Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “APPETITE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed2001

Assessing appetite in Dutch elderly with the Appetite, Hunger and Sensory Perception (AHSP) questionnaire.

BACKGROUND: In investigating anorexia of ageing, attention is often given to physical and psychological determinants of appetite in the elderly but little has been done to provide information on self-assessment of appetite and sensory perceptions in the elderly. OBJECTIVES: to provide data and detect possible differences in self-assessment of appetite, hunger feelings and sensory perception in different health group of elderly using the Appetite, Hunger feelings and Sensory Perception (AHSP) questionnaire. METHODS: three health categories of elderly subjects were used for the present study: free-living with no help, free-living with help and nursing home elderly. For each group, collected data were general characteristics, anthropometry and answers to the AHSP. The AHSP questionnaire includes 29-items focusing on feelings of hunger and appetite as well as taste and smell perception addressing both the present situation and the period before retirement. RESULTS: Significant differences were observed between the 3 health groups for appetite, hunger feelings, present taste perception and present smell perception (P<0.05). Appetite and hunger were found to be related to body weight in the healthiest but not in the others. CONCLUSION: A decline in health status is paired with a decrease in appetite, hunger feelings and sensory perceptions of elderly subjects.

Aged↗
PubMed1993

Appetite and appetite stimulants.

Poor appetite is a common symptom among cancer patients. It can lead to inadequate food intake, weight loss, physical debilitation and reduced tolerance to anti-neoplastic treatment. Although cancer-induced anorexia is not fully understood, there are some theories relating to its development. Interventions may be aimed at improving nutritional intake to prevent excessive weight loss when poor appetite exists, or it may concentrate on improving appetite by pharmacological means. Appetite should be considered alongside other aspects of symptom control and tackled aggressively when it is contributing to a poor quality of life.

Anorexia↗
PubMed2004

The future of research on appetitive behavior: 30th Anniversary of the Columbia University Seminar on Appetitive Behavior.

The first 30 years of Columbia's Appetitive Seminar were celebrated by speakers extrapolating from the past to the future for six areas of research on appetite. This editorial introduces reviews of three of the selected topics and briefly summarizes the other three presentations-on the sensing of glucose utilization, gastrointestinal controls of satiety and mechanisms of learning and conditioning.

Appetite↗
PubMed2001

Description and evaluation of a Newton-based electronic appetite rating system for temporal tracking of appetite in human subjects.

This study assessed the reliability and validity of a palm-top-based electronic appetite rating system (EARS) in relation to the traditional paper and pen method. Twenty healthy subjects [10 male (M) and 10 female (F)] - mean age M=31 years (S.D.=8), F=27 years (S.D.=5); mean BMI M=24 (S.D.=2), F=21 (S.D.=5) - participated in a 4-day protocol. Measurements were made on days 1 and 4. Subjects were given paper and an EARS to log hourly subjective motivation to eat during waking hours. Food intake and meal times were fixed. Subjects were given a maintenance diet (comprising 40% fat, 47% carbohydrate and 13% protein by energy) calculated at 1.6xResting Metabolic Rate (RMR), as three isoenergetic meals. Bland and Altman's test for bias between two measurement techniques found significant differences between EARS and paper and pen for two of eight responses (hunger and fullness). Regression analysis confirmed that there were no day, sex or order effects between ratings obtained using either technique. For 15 subjects, there was no significant difference between results, with a linear relationship between the two methods that explained most of the variance (r(2) ranged from 62.6 to 98.6). The slope for all subjects was less than 1, which was partly explained by a tendency for bias at the extreme end of results on the EARS technique. These data suggest that the EARS is a useful and reliable technique for real-time data collection in appetite research but that it should not be used interchangeably with paper and pen techniques.

Adult↗
PubMed2004

Low dose daily iron supplementation improves iron status and appetite but not anemia, whereas quarterly anthelminthic treatment improves growth, appetite and anemia in Zanzibari preschool children.

Iron deficiency and helminth infections are two common conditions of children in developing countries. The consequences of helminth infection in young children are not well described, and the efficacy of low dose iron supplementation is not well documented in malaria-endemic settings. A 12-mo randomized, placebo controlled, double-blind trial of 10 mg daily iron and/or mebendazole (500 mg) every 3 mo was conducted in a community-based sample of 459 Zanzibari children age 6-71 mo with hemoglobin > 70 g/L at baseline. The trial was designed to examine treatment effects on growth, anemia and appetite in two age subgroups. Iron did not affect growth retardation, hemoglobin concentration or mild or moderate anemia (hemoglobin < 110 g/L or < 90 g/L, respectively), but iron significantly improved serum ferritin and erythrocyte protoporphyrin. Mebendazole significantly reduced wasting malnutrition. but only in children <30 mo old. The adjusted odds ratios (AORs) for mebendazole in this age group were 0.38 (95% CI: 0.16, 0.90) for weight-for-height less than -1 Z-score and 0.29 (0.09, 0.91) for small arm circumference. In children <24 mo old, mebendazole also reduced moderate anemia (AOR: 0.41, 0.18, 0.94). Both iron and mebendazole improved children's appetite, according to mothers' report. In this study, iron's effect on anemia was limited, likely constrained by infection, inflammation and perhaps other nutrient deficiencies. Mebendazole treatment caused unexpected and significant reductions in wasting malnutrition and anemia in very young children with light infections. We hypothesize that incident helminth infections may stimulate inflammatory immune responses in young children, with deleterious effects on protein metabolism and erythropoiesis.

Anemia, Iron-Deficiency↗
PubMed1986

Angiotensin and salt appetite: physiological amounts of angiotensin given peripherally increase salt appetite in the rat.

Two experiments were conducted in which adrenalectomized male Sprague-Dawley rats were maintained ad lib on distilled water, 3% saline, and sodium-free food. In Experiment 1, 45 rats were given 100, 200, 400, 800, and 1,000 micrograms/kg/day desoxycorticosterone acetate (DOCA) im for 5 days to determine the dose of DOCA that would produce the lowest voluntary saline intake, and 800 micrograms/kg/day was found to produce the nadir in saline intake. In Experiment 2, 40 rats were placed ad lib on distilled water, saline, and sodium-free food as described above, maintained on 800 micrograms/kg/day DOCA, and infused with 4, 25, 100 micrograms/kg/day angiotensin II (A II) or 0.9% saline. The three A II groups showed significant percentage changes in their saline intake above pre-A II levels; the saline control group showed no change in saline intake from pre-A II level. These results are interpreted to demonstrate the production of salt appetite in rats by peripheral administration of physiological doses of angiotensin II.

Angiotensin II↗
PubMed2003

Cross talk between physical activity and appetite control: does physical activity stimulate appetite?

Physical activity has the potential to modulate appetite control by improving the sensitivity of the physiological satiety signalling system, by adjusting macronutrient preferences or food choices and by altering the hedonic response to food. There is evidence for all these actions. Concerning the impact of physical activity on energy balance, there exists a belief that physical activity drives up hunger and increases food intake, thereby rendering it futile as a method of weight control. There is, however, no evidence for such an immediate or automatic effect. Short (1-2 d)-term and medium (7-16 d)-term studies demonstrate that men and women can tolerate substantial negative energy balances of < or = 4 MJ energy cost/d when performing physical activity programmes. Consequently, the immediate effect of taking up exercise is weight loss (although this outcome is sometimes difficult to assess due to changes in body composition or fluid compartmentalization). However, subsequently food intake begins to increase in order to provide compensation for about 30% of the energy expended in activity. This compensation (up to 16 d) is partial and incomplete. Moreover, subjects separate into compensators and non-compensators. The exact nature of these differences in compensation and whether it is actually reflective of non-compliance with protocols is yet to be determined. Some subjects (men and women) performing activity with a cost of < or = 4 MJ/d for 14 d, show no change in daily energy intake. Conversely, it can be demonstrated that when active individuals are forced into a sedentary routine food intake does not decrease to a lower level to match the reduced energy expenditure. Consequently, this situation creates a substantial positive energy balance accompanied by weight gain. The next stage is to further characterize the compensators and non-compensators, and to identify the mechanisms (physiological or behavioural) that are responsible for the rate of compensation and its limits.

Anorexia↗
PubMed1978

Endocrine control of appetite: gastrointestinal hormonal effects on CNS appetitive structures.

Permanent semi-microelectrodes were implanted in the ventromedial hypothalamus (VMH), lateral hypothalamus (LH), amygdala (AMYG), medial forebrain bundle (MFB), anterior hypothalamus (AH), inferior colliculus (IC), and caudate nucleus (CN). Average evoked responses were recorded simultaneously from the above sites in freely behaving rats before and after administration of pentagastrin (100 microgram/kg), secretin 1 microgram/kg or cholecystokinin octapeptide (CCK-OP) (1 microgram/kg) in search of satiety signal. Gastrin and secretin had little effect while it appears that CCK may perform a regulatory function in a neurohumoral feedback mechanism.

Amygdala↗
PubMed1999

Correlates of poor appetite among hemodialysis patients.

OBJECTIVE: Poor appetite is an important barrier to adequate nutrition among hemodialysis patients. We sought to determine the relationship between overall appetite and (1) patient demographic and medical characteristics and (2) appetite for specific foods. DESIGN: Cross-sectional study. SETTING: All 22 chronic hemodialysis units in northeast Ohio. PATIENTS: Two hundred ninety-eight randomly selected patents. INTERVENTION: Interview and chart abstraction. MAIN OUTCOME MEASURE: Overall patient appetite. RESULTS: Of all patients, 12% reported poor overall appetite, 20% reported fair appetite, and 69% reported good appetite. There was no relationship between overall appetite and patient demographic (age, gender, race, education, health insurance) or medical (cause of renal failure, years on dialysis, number of comorbid conditions, Kt/V) characteristics. There was little relationship between overall appetite and appetite for 20 specific foods. Of 34 patients with poor overall appetite, 29 (85%) identified at least three specific protein foods for which they had good appetite and 28 (82%) identified at least three nonprotein foods for which they had good appetite. CONCLUSION: Poor overall appetite is not associated with patient characteristics or appetite for specific foods. Most patients with poor overall appetite have good appetite for several specific foods. Helping patients increase the intake of these foods may be beneficial in improving nutritional status.

Adult↗
PubMed1991

Neuroendocrine factors in salt appetite.

We dedicate this paper to Curt P. Richter, father of the study of salt appetite, who died recently at the age of 94. Richter first demonstrated that the adrenalectomized rat's voracious appetite for salt kept it alive (1936) and showed the same in humans (1940). Our first paper in 1955 demonstrated that salt appetite was an innate response to salt depletion. Since then, we have pursued the notion that the neuroendocrine consequences of sodium depletion create a brain state that raises salt appetite. In Epstein's laboratory, it was shown that angiotensin and aldosterone, the hormones of salt retention in the periphery, act synergistically in the brain to produce salt appetite in the rat. Block either hormone and the appetite is reduced by half; block both and the appetite is eliminated despite severe bodily need. With repeated depletions or treatments of the brain with angiotensin and aldosterone, salt ingestion increases, reaching an asymptote by the third depletion. Need-free intake of NaCl also increases, especially in female rats which ingest more NaCl than male rats. In Stellar's laboratory, running speed to salt solutions in a runway is used as a measure of salt appetite. When the appetite is raised with large doses of DOCA, a mimic of aldosterone, rats run rapidly for a taste of strong salt solutions as high as 24% (almost 4 molar). Using ingestion as a measure, the role of the atrial natriuretic peptide (ANP), an antagonist of angiotensin's physiological effect, was investigated as a modulator of salt appetite. When angiotensin is involved is producing salt appetite, following sodium depletion by a diuretic combined with a low-salt diet, ANP reduced salt intake by 40%. When salt appetite was raised by DOCA, however, ANP either had no effect or reduced salt ingestion by only 10%. The subfornical organ, the lateral preoptic area, and the central and medial nuclei of the amygdala are being investigated as major components of the limbic circuit underlying salt appetite produced by the actions of angiotensin, aldosterone and ANP in the brain.

Animals↗
PubMed2001

Pharmacology of appetite suppression: implication for the treatment of obesity.

Given the current global epidemic of obesity there is a demand for new anti-obesity drugs to overcome the problem. Many pharmacological agents reduce food intake and significantly decrease body mass when administered to animals but affect feeding behaviour in a profoundly different way indicating the variety of biological mechanisms by which such agents act (appetite verses non-appetite). More limited clinical data demonstrates that some of the same drugs produce decreases in food intake and weight loss in humans. A few of these drugs do so by modifying the functioning of the appetite system as measured by subjective changes in feelings of hunger and fullness (indices of satiety). These drugs that modify the daily flux of appetite could be considered as 'appetite suppressants' with clinical potential as anti-obesity agents. Drugs that can be considered suitable candidates for appetite suppressants are agents that enhance peripherally satiety peptide systems (such as CCK, Bombesin/GRP, Enterostatin and GLP-1), alter the CNS levels of various hypothalamic neuropeptides (NPY, Galanin, Orexin, CART and Melanocortins) or monoamine neurotransmitters (such as serotonin, nor-adrenaline and possibly dopamine). Recently, the hormone leptin has become regarded as a key hormonal signal linking adipose tissue status with a number of key central nervous system circuits (NPY, CART, CRF, Melanocortins and possibly Orexins). This tonic system may also provide drug targets for the control of appetite. Any changes induced by a potential appetite suppressant should be considered in terms of the (i) psychological experience and behavioural expression of appetite, (ii) metabolism and peripheral physiology, and (iii) functioning of CNS neural pathways. In humans, such modulation of appetite will involve changes in total caloric consumption, subjective changes in feelings of hunger and fullness, preferences for specific food items, and general macronutrient preferences. These may be expressed behaviourally as changes in meal patterns, snacking behaviour and food choice. Within the next 20 years it is certain that clinicians will have a new range of anti-obesity compounds available to choose from. Such novel compounds may act on a single component of the appetite system or target a combination of these components detailed in this review. Such compounds used in combination with life style changes and dietary intervention may be critical in dealing with the rising world epidemic of obesity.

Animals↗
PubMed2001

Acute effects of peritoneal dialysis solutions on appetite in non-uremic rats.

BACKGROUND: Standard peritoneal dialysis (PD) solutions may contribute to anorexia in PD patients due to the peritoneal absorption of glucose from the dialysate, abdominal discomfort and other factors. New PD solutions containing alternative osmotic agents, neutral pH and bicarbonate as buffer were recently developed. To test the effect of these solutions on appetite, we investigated how intraoral (IO) intake of sucrose via an IO cannula was influenced by intraperitoneal (IP) infusion of different PD solutions in an appetite model in rats. METHODS: The IO intake was measured in male Wistar rats after an IP dwell of 30 and 120 minutes with the following PD solutions: 1.36%, 2.27% and 3.86% glucose based and lactate buffered solutions (D); 1.36%, 2.27% and 3.86% glucose based and bicarbonate/lactate buffered solutions (P); 7.5% icodextrin based solution (E); 1.1% amino acid-based solution (N); and, 2.5% glucose-based lactate-buffered solution (GB), using sham injection (injection without infusion) as control. Prior to the tests, rats were provided with an IO cannula, and were trained for two weeks until the rate of IO intake had stabilized. RESULTS: The D and N solutions inhibited IO intake. For the D solutions, the degree of appetite suppression was higher with the higher concentration of glucose. P 3.86%, but not P 1.36% and P 2.27% solutions, inhibited the IO intake. However, a comparison of the degree of appetite inhibition between D and P showed less inhibition with P 1.36%, 2.27% and 3.86% solutions than with corresponding D solutions. The E solution did not seem to suppress appetite. Finally, no significant difference in IO intake was found between rats given GB 2.5% and D 2.27%. CONCLUSIONS: In this appetite model in rats, the measurement of IO intake after the IP infusion of different dialysis solutions showed that (1) N and D solutions may reduce appetite, and for the D solutions the degree of appetite inhibition was related to the dialysate concentrations of glucose; (2) the P solutions had less impact on appetite than the D solutions; (3) the E solution had no impact on appetite during the short dwells of 30 and 120 minutes. The demonstrated differences between the different solutions appear to be due to different concentrations, and type, of nutrients used as osmotic agent (glucose, amino acids, icodextrin) or buffer (lactate), although differences in dialysate pH, tonicity and concentration of glucose degradation products also may be important. The present studies suggest a possible positive effect on appetite by using bicarbonate/lactate buffered solutions instead of lactate buffered solutions.

Administration, Oral↗
PubMed1981

The effect on salt appetite and the renin-aldosterone system on replacing the depleted ions to sodium-deficient cattle.

1. Sodium depletion which occurred in cattle following exteriorization of a parotid duct produced depression of both plasma and salivary sodium, acidosis, elevated plasma aldosterone and renin activity. Increased sodium appetite, characteristic of sodium depletion, was assessed by operant behaviour where scoring of panel pressing for NaHCO(3) rewards showed change in sodium appetite.2. Sodium-depleted calves readily drank the calculated ionic deficit as a hypertonic solution (4 l.) in a few minutes, or as an isotonic solution (16 l.) usually within 30 min.3. When the ionic deficit was restored by either i.v. infusion or drinking, sodium appetite was reduced significantly. The suppression of sodium appetite was more rapid when the depleted ions were replaced by drinking (30 min) than by i.v. infusion (2 hr) but in both circumstances the effect was short lived since sodium appetite redeveloped within 3 hr.4. The rapid return of sodium appetite following restoration of the ionic deficit occurred even when the plasma sodium level was normal. Other biochemical changes resulting from sodium depletion, such as acidosis and reduced salivary sodium, could not be correlated with variation in sodium appetite.5. Rapid infusion of Ringer saline (4 l.) did not inhibit the sodium appetite, which suggests that neither vascular volume changes per se nor vascular baroreceptors control sodium appetite in sodium-deficient calves.Plasma aldosterone fell rapidly following infusion of the hypertonic solution but only slightly with the isotonic infusion. The change in plasma hormone level was not related to changes in sodium appetite.6. Drinking the hypertonic solution produced a marked reduction in panel pressing for NaHCO(3) with a rapid rise in plasma sodium. Consumption of the larger volume of isotonic solution also inhibited sodium intake but plasma sodium remained low. A secondary increase in plasma renin activity (p.r.a.) occurred following ingestion of the hypertonic solution, but both p.r.a. and aldosterone fell to normal levels over the next 6 hr when the cattle again showed marked sodium appetite. It is possible that these effects may be due to ion and fluid movement between gut and extracellular fluid and reflect osmolality changes or tissue dehydration.7. It is concluded that the sodium appetite of sodium deficient cattle is only temporarily alleviated by restoration of the depleted ionic loss, and that the behavioural response to seek sodium rewards is independent of plasma sodium, p.r.a., aldosterone and volume changes in the gut and vascular system.8. Recent reports suggest that sodium appetite may be controlled by receptors in the hypothalamus or by angiotensin II in the brain. In cattle the capacious gut may also be involved, since sodium appetite is inhibited more rapidly when the depleted ions are taken orally than by i.v. infusion.

Aldosterone↗