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Results for “Appetite Alterations”

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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↗
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↗
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↗
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↗
PubMed1988

Monoamine oxidase inhibitors and weight gain.

Weight gain associated with antidepressant therapy is a common problem that often results in noncompliance. Some authors suggest that monoamine oxidase inhibitors (MAOI) are less likely to produce weight gain than tricyclic antidepressants. This paper addresses the relative potential for weight gain with the MAOI. Assessing the potential for antidepressant-induced weight gain necessitates separating the weight changes associated with alterations in mood disorders from those due to drug-induced alterations in appetite control. The mechanisms of appetite control are reviewed briefly followed by proposed mechanisms by which the MAOI may alter this control. A literature review suggests that phenelzine is the MAOI most likely to induce weight gain; reports of isocarboxazid-induced weight gain are less common. There are no cases of tranylcypromine-induced weight gain in the literature that are clearly associated with the drug. The MAOI probably have different effects on the mechanisms of appetite control.

Humans↗
PubMed1976

Anorexia and weight loss in the portacaval-shunted pig.

The pig shows a marked response to end-to-side portacaval shunt. Survival is short and levels of alkaline phosphatase and cholesterol fall. This study was designed to determine the role of the reduced food intake which follows the operation upon these results. In pair-fed, sham-operated pigs, survival was short and levels of alkaline phosphatase and cholesterol also fell. Sham-operated animals fed normally did not show this response. Reduced appetite has been recorded in many experimental animals after portacaval shunt, but the cause remains to be elucidated. Encephalopathy, bacteremia, peptic ulceration, or hormonal imbalance could be implicated. Similar alteration in appetite and weight loss have not been observed in children who have been treated by portacaval shunt for glycogen storage disease or hypercholesterolemia; however, the underlying metabolic disorder or the species difference may be a contributory cause.

Alkaline Phosphatase↗
PubMed1997

Effects of naltrexone on food intake and changes in subjective appetite during eating: evidence for opioid involvement in the appetizer effect.

The effects of 50 mg naltrexone on eating and subjective appetite were assessed in a double-blind placebo-controlled study with 20 male volunteers. Appetite was monitored using a disguised digital balance connected to a micro-computer, which constantly monitored the amount of food remaining, and which automatically interrupted feeding for 30 s after every 50 g consumed to allow appetite ratings to be made. Half the subjects ate pasta with a cheese sauce, and the remainder pasta with a tomato sauce. Subjects ate significantly less of both foods after 50 mg naltrexone than in either the placebo condition or on the initial (familiarisation) day. Naltrexone also reduced the rated pleasantness of both foods, and reduced overall eating rate. When best-fit quadratic functions were used to describe changes in rated hunger in relation to intake within the meal, naltrexone abolished the positive linear component reflecting the initial stimulation of appetite without altering either intercept or the negative quadratic function. Although mood ratings suggested that naltrexone had a mild sedative effect, mood changes alone could not explain the effects of naltrexone on appetite. Overall, these data suggest a specific role for opioids in the stimulation of appetite through palatability.

Adult↗
PubMed1981

Endocrine profile of patients with post-tubal-ligation syndrome.

The endocrine profile of the midluteal phase was assessed in 29 patients with the post-tubal-ligation syndrome, consisting of pain, bleeding and premenstrual tension. Compared to normal controls, the patients had a high serum estradiol and a low serum progesterone level. This abnormal luteal function may be responsible for the symptoms observed and may also explain the failure to conceive following successful reversal of tubal ligation. It is recommended that patients seeking sterilization reversal be screened for abnormal luteal function preoperatively. Selection of sterilization procedures that minimize alteration in luteal function should be given high priority.

Adult↗