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At least 19 recordsLinked to original sources
PubMed2002

Induction of a salt appetite alters dendritic morphology in nucleus accumbens and sensitizes rats to amphetamine.

Sensitization to drugs, such as amphetamine, is associated with alterations in the morphology of neurons in the nucleus accumbens, a brain region critical to motivation and reward. The studies reported here indicate that a strong natural motivator, sodium depletion and associated salt appetite, also leads to alterations in neurons in nucleus accumbens. Medium spiny neurons in the shell of the nucleus accumbens of rats that had experienced sodium depletions had significantly more dendritic branches and spines than controls. In addition, a history of sodium depletions was found to have cross-sensitization effects, leading to enhanced psychostimulant responses to amphetamine. Thus, neuronal alterations common to salt and drug sensitization may provide a general mechanism for enhanced behavioral responses to subsequent exposures to these challenges.

Amphetamine↗
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↗
PubMedDate not supplied

Toluene alters appetite, NPY, and galanin immunostaining in the rat hypothalamus.

Toluene is a neurotoxic organic solvent widely used in industry and extensively inhaled by solvent abusers. Toluene, diluted 1:1 in olive oil, was administered intraperitoneally at a dose of 1.3 ml/kg/day for 4 days. Controls received the vehicle in the same dose and duration. Food intake and body weight were measured daily. A regional hypothalamic NPY and galanin immunocytochemical study was also performed. Acute toluene administration in rats generated a reduction in food intake and body weight gain. A significant decrease in NPY immunostaining in the paraventricular nucleus and an increase in arcuate nucleus without changes in other hypothalamic regions were observed. Also, acute toluene administration increased galanin immunostaining in paraventricular and arcuate nuclei. These results suggest that the hypothalamic NPY arcuate-paraventricular projection is involved in the anorectic effect of acute high-dose toluene administration. Changes in regional hypothalamic galanin expression could represent a compensatory mechanism against toluene-induced anorexia.

Animals↗
PubMed2003

Chronic MCH-1 receptor modulation alters appetite, body weight and adiposity in rats.

Central administration of the neuropeptide melanin-concentrating hormone (MCH) stimulates feeding in rodents. We studied the effects of intracerebroventricular (i.c.v.) administration of an MCH-1 receptor agonist (Compound A) and an MCH-1 receptor antagonist (Compound B) on feeding in satiated rats. Compound B (10 microg, i.c.v.) blocked the acute orexigenic effect of Compound A (5 microg, i.c.v.). In an experiment designed to either stimulate or inhibit MCH-1 receptor signaling over an extended period, rats received continuous i.c.v. infusions of vehicle (saline), Compound A (30 microg/day), Compound B (30 or 48 microg/day) or neuropeptide Y (24 microg/day, as positive control) via implantable infusion pumps. Continuous MCH-1 receptor activation recapitulated the obese phenotype of MCH-over-expressor mice, manifest as enhanced feeding (+23%, P<0.001), caloric efficiency and body weight gain (+38%, P<0.005) over the 14-day period relative to controls. Chronic MCH-1 receptor activation also elevated plasma insulin and leptin levels significantly. Conversely, continuous MCH-1 receptor antagonism led to sustained reductions in food intake (-16%, P<0.001), body weight gain (-35%, P<0.01), and body fat gain relative to controls, without an effect on lean mass. Antagonism of the MCH-1 receptor may be an effective approach for the treatment of obesity.

Adipose Tissue↗
PubMed2006

Design and synthesis of (ant)-agonists that alter appetite and adiposity.

Over the past decade, hypothalamic circuits have been described that impact energy homeostasis in rodents and humans. Our drug development efforts for the treatment of obesity and the metabolic syndrome have largely focused on selected genetic and/or pharmacologically validated pathways. The translation of these pathways into therapeutics for the treatment of obesity will find its first clinical successes over the coming decade. Initial efforts have focused on gaining a better understanding of the relevance of rodent pharmacological and genetic observations for the development of therapeutics for the treatment of human obesity. We pursue pathways defined by the expression of the ghrelin receptor, melanin-concentrating hormone receptors, melanocortin receptors, cannabinoid receptors and neuropeptide Y1 and Y5 receptors. In this review, we will discuss drug development efforts for the treatment of obesity, focused on selective melanocortin 4 receptor agonists and neuropeptide Y1 and Y5 receptor antagonists. These drug development efforts required an in-depth understanding of cell-based observations which drive the development of compound structure-activity relationships. These include understanding of receptor function in selected cell-based backgrounds and early evaluation and validation of ex vivo observations in appropriate in vivo models. In order to develop selective and safe anti-obesity drugs, diverse approaches are needed to increase the likelihood of clinical success, including: (i) developing a detailed understanding of the predictive value of rodent pathways for treatment of human disease; (ii) knowledge of the exact location of targeted receptor subtypes for the clinical indication under study in order to derive a suitable compound profile; (iii) predictive measures of in vivo and/or ex vivo receptor occupancy required to bring about a desired physiological effect; (iv) predictive parameters that outline that the drug-derived effects are safe and mechanism-based; and (v) the refinement of selected compound classes, aimed at their clinical use.

Adiposity↗
PubMed2001

Altered subjective appetite parameters in Crohn's disease patients.

BACKGROUND AND AIM: Altered appetite and early satiety may promote anorexia associated with Crohn's disease. The aim of this study was to assess the impact of disease activity on subjective appetite parameters in Crohn's disease patients. METHODS: Seventeen patients with Crohn's disease and 15 healthy controls (8 M: 7 F, 34 (20-35) years) were studied. Subjects rated their hunger, desire to eat, fullness and level of satiety using visual analogue scales after an overnight fast. Subjects were reassessed after ingestion of 500 and 1000 ml water. Anthropometry was used to determine percentage body fat. Serum leptin & TNF- alpha levels were assessed using immunoassay. Disease activity was determined using the Harvey-Bradshaw index. RESULTS: Hunger ratings for active Crohn's disease patients were significantly lower than controls at baseline (P<0.05). Desire to eat was lower in patients with active Crohn's disease than controls both at baseline (95% CI, 0.3 mm, 40.7 mm) and after ingestion of 500 ml water (95% CI, 1.25 mm, 51.9 mm) (P<0.05). Serum leptin concentrations were significantly associated with percent body fat (r=0.57;P<0.001) and, after correcting for body fat status, tended to be higher in patients with active Crohn's disease (mean 0.9 ng/ml/% body fat; SD 0.8 ng/ml/% body fat) compared with either patients with inactive disease (mean 0.4 ng/ml/% body fat; SD 0.3 ng/ml/% body fat) or healthy controls (mean 0.3 ng/ml/% body fat; SD 0.2 ng/ml/% body fat) (P=0.15, ns). Appetite parameters and serum leptin concentrations showed no significant correlation. CONCLUSIONS: Subjective appetite parameters were altered in patients with active Crohn's disease. At baseline, patients with active Crohn's disease were less hungry than healthy controls and had less desire to eat. After ingestion of 500 ml of water, desire to eat was significantly less in patients with active disease as compared with healthy controls. Serum leptin concentration corrected for percent body fat tended to be higher in patients with active Crohn's disease compared with inactive Crohn's disease and healthy controls, but the differences did not reach statistical significance.

Adult↗
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↗
PubMed2005

Fetal and perinatal programming of appetite.

There is increasing concern about the rapidly rising incidence of obesity worldwide and its impact both on mortality, morbidity and the cost of healthcare. In the last 15 years, a large volume of research has linked low birth weight to many adult diseases in humans, such as Type II diabetes, cardiovascular disease, hypertension and the metabolic syndrome. Obesity is a causal factor in all these conditions. There are epidemiological studies linking low birth weight to increased adiposity, but the timing of the insult during gestation seems crucial, as reducing maternal nutrition in late gestation and during lactation causes a reduction in later obesity. Recent studies in animal models have provided clues towards mechanisms of altered appetite regulation following alterations in fetal and neonatal growth. The outcome of these and future studies could prove clinically crucial, particularly in the debate over the benefits of breast feeding, which provides a lower plane of nutrition compared with formula feeding.

Appetite Regulation↗
PubMed2000

Role of serotonergic and noradrenergic systems in the pathophysiology of depression and anxiety disorders.

There is abundant evidence for abnormalities of the norepinephrine (NE) and serotonin (5HT) neurotransmitter systems in depression and anxiety disorders. The majority of evidence supports underactivation of serotonergic function and complex dysregulation of noradrenergic function, most consistent with overactivation of this system. Treatment for these disorders requires perturbation of these systems. Reproducible increases in serotonergic function and decreases in noradrenergic function accompany treatment with antidepressants, and these alterations may be necessary for antidepressant efficacy. Dysregulation of these systems clearly mediates many symptoms of depression and anxiety. The underlying causes of these disorders, however, are less likely to be found within the NE and 5HT systems, per se. Rather their dysfunction is likely due to their role in modulating, and being modulated by, other neurobiologic systems that together mediate the symptoms of affective illness. Clarification of noradrenergic and serotonergic modulation of various brain regions may yield a greater understanding of specific symptomatology, as well as the underlying circuitry involved in euthymic and abnormal mood and anxiety states. Disrupted cortical regulation may mediate impaired concentration and memory, together with uncontrollable worry. Hypothalamic abnormalities likely contribute to altered appetite, libido, and autonomic symptoms. Thalamic and brainstem dysregulation contributes to altered sleep and arousal states. Finally, abnormal modulation of cortical-hippocampal-amygdala pathways may contribute to chronically hypersensitive stress and fear responses, possibly mediating features of anxiety, anhedonia, aggression, and affective dyscontrol. The continued appreciation of the neural circuitry mediating affective states and their modulation by neurotransmitter systems should further the understanding of the pathophysiology of affective and anxiety disorders.

Adrenocorticotropic Hormone↗
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↗
PubMed2005

Programming of appetite and type 2 diabetes.

In the past decade, epidemiological findings and data from experimental studies in animals have shown that the structure and function of the organism can be programmed during critical periods of development which can lead to detrimental long-term consequences for the health of an individual. Low birth weight has been linked to many adult diseases in humans including type 2 diabetes. The full detrimental effects of early growth restriction are often accompanied by the presence of obesity, which itself might be a manifestation of programmed appetite regulation in fetal and neonatal life. The understanding of interactions between leptin and insulin and their roles in glucose and body weight regulation provides clues towards mechanisms underlying altered appetite regulation and increased risk of type 2 diabetes in low birth weight individuals. Molecular mechanisms involved might include epigenetic alteration of the fetal genome in response to maternal nutrition.

Animals↗
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↗
PubMed2001

[Endocrine and reproductive disturbances in anorexia nervosa and bulimia nervosa].

Numerous endocrine abnormalities are associated with anorexia nervosa and bulimia nervosa. The principal complication is amenorrhoea. Hypothyroidism and hypercortisolism have been described as a protective mechanism to conserve energy. Growth hormone concentrations are often increased as a result of starvation. Insulin and blood sugar concentrations are decreased, but prolactin concentrations are remain normal. Considerable evidence exists of hypothalamic dysfunction in patients with eating disorders. This dysfunction is reflected in disturbances of endocrine function. Endocrine disturbances may be not solely related to the low body weight. Hypothalamic monoamines, neuropeptides and leptin are involved in the regulation of human appetite, and in several ways they are changed in eating disorders. However, it remains to be clarified whether the altered appetite regulation is secondary or etiologic.

Amenorrhea↗
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↗
PubMed2002

Chronic intermittent amphetamine pretreatment enhances future appetitive behavior for drug- and natural-reward: interaction with environmental variables.

Appetitive behavior for drug and sexual reward is enhanced in animals with a history of amphetamine-experience. The present experiment investigated whether prior exposure to a sensitizing regimen of amphetamine treatment would 'globally' enhance future appetitive behaviors of adult male Sprague-Dawley rats, and whether the drug preexposure-environment or intermittency of administration would affect this development. Reward appetite was compared in drug-experienced versus drug-naive rats using amphetamine place-preference conditioning (CPP) and a natural-incentive sensitization task, which measured appetitive approach for food and sexual reward. Experiment I found that 10 daily exposures to 1 mg/kg amphetamine did not alter future psychostimulant CPP, regardless of abstinence schedule. Although daily exposure to a higher amphetamine dose also did not alter appetitive behavior when measured after 2-weeks drug abstinence in Experiment II, alternate-day amphetamine experience (5.0 mg/kg, twice-a-day) in an initially unfamiliar environment persistently enhanced future amphetamine CPP and appetitive behavior for natural reward. Identical treatment administered in the homecage did not. Furthermore, sensitized reward-seeking behaviors were not globally evident. Animals that showed sensitized amphetamine CPP did not show sensitized food-seeking behavior and vice versa. Thus, the environment surrounding chronic psychostimulant drug experience can greatly affect subsequent reward appetite, but the sensitized expression may be individually determined.

Amphetamine↗