997

Intracerebroventricular Administration of Mineralocorticoid Receptor Antisense Oligonucleotides Attenuates Salt Appetite in the Rat.

The anterior ventral third ventricle (AV3V) region of the brain contains high concentrations of mineralocorticoid receptors (MR) and glucocorticoid receptors (GR) that are important in the maintenance of body fluid and electrolyte balance as well as other physiological processes. Daily intracerebroventricular pulse injections of MR antisense oligonucleotides significantly suppressed deoxycorticosterone acetate (DOCA) induced salt appetite in a dose-related manner. Similar administration of GR antisense or scrambled/sense oligonucleotide into the third ventricle failed to inhibit salt appetite. Salt appetite aroused after adrenalectomy was not suppressed by MR antisense oligonucleotide treatments but was suppressed by an antisense oligonucleotide directed against the angiotensin II AT1 receptor subtype. Receptor binding analysis demonstrated that MR and GR oligonucleotide treatments each reduced their respective receptor subtypes. Finally, although GR antisense oligonucleotide treatment was ineffective in suppressing DOCA-induced salt appetite, this treatment did increase stress induced corticosterone release as well as delayed the recovery of corticosterone to basal levels after stress.

Journal Article↗
PubMed1999

[Efficacy of combination with granisetron and methylprednisolone for nausea, vomiting and appetite loss in remission induction chemotherapy of acute myeloid leukemia--a randomized comparative trial between granisetron alone and granisetron plus methylprednisolone].

The prevention of nausea, vomiting and appetite loss induced by remission induction chemotherapy for acute myeloid leukemia was compared by randomization between granisetron alone and combination with granisetron plus methylprednisolone. Granisetron was administered at 40 micrograms/kg during chemotherapy, and methylprednisolone was administered concomitantly at 125 mg/body for 3 days or more in the combination group. The single and combination groups comprised 14 and 13 patients, respectively, and there was no significant difference between the background of both groups. To evaluate the effect they were scored according to 4 grades, and evaluated every 24 hours from the start of chemotherapy to 5 days after its completion. The complete inhibition rate of vomiting was as high as 71.4% and 92.3% in the single and combination groups, respectively, showing no significant difference. The grade of vomiting was mild in both groups. Nausea was noted in 71.4% and 46.2%, respectively, and the inhibitory effect tended to be higher in the combination group. Appetite loss developed in 92.9% and 41.7%, respectively, and the prevention effect was clearly higher in the combination group. The prevention effects on nausea 7, 8 and 10 days after the start of chemotherapy, on appetite loss 2-10 days after it, and 2-5 days after its completion, were higher in the combination group. Granisetron revealed an excellent inhibitory effect on vomiting induced by remission induction chemotherapy for acute myeloid leukemia, but combination with granisetron and methylprednisolone was considered useful for nausea in the latter half of the treatment period and for appetite loss during the whole period.

Acute Disease↗
PubMed1987

Assessment of the effects of phenylpropanolamine on appetite and food intake.

Single 37.5 mg doses of phenylpropanolamine (PPA) were given on each of two separate, nonconsecutive days to each of twelve nonobese women. PPA's effects on reported appetite and food intake were compared to those of a placebo also given on two nonconsecutive days. To control for possible effects on appetitive behavior of knowledge about the drug's putative role as an appetite suppressant, the subjects were told that PPA was a nasal decongestant which was expected to affect their sensitivity to flavors. Hunger rating before eating was significantly lower on trials after PPA than on trials after placebo (carry-over effect), but the direct effect of PPA on hunger was not significant. Although food intake was 26 g less under the PPA condition (407 g) than under placebo (433 g), this difference was not significant. However, because of insufficient power, the null hypothesis could not be accepted. The true effect of PPA on intake remains inconclusive. Either more subjects must be tested at this dose or the effect must be made larger by changing the dose, in order to obtain conclusive results.

Adolescent↗
PubMed1994

Pharmacological aspects of appetite: implications for the treatment of obesity.

The properties of an ideal weight-reducing drug would be to produce a sustained decrease in body fat, to oppose the recidivism in obese patients and to improve compliance to dietary requirements. More specifically the drug would have to decrease hunger, be active in the long term, preferably produce no tolerance or rebound effects, and prevent any decrease in basal metabolic rate. Moreover, the drug should reduce the intake of dietary fat which is now regarded as a major cause of weight gain (and regain) [14]. Can this be achieved? Can drug-induced appetite control be used to combat obesity? Some drugs have already demonstrated a capacity to adjust appetite so as to produce significant improvements in the pattern of eating and the control of body weight. What mechanisms are responsible for such an action and how can new drugs be developed so as to advance the pharmacological control of appetite?

Appetite↗
PubMed2002

Safety and mechanism of appetite suppression by a novel hydroxycitric acid extract (HCA-SX).

A growing body of evidence demonstrates the efficacy of Garcinia cambogia-derived natural (-)-hydroxycitric acid (HCA) in weight management by curbing appetite and inhibiting body fat biosynthesis. However, the exact mechanism of action of this novel phytopharmaceutical has yet to be fully understood. In a previous study, we showed that in the rat brain cortex a novel HCA extract (HCA-SX, Super CitriMax) increases the release/availability of radiolabeled 5-hydroxytryptamine or serotonin ([3H]-5-HT), a neurotransmitter implicated in the regulation of eating behavior and appetite control. The aim of the present study was 2-fold: (a) to determine the effect of HCA-SX on 5-HT uptake in rat brain cortex in vitro; and (b) to evaluate the safety of HCA-SX in vivo. Isolated rat brain cortex slices were incubated in oxygenated Krebs solution for 20 min and transferred to buffer solutions containing [3H]-5-HT for different time intervals. In some experiments, tissues were exposed to HCA-SX (10 microM - 1 mM) and the serotonin receptor reuptake inhibitors (SRRI) fluoxetine (100 microM) plus clomipramine (10 microM). Uptake of [3H]-5-HT was expressed as d.p.m./mg wet weight. A time-dependent uptake of [3H]-5-HT occurred in cortical slices reaching a maximum at 60 min. HCA-SX, and fluoxetine plus clomipramine inhibited the time-dependent uptake of [3H]-5-HT. At 90 min, HCA-SX (300 microM) caused a 20% decrease, whereas fluoxetine plus clomipramine inhibited [3H]-5-HT uptake by 30%. In safety studies, acute oral toxicity, acute dermal toxicity, primary dermal irritation and primary eye irritation, were conducted in animals using various doses of HCA-SX. Results indicate that the LD50 of HCA-SX is greater than 5,000 mg/kg when administered once orally via gastric intubation to fasted male and female Albino rats. No gross toxicological findings were observed under the experimental conditions. Taken together, these in vivo toxicological studies demonstrate that HCA-SX is a safe, natural supplement under the conditions it was tested. Furthermore, HCA-SX can inhibit [3H]-5-HT uptake (and also increase 5-HT availability) in isolated rat brain cortical slices in a manner similar to that of SRRIs, and thus may prove beneficial in controlling appetite, as well as treatment of depression, insomnia, migraine headaches and other serotonin-deficient conditions.

Administration, Cutaneous↗
PubMed2004

Megestrol acetate promotes euglycemia and appetite in a child with persistent hyperinsulinemic hypoglycemia of infancy.

UNLABELLED: This report describes a successful treatment with megestrol acetate in a child with persistent hyperinsulinemic hypoglycemia of infancy (PHHI). An 8-y-old child with PHHI treated with octreotide had marked impairment of appetite sensation and feeding skills. Within 3 wk of starting megestrol acetate (8 mg/kg/d) to stimulate her appetite, she had a significant improvement. By 1 y postinitiation, she had acquired age-appropriate eating habits. The megestrol acetate caused hyperglycemia, necessitating the discontinuation of all other therapy for her hypoglycemia. Her height growth remained normal but she was found to have asymptomatic adrenal suppression. CONCLUSION: Megestrol acetate appeared to stimulate appetite and regulate glucose homeostasis in this child with PHHI. Additional studies will be required to document its efficacy and safety in other children with this disorder.

Appetite↗
PubMed2000

The acquisition of an appetite.

Unlike older animals, weanling-age rats do not seek water to drink when they are dehydrated, despite the fact that a physiological sensitivity to dehydration is present very soon after birth. We demonstrate here that the appetitive behaviors needed to approach and obtain water become linked to dehydration only as a result of specific postnatal learning experience. Preventing early experience with dehydration retards the developmental emergence of dehydration-induced, water-oriented behavior in young rats. But a single pairing of water with dehydration can establish an appetitive response. These findings reveal a critical role of early learning in the development of goal-oriented behavior. Such a learning process is potentially characteristic of other behavioral systems, from the most basic appetites to complex motives.

Aging↗
PubMed1990

Synthesis and resolution of the novel appetite suppressant 2-benzylmorpholine, a nonstimulant isomer of phenmetrazine.

The synthesis of 2-benzylmorpholine from allylbenzene together with its resolution into its (+)- and (-)-enantiomers is reported. Oral dosing of the racemate to dogs caused appetite suppression with an ED50 of 3 and 5.5 mg kg-1 at 1 and 2 h, respectively, after access to a meat meal. No stimulant activity was observed in dogs given oral doses of 200 mg kg-1 but the appetite suppressant effect in dogs declined during 20 days of chronic oral dosing at 10 mg kg-1. Appetite suppression activity was shown to reside in the (+)-enantiomer.

Administration, Oral↗
PubMed1996

Appetite-suppressing effects of urocortin, a CRF-related neuropeptide.

The neuropeptide corticotropin-releasing factor (CRF) is well known to act on the central nervous system in ways that mimic stress and result in decreases in exploration, increases in sympathetic activity, decreases in parasympathetic outflow, and decreases in appetitive behavior. Urocortin, a neuropeptide related to CRF, binds with high affinity to the CRF2 receptor, is more potent than CRF in suppressing appetite, but is less potent than CRF in producing anxiety-like effects and activation. Doses as low as 10 nanograms injected intracerebroventricularly were effective in decreasing food intake in food-deprived and free-feeding rats. These results suggest that urocortin may be an endogenous CRF-like factor in the brain responsible for the effects of stress on appetite.

Animals↗
PubMed2001

Diet, monoamine neurotransmitters and appetite control.

This article has attempted to point out some of the relationships between 5-HT and catecholamine (NE, DA) neurons in brain and the control of appetite and food intake. At least two bodies of evidence support this connection. The first is pharmacologic, and demonstrates that drugs that stimulate transmission across 5-HT and/or catecholamine synapses suppress hunger and food intake. The second is physiologic and metabolic, and reveals that the ingestion of foods, on either an acute (single meal) or chronic basis, can reliably modify the uptake of TRP and TYR into brain (and hypothalamus), and directly alter the synthesis of their transmitters (5-HT and the catecholamines, respectively). The synthesis of these two bodies of information has led to models by which (1) changes in dietary carbohydrate ingestion, by modifying brain TRP uptake and 5-HT production, may cause like changes in 5-HT release, and in the stimulation of 5-HT receptors in brain circuits that control carbohydrate appetite, and (2) dietary protein intake, by altering brain TYR uptake, directly influences DA and NE synthesis (notably in hypothalamus), perhaps providing a signal to brain circuits monitoring dietary protein adequacy regarding protein intake. In this case, one might imagine that stimulating DA and/or NE receptors in such circuits might suppress protein intake, a possibility we are now examining in rats. As indicated in the Introduction, the broader issue being touched upon in this article concerns the body's need to acquire and maintain an optimal (or adequate) nutritional balance (for growth and ultimately, reproductive success). Rats and humans evolved in an environment that does not provide continuous access to all essential nutrients, and one that presents nutrients in a complex matrix (other animals, plants) that can also include toxic compounds. Together with the fact that animals and humans do not carry a guidebook to healthy eating, we must presume that the brain mechanisms that have evolved to optimize the acquisition of essential nutrients are 'automatic' (i.e., not conscious) and quite complex. In this context, the relationships described here must be viewed as rudimentary, touching only a small portion of this complex regulatory mechanism. The hope is, as further insights develop, that we will gain a better understanding of the workings of these mechanisms, and also be able to apply this knowledge to the development of better pharmacologic (and other) aids for controlling appetite and obesity in our modern, man-made environment.

Animals↗
PubMed2004

Appetite and cancer-associated anorexia: a review.

Appetite is governed by peripheral hormones and central neurotransmitters that act on the arcuate nucleus of the hypothalamus and nucleus tactus solitarius of the brainstem. Cancer anorexia appears to be the result of an imbalance between neuropeptide-Y and pro-opiomelanocortin signals favoring pro-opiomelanocortin. Many of the appetite stimulants redress this imbalance. Most of our understanding of appetite neurophysiology and tumor-associated anorexia is derived from animals and has not been verified in humans. There have been few clinical trials and very little translational research on anorexia despite its prevalence in cancer.

Animals↗
PubMed2003

Oxyntomodulin suppresses appetite and reduces food intake in humans.

Oxyntomodulin (OXM) is released from the gut postprandially, in proportion to energy intake, and circulating levels of OXM are elevated in several conditions associated with anorexia. Central injection of OXM reduces food intake and weight gain in rodents, suggesting that OXM signals food ingestion to hypothalamic appetite-regulating circuits. We investigated the effect of iv OXM (3.0 pmol/kg.min) on appetite and food intake in 13 healthy subjects (body mass index, 22.5 +/- 0.9 kg/m(2)) in a randomized, double-blind, placebo-controlled, cross-over study. Infusion of OXM significantly reduced ad libitum energy intake at a buffet meal (mean decrease, 19.3 +/- 5.6%; P < 0.01) and caused a significant reduction in scores for hunger. In addition, cumulative 12-h energy intake was significantly reduced by infusion of OXM (mean decrease, 11.3 +/- 6.2%; P < 0.05). OXM did not cause nausea or affect food palatability. Preprandial levels of the appetite-stimulatory hormone, ghrelin, were significantly suppressed by OXM (mean reduction, 44 +/- 10% of postprandial decrease; P < 0.0001). Elevated levels of endogenous OXM associated with disorders of the gastrointestinal tract may contribute to anorexia.

Adult↗
PubMed2003

Pancreatic polypeptide reduces appetite and food intake in humans.

Pancreatic polypeptide (PP) is a gut hormone released from the pancreas in response to ingestion of food. Plasma PP has been shown to be reduced in conditions associated with increased food intake and elevated in anorexia nervosa. In addition peripheral administration of PP has been shown to decrease food intake in rodents. These findings suggest that PP may act as a circulating factor that regulates food intake. Therefore we investigated the effect of intravenous infusion of PP (10 pmol/kg/min) on appetite and food intake in a randomised double-blind placebo-controlled crossover study in ten healthy volunteers. Infusion of PP reduced appetite and decreased the energy intake at a buffet lunch two hours post-infusion by 21.8 +/- 5.7% (P < 0.01). More importantly the inhibition of food intake was sustained, such that energy intake, as assessed by food diaries, was significantly reduced both the evening of the study and the following morning. Overall PP infusion reduced cumulative 24-hour energy intake by 25.3 +/- 5.8%. In conclusion our data demonstrates that PP causes a sustained decrease in both appetite and food intake.

Adolescent↗
PubMed1985

Mechanisms of appetite modulation by drugs.

The regulation of appetite is a complex process that we are just beginning to understand. It consists of both central and peripheral elements and involves the integration by the brain of a variety of signals from peripheral organs transmitted by neurotransmitters, peptides, hormones, and metabolites. All available anorectic drugs act by central mechanisms and have several disadvantages including limited effectiveness, side effects on the central nervous system, the development of tolerance, abuse potential, and rebound hyperphagia on discontinuance. Several appetite-modulating agents have been tested in animals that act by peripheral mechanisms and do not produce tolerance or rebound hyperphagia, which suggests that peripherally acting anorectic drugs may provide novel therapeutic approaches to disorders of appetite regulation in humans.

Animals↗