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At least 19 recordsLinked to original sources
PubMed1994

Fetal experience with milk or an artificial nipple alters appetitive and aversive responses to perioral cutaneous stimuli.

Fetal rats exhibit oral grasping of an artificial nipple. The authors examined interactive effects of sensory stimuli normally encountered in the suckling environment on subsequent responses to the nipple. Embryonic Day 20 rat fetuses received an infusion of milk, lemon, or saline through a hollow artificial nipple or an intraoral cannula (producing no nipple stimulation). One minute after sensory pretreatment, behavioral responses of fetuses to an artificial nipple were recorded on videotape for frame-by-frame analysis. Preexposure to the artificial nipple decreased the number of oral grasps and facial wipes directed toward the artificial nipple but increased the duration of grasp responses. Milk uniformly reduced fetal responsiveness to the nipple. Furthermore, the artificial nipple enhanced fetal responses to perioral cutaneous stimulation, whereas milk suppressed perioral responsiveness. These data suggest that the perinatal rat's 1st experience with milk or the nipple can alter subsequent responses to suckling stimuli.

Animals↗
PubMed1999

Neuropeptide Y restores appetite and alters concentrations of GH after central administration to endotoxic sheep.

The objective of this study was to determine whether neuropeptide Y (NPY) and recombinant human interleukin-1 receptor antagonist (IL-1ra) would: first, increase food intake; secondly, decrease concentrations of GH; thirdly, reduce GHRH-induced release of GH; and fourthly, reduce changes to concentrations of IGF-I in plasma during experimental endotoxemia in sheep. Six treatments were given to six castrated male sheep in a 6x6 Latin square treatment order. Osmotic mini-pumps were implanted at 0 h and a jugular vein was cannulated. Each sheep was continuously infused with saline (0.9%) or lipopolysaccharide (LPS) (20 micrograms/kg per 24 h, s.c.) at 10 microliters/h for 72 h via the osmotic mini-pumps. Blood samples (3 ml) were collected at 15-min intervals from 24 to 33 h. At 26 h, one of three treatments (artificial cerebrospinal fluid, NPY or IL-1ra) was injected i.c.v. within 30 s (0.3 microgram/kg), then infused i.c.v. from 26 to 33 h (600 microliters/h) at 0.3 microgram/kg per h. GHRH was injected i.v. (0.075 microgram/kg) at 32 h after which blood samples were collected at 5, 10, 15, 30, 45 and 60 min. Feed intake was reduced up to 50% for 48 h in LPS-treated compared with non-LPS-treated sheep. NPY restored feed intake in LPS-treated sheep and induced hyperphagia in non-LPS-treated sheep from 24 to 48 h. In contrast, IL-1ra did not affect appetite. Injection of NPY increased concentrations of GH from 26 to 27 h, while IL-1ra had no effect. Infusion of NPY suppressed GHRH-induced release of GH. However, no treatment altered pulse secretion parameters of GH. Concentrations of IGF-I were 20% higher at 72 h in LPS-treated sheep given NPY than in sheep treated with LPS alone, and this may reflect increased appetite from 24 to 48 h. We concluded that reduced appetite during endotoxemia is due to down-regulation of an NPY-mediated mechanism. Furthermore, NPY stimulates release of GH in healthy sheep, does not reduce pulse secretion parameters of GH, but does suppress GHRH-induced release of GH in endotoxic sheep. Therefore, NPY may be an important neurotransmitter linking appetite with regulation of GH during endotoxemic and healthy states in sheep.

Animals↗
PubMed1998

The role of the central nervous system in the psychoneuroendocrine disturbances of anorexia and bulimia nervosa.

It has been well-recognized that starvation in anorexia and bulimia nervosa causes endocrine disturbances. Such disturbances may help understand why many people with eating disorders cannot easily reverse their illness since people with eating disorders often enter a downward spiraling circle with malnutrition sustaining and perpetuating the desire for more weight loss and dieting. Symptoms, such as obsessions and dysphoric mood, and altered appetitive behavior, may be exaggerated by neuropeptide alterations and thus contribute to this downward spiral. While neuropeptide disturbances do not appear to be a permanent feature or cause or anorexia nervosa, these disturbances are strongly entrenched, and are not easily corrected by improved nutrition or short-term weight normalization. This suggests that therapy should be sustained for months after nutritional normalization.

Anorexia Nervosa↗
PubMedDate not supplied

Amylin decreases food intake in mice.

The isolation of amylin from pancreatic islets has stimulated interest in its potential role in the pathogenesis of type II diabetes mellitus and in its possible physiological roles. Amylin administered intraperitoneally decreased food intake in non-food-deprived and food-deprived diabetic and nondiabetic mice. Amylin also decreased feeding induced by insulin administration without significantly affecting blood glucose levels. Amylin also decreased food intake following intracerebroventricular administration. It is possible that amylin plays a physiological role in appetite regulation and may play a pathophysiological role in the altered appetites seen in some persons with type II diabetes mellitus.

Amyloid↗
PubMed1989

Tobacco use in Alzheimer's disease.

Cholinergic abnormalities in Alzheimer's disease (AD) may be important in the pathogenesis of memory impairment. Tobacco use, which might reflect changes in central nicotinic receptors, was examined by chart review of 272 patients (M:F 86:186) with "probable" AD by NIH criteria, and by interviewing next-of-kin of 39 patients (M:F 15:24) and spouse controls. On chart review, 37% of females and 98% of males had used tobacco, but only 10% of females and 14% of males were still smoking at AD onset. Interval between stopping smoking and AD onset was 18.3 +/- 7.7 years in females and 16.6 +/- 6.8 years in males. Losing the taste for smoking preceded cessation in 60.3% of females and 16.2% of males. Only 7.9% of females and 4.4% of males had withdrawal symptoms. Next-of-kin interview revealed that patients and controls were comparable in demographic data, alcohol use, and smoking habits. 24% of patients and 37% of controls had stopped smoking, often due to losing the taste for smoking (32% of patients; 18% of controls). Withdrawal symptoms occurred in 21% of patients and 41% of controls. Relative to controls, patients less frequently had increased appetite (28% vs 47%), but more often had changed sex drive (22% vs 0%) and altered preference for specific alcoholic beverages (11% vs 0%), after stopping smoking. In AD, the loss of desire to smoke, lack of nicotine withdrawal, and altered appetites long precede cognitive symptoms, suggesting preclinical changes in central nicotinic receptors, as well as possible diagnostic and therapeutic strategies.

Aged↗
PubMedDate not supplied

A review of endocrine changes in anorexia nervosa.

Anorexia nervosa is a syndrome of unknown etiology. It is associated with multiple endocrine abnormalities. Hypothalamic monoamines (especially serotonin), neuropeptides (especially neuropeptide Y and cholecystokinin) and leptin are involved in the regulation of human appetite, and in several ways they are changed in anorexia nervosa. However, it remains to be clarified whether the altered appetite regulation is secondary or etiologic. Increased secretion of corticotropin-releasing hormone and proopiomelanocortin seems to be secondary to starvation, however, there is evidence that it may maintain and intensify anorexia, excessive physical activity and amenorrhea. Hypothalamic amenorrhea, which is a diagnostic criterion in anorexia nervosa, is not solely related to the low body weight and exercise. Growth hormone resistance with low production of insulin-like growth factor I and high growth hormone secretion reflect the nutritional deprivation. The nutritional therapy of patients with anorexia nervosa might be improved by administering an anabolic agent such as growth hormone or insulin-like growth factor I. So far none of the endocrine abnormalities have proved to be primary, however, there is increasing evidence that some of these might participate in a vicious circle.

Anorexia Nervosa↗
PubMed1990

Sexual motivation: a neural and behavioural analysis of the mechanisms underlying appetitive and copulatory responses of male rats.

Experiments investigating the neural mechanisms underlying the expression of masculine sexual behaviour are discussed in the context of the hypothesis set out by Frank Beach that suggested the existence of separate sexual arousal and performance mechanisms. The results indicate that the medial preoptic area is crucially involved in consummatory aspects of sexual behaviour: lesions and chemical manipulations of the area profoundly affect mounts, intromissions and ejaculation, but tend not to alter appetitive sexual responses. By contrast, ventral striatal dopamine-dependent mechanisms primarily affect appetitive sexual responses, measured in a variety of paradigms, but tend not to alter copulatory behaviour itself. Finally, associative mechanisms, for example those by which arbitrary environmental stimuli come to control appetitive sexual responses through their predictive association with sexual reinforcement, are shown to depend at least in part on interactions between the basolateral amygdala and dopamine-dependent events in the ventral striatum. Thus, diverse neural and behavioural procedures have revealed that separable neural mechanisms appear to be involved more or less selectively with different components of the male rat's sexual response system. It may still be useful to conceptualize separate sexual arousal and intromission/ejaculatory mechanisms when studying the neuroendocrine basis of sexual behaviour. However, a major challenge is to understand the way in which elements of the telencephalic limbic system, the striatum and preoptic area, some of which are targets for the action of sex steroids, interact to produce an integrated pattern of sexual behaviour.

Animals↗
PubMed1985

Cerebrospinal fluid sodium concentration and salt appetite.

Infusion into a lateral brain ventricle (IVT) of different hypertonic (0.7 M) saccharide solutions decreased [Na+] of cerebrospinal fluid (CSF). Increased Na appetite of moderately Na-deplete sheep was observed during infusion of mannitol, L-glucose or L-fucose, while no change was observed during infusion of D-glucose, D-fucose, D-mannose, 2-deoxy-D-glucose, 3-O-methyl-glucose or fructose. In other experiments, increased Na appetite was observed during infusion of 2.3 mM phlorizin (a relatively specific blocker of Na-coupled glucose transport into cells) or 2.3 mM phlorizin plus 0.7 M D-glucose. In addition, phlorizin eliminated the characteristic decrease in Na appetite but did not affect the increase in water intake caused by IVT infusion of hypertonic NaCl which increased [Na+] of CSF. The results suggest that: (a) there are sensors within the neuropil which respond to change of [Na+] and influence Na appetite, and that these changes of [Na+] are induced deep within the neuropil by those saccharides which do not cross the blood-brain barrier or enter cells; change of CSF[Na+] alone is not sufficient to alter appetite but a change in brain extracellular fluid (ECF)[Na+] is probably necessary; (b) the theory is advanced that the stimulus for altered Na intake could be altered brain ECF[Na+] producing a change in cerebral intracellular fluid (ICF)[Na+] of the sensors; and (c) phlorizin, in reducing or blocking Na-coupled glucose transport, could increase Na appetite by producing a fall in ICF[Na+] of the specific neurones subserving sodium appetite or prevent a decrease in Na appetite caused by IVT infusion of hypertonic NaCl by preventing an increase in ICF[Na+] of this same neuronal system.

Animals↗
PubMed2000

Conjugated linoleic acid supplementation in humans: effects on circulating leptin concentrations and appetite.

Conjugated linoleic acid (CLA) has been demonstrated to reduce body fat in animals. However, the mechanism by which this reduction occurs is unknown. Leptin may mediate the effect of CLA to decrease body fat. We assessed the effects of 64 d of CLA supplementation (3 g/d) on circulating leptin, insulin, glucose, and lactate concentrations in healthy women. Appetite was assessed as a physiological correlate of changes in circulating leptin levels. Analysis of plasma leptin concentrations adjusted for adiposity by using fat mass as a covariate showed that CLA supplementation significantly decreased circulating leptin concentrations in the absence of any changes of fat mass. Mean leptin levels decreased over the first 7 wk and then returned to baseline levels over the last 2 wk of the study in the CLA-treated group. Appetite parameters measured at around the time when the greatest decreases in leptin levels were observed showed no significant differences between supplementation and baseline determinations in the CLA-supplemented group or between the CLA and placebo-supplemented groups. There was a nonsignificant trend for mean insulin levels to increase toward the end of the supplementation period in CLA-treated subjects. CLA did not affect plasma glucose and lactate over the treatment period. Thus, 64 d of CLA supplementation in women produced a transient decrease in leptin levels but did not alter appetite. CLA did not affect these parameters in a manner that promoted decreases of adiposity.

Adipose Tissue↗
PubMedDate not supplied

Intestinal transit and body weight responses to ovarian hormones and dietary fiber in rats.

A two-part experimental design was used to study the effects of ovarian hormone cessation, hormone supplementation, and dietary fiber composition on body weight, appetite, and intestinal transit. In Part 1, effects of ovarian hormone status on body weight and baseline and stimulated intestinal transit were measured in chow-fed rats. Sprague-Dawley rats were ovariectomized (OVX), then injected daily (22 days) with estrogen (E), progesterone (P), the combination (E + P), or placebo. Controls were sham operated and placebo injected. Among OVX rats, E and E + P had the least body weight gain (9%, 6%); placebo and P had the greatest (36%, 34%). In OVX-P, baseline intestinal transit (measured in anesthetized rats as distance traveled by a charcoal marker) was relatively low, but vagal stimulation via centrally administered thyrotropin-releasing hormone evoked an increase significantly larger than that in other groups. In Part 2, experiments probed the interacting effects of ovarian hormone cessation and dietary fiber composition on body weight and baseline intestinal transit. Caloric intake was measured to determine the contribution of altered appetite. Rats were OVX or sham operated, then fed liquid diets with or without dietary fiber (25 days). OVX fiber-fed rats had significantly higher caloric intake, weight gain, and baseline intestinal transit than other groups. Caloric intake did not fully account for group differences. These results demonstrate modulation of GI function by ovarian hormones and dietary fiber.

Animals↗
PubMed1978

Effect of diazepam on food consumption in rats.

Diazepam significantly increased milk consumption in rats that had never been exposed to this food before but not in rats trained to drink milk. Diazepam failed to increase lever-pressing for food reward except when this behavior had been previously suppressed by the simultaneous administration of electric shock. These data suggest that diazepam does not alter appetite, but enhances the expression of motivation suppressed by instinct or training.

Animals↗
PubMed1990

What do we mean when we say "palatable food"?

The word palatability and related words have not been used in a consistent way. Palatability may be a property of a food, of the organism eating the food, or both. Investigators have failed to distinguish different possible meanings of the statement: "palatable foods increase intake". This may indicate: (1) a simple observation that some foods stimulate more intake than others, (2) an innate response to the taste of foods that alters appetite, (3) a correlate of food intake that does not itself affect intake, and (4) a link in a causal chain involving prior associations between foods and their postingestive consequences.

Appetite↗
PubMed2000

Psychobiological problems in heavy 'ecstasy' (MDMA) polydrug users.

Twelve heavy recreational ecstasy drug users (30-1000 occasions), 16 light ecstasy users (1-20 occasions) and 22 non ecstasy user controls, with group mean ages around 21 years, were compared. Three self-rating questionnaires were completed when drug-free: the SCL-90 (an outpatient psychiatric symptom checklist), the impulsiveness venturesomeness and empathy (IVE) scale; and the uplifts, hassles, stresses and cognitive failures questionnaire. Heavy Ecstasy users reported significantly higher scores than controls on the following SCL-90 factors: paranoid ideation, psychoticism, somatisation, obsessionality, anxiety, hostility, phobic anxiety, altered appetite and restless sleep, together with greater IVE impulsiveness. Light ecstasy users generally produced intermediate scores, with significantly higher scores than controls on two factors and significantly lower scores than heavy ecstasy users on another two. Previous reports have described various psychiatric and psychobiological disorders in recreational ecstasy users, but it is not known how typical they are, being mainly based on individual case studies. This is the first study to describe psychological problems in a non clinical sample of young recreational ecstasy users. However, our ecstasy users were polydrug users, with both groups showing significantly greater usage of amphetamine, LSD and cocaine, than the controls. These other illicit drugs probably contributed to their adverse psychobiological profiles, while there is also the possibility of pre-existing differences between ecstasy users and non users. However, since repeated MDMA can cause serotonergic neurotoxicity in laboratory animals and man, these problems may reflect reduced serotonin activity induced by regular ecstasy use.

Adolescent↗
PubMed2000

Brain-derived neurotrophic factor regulates glucose metabolism by modulating energy balance in diabetic mice.

We previously reported that brain-derived neurotrophic factor (BDNF) regulates both food intake and blood glucose metabolism in rodent obese diabetic models such as C57BL/KsJ-lepr(db)/lepr(db) (db/db) mice. To elucidate the effect of BDNF on glucose metabolism, we designed a novel pellet pair-feeding apparatus to eliminate the effect of appetite alteration on glucose metabolism. The apparatus was used to synchronize food intake precisely between BDNF-treated and vehicle-treated db/db mice. It was shown using this pellet pair-feeding apparatus that BDNF administered daily (20 mg x kg(-1) x day(-1)) to db/db mice significantly lowered blood glucose compared with pellet pair-fed db/db mice. To evaluate the effect of BDNF on insulin action, we used streptozotocin-induced type 1 diabetic mice. In this case, BDNF did not lower blood glucose concentration but rather enhanced the hypoglycemic action of insulin. In hyperglycemic db/db mice, pancreatic insulin content was reduced and glucagon content was increased compared with normoglycemic db/m mice. BDNF administered to db/db mice significantly restored both pancreatic insulin and glucagon content. Histological observations of aldehyde-fuchsin staining and immunostaining with anti-insulin indicated that insulin-positive pancreatic beta-cells were extensively regranulated by BDNF administration. We also studied the effect of BDNF on KK mice, normoglycemic animals with impaired glucose tolerance. In these mice, BDNF administration improved insulin resistance in the oral glucose tolerance test. To elucidate how blood glucose was metabolized in BDNF-treated animals, we investigated the effect of BDNF on the energy metabolism of db/db mice. Body temperature and oxygen consumption of the pellet pair-fed vehicle-treated mice were remarkably lower than the ad libitum-fed vehicle-treated mice. Daily BDNF administration for 3 weeks completely ameliorated both of the reductions. Finally, to clarify its action mechanism, the effect of intracerebroventricular administration of BDNF on db/db mice was examined. Here, a small dose of BDNF was found to be effective in lowering blood glucose concentration. This indicates that BDNF regulates glucose metabolism by acting directly on the brain.

Animals↗
PubMed1991

Relationships between weight and caloric intake of men who stop smoking: the Multiple Risk Factor Intervention Trial.

Data from 6,569 middle-aged men in the Multiple Risk Factor Intervention Trial were analyzed to determine whether the weight change associated with smoking cessation resulted primarily from appetite or metabolic alterations. The appetite hypothesis attributes weight gain to an enhanced appetite and subsequent increase in caloric intake. The metabolic change hypothesis attributes weight gain to a metabolic alteration and subsequent decrease in basic caloric needs. Caloric intake and weight changes were tabulated for men who quit smoking and were compared to similar changes in men who continued smoking over 12 months. The difference between caloric intake changes in men quitting smoking versus men continuing smoking, controlled for weight change, was attributed to the metabolic change hypothesis. Men who quit smoking consumed 103 calories per day less (95% confidence interval = 29 to 177) than men who continued smoking with similar body weight changes. The decrease in caloric intake attributed to smoking cessation was proportional to the number of cigarettes smoked prior to cessation [corrected].

Adult↗
PubMed1997

Altered concentrations of appetite regulators may contribute to the development and maintenance of HIV-associated wasting.

OBJECTIVE: To examine the relation of circulating appetite neuropeptides, CCK-8 sulphate (CCK-8s) and beta-endorphin, and the tumour necrosis factor-alpha (TNF-alpha) and soluble TNF receptors (sTNFR) to the anorexia and wasting associated with HIV-infection. DESIGN: Cross-sectional analysis. SETTING: A university-based HIV/AIDS ambulatory clinic in Madrid, Spain. PARTICIPANTS: Thirty-six randomly selected AIDS patients without concomitant diseases or secondary infections were classified into two groups: 19 patients with wasting and 17 with normal body weight, and 18 healthy controls. MEASUREMENTS: Nutritional status was evaluated by anthropometry, laboratory parameters and self-report of appetite. Plasma levels of TNF-alpha and sTNFR proteins p55 (sTNFR-p55) and p75 (sTNFR-p75) were determined by enzyme immunoassay, whereas CCK-8s and beta-endorphin levels were measured by radioimmunoassay. RESULTS: AIDS patients with wasting had significantly higher plasma concentrations of CCK-8s, but lower levels of beta-endorphin when compared to well-nourished AIDS patients (P < 0.01) or controls (P < 0.001). Mean levels of TNF-alpha, and sTNFR-p55 and sTNFR-p75 were greater in AIDS patients with wasting than in asymptomatic AIDS patients or in controls. No significant association was observed between any of these circulating peptides and the parameters of malnutrition. CONCLUSIONS: An activation of the TNF system, together with reciprocal changes in plasma concentrations of two neuropeptides with opposing appetite regulation, that is increased concentrations of CCK-8s but lower levels of beta-endorphin, are associated with the presence of HIV wasting. We hypothesize that these changes may contribute to the development of HIV wasting by producing a pathological inhibition of appetite.

Acquired Immunodeficiency Syndrome↗
PubMed1990

How not to think about immediate dietary and postingestional influences on appetites and satieties.

Palatabilities and also satieties are assumption-loaded abstractions from the observable momentary causal relationships between eating or drinking and the situations in which it occurs. Palatability is neither in the food nor in the ingestive movements. Relative preference can vary with context, contrary to the usual concept of stable palatability. Satieties exemplify this, for they can be food-specific, i.e. ingestion-induced suppression of appetite may alter the supposed palatability hierarchy.

Appetite↗