cholecystokinin and Feeding-and-Eating-Disorders

Although food intake is necessary to provide energy for all bodily activities, considering food intake as a motivated behavior is complex. Rather than being a simple unconditioned reflex to energy need, eating is mediated by diverse factors. These include homeostatic signals such as those related to body fat stores, to food available and being eaten, and to circulating energy-rich compounds like glucose and fatty acids. Eating is also greatly influenced by non-homeostatic signals that convey information related to learning and experience, hedonics, stress, the social situation, opportunity, and many other factors. Recent developments identifying the intricate nature of the relationships between homeostatic and non-homeostatic influences significantly add to the complexity underlying the neural basis of the motivation to eat. The future of research in the field of food intake would seem to lie in the identification of the neural circuitry and interactions between homeostatic and non-homeostatic influences.

Topics: Amygdala; Brain; Cholecystokinin; Feeding and Eating Disorders; Feeding Behavior; Homeostasis; Humans; Hypothalamus; Insulin; Leptin; Motivation; Satiation; Stress, Psychological

Disturbances in gastrointestinal hormones have been implicated in the pathogenesis of eating disorders such as anorexia nervosa and bulimia nervosa. However, the contribution of these hormonal changes to the onset and maintenance of eating disorder remains unclear. We focus our review on a selective number of gastrointestinal hormones that are known to play a role in the regulation of short-term or long-term energy balance and examine their association with eating disorder in recently published literature.. Several new studies reported differential changes of ghrelin isoforms during fasting and following nutrient ingestion. New findings on other appetite-regulating hormones (peptide YY, cholecystokinin, incretin hormones and pancreatic polypeptide) at different nutritional states and disease stage have also been reported in subtypes of eating disorder. Most of the changes in peripheral hormones disappeared or partially recovered after the restoration of weight with nutritional and behavioral therapy.. Dysregulation of gastrointestinal hormones is more likely to contribute to the maintenance of the disordered eating behavior and related metabolic outcomes as well as the clinical course rather than causing them. A better understanding of this relationship also carries implications for developing targeted hormone-base treatment for eating disorder.

Topics: Animals; Cholecystokinin; Feeding and Eating Disorders; Gastrointestinal Hormones; Ghrelin; Glucagon-Like Peptide 1; Humans; Peptide Hormones; Peptide YY

Disturbances in gastrointestinal hormones have been widely identified in persons with eating disorders (EDs) and have been implicated in their clinical pathologies.. The objective was to identify, critically examine, and summarize studies investigating the short-term response of gastrointestinal hormones to food in persons with an ED, including the subtypes anorexia nervosa and bulimia nervosa.. A priori inclusion and exclusion criteria were set and included a procedure in which a test meal or glucose load was given and blood hormone concentrations measured. All studies included a healthy control group for comparison. The outcome variable was defined as the mean difference between fasting plasma hormone concentrations and the maximum postprandial peak or nadir. The difference in baseline values between groups was also examined. Pooled standardized mean differences were calculated and analyzed where possible.. A total of 28 studies were identified, including sufficient studies to perform a meta-analysis for ghrelin, peptide YY, cholecystokinin, insulin, and pancreatic polypeptide. Persons with an ED had higher baseline concentrations of ghrelin (large effect), peptide YY (medium effect), and cholecystokinin (medium effect for ED, large effect for anorexia nervosa). The response of insulin to food was decreased in persons with an ED (medium effect). No further differences were found in the release of gut peptides to a standardized test meal.. All of the studies had low power for the different subtypes of EDs. High heterogeneity among the studies was observed, and limitations are discussed. The findings suggest that the physiologic changes observed in patients with EDs are highly variable and subject to multiple confounding factors.

Topics: Cholecystokinin; Feeding and Eating Disorders; Gastrointestinal Hormones; Gastrointestinal Tract; Ghrelin; Humans; Insulin; Pancreatic Polypeptide; Peptide YY

The etiology of eating disorders has not been defined yet. It is generally thought of as multi-dimensional, consisting of socio-cultural, psychological and biological factors. The biological factors include predisposing, precipitating and perpetuating factors. In recent years, genetics have been reported as predisposing factors, various neuropeptides which play an important role in regulation of feeding behavior have been discovered to be precipitating factors, and brain imaging studies investigating morphological changes have revealed perpetuating factors. This review gives an outline of recent information about biological factors in eating disorders.

Topics: Brain; Cholecystokinin; Corticotropin-Releasing Hormone; Diagnostic Imaging; Dopamine; Estrogens; Feeding and Eating Disorders; Feeding Behavior; Gastrin-Releasing Peptide; Genetic Predisposition to Disease; Humans; Leptin; Neuropeptide Y; Polymorphism, Genetic; Serotonin

Estradiol has long been known to inhibit feeding in animals, but the mechanism(s) mediating its effects have not been clear. Demonstrations that estradiol's feeding effects are expressed as decreases in meal size coupled with the emerging consensus that cholecystokinin (CCK) released from the small intestines during meals is a physiological negative-feedback signal controlling meal size (i.e. satiation) suggested a new approach to the problem of the mechanisms of estradiol's inhibitory effect on feeding. Progress on this approach is reviewed here. Experimental manipulations of exogenous and endogenous CCK and estradiol have produced converging evidence that estradiol cyclically increases the activity of the CCK satiation-signaling pathway so that meal size and food intake decrease during the ovulatory or estrus phase of the ovarian cycle. This is a striking example of the modulation of the operation of a control of meal size by the physiological context in which the meal occurs. Estradiol also produces a tonic decrease in meal size, but this apparently does not involve the CCK satiation-signaling pathway. Where and how estradiol acts to increase the potency of the CCK satiating-signaling pathway are not known. Several possible sites are suggested by the observations that estradiol treatment increases feeding- and CCK-induced expression of c-Fos in ovariectomized animals in brain areas including the nucleus tractus solitarius, paraventricular nucleus of the hypothalamus, and central nucleus of the amygdala. Tests with null mutation mice indicate that estrogen receptor-alpha is necessary for estradiol's feeding effects. Finally, the possibilities that estradiol exerts important influences on normal or disordered eating in women are discussed. It is concluded that estradiol exerts a biologically significant action on CCK satiation in animals. Further research to determine whether this action of estradiol has a role in the pathogenesis, course, or treatment of disordered eating in women is indicated.

Topics: Animals; Brain; Cholecystokinin; Estradiol; Feeding and Eating Disorders; Feeding Behavior; Female; Humans; Hypothalamus; Ovulation; Satiation; Signal Transduction; Time Factors

The present review of the satiating effect of cholecystokinin in humans has revealed that cholecystokinin is a physiological satiety factor in humans. The results demonstrate the efficacy of the satiating actions of exogenous and endogenous CCK in humans. The therapeutic potential of CCK analogues cannot be estimated until further studies are performed that demonstrate the efficacy of CCK analogues for decreasing body weight, and the safety of CCK when administered repetitively for prolonged periods.

Topics: Animals; Appetite; Body Weight; Cholecystokinin; Feeding and Eating Disorders; Feeding Behavior; Gastric Mucosa; Humans

The satiety-inducing effects of centrally and peripherally administered cholecystokinin (CCK) in experimental animals have been well documented. Recently, studies in humans showed that CCK is released into plasma following food ingestion, a phenomenon postulated to promote meal-related satiety. To explore whether abnormal CCK secretion during feeding may be related to pathophysiological mechanisms in disorders associated with appetite abnormalities, we report here studies of the plasma CCK response to a test meal in patients with bulimia nervosa, as well as seasonal (hyperphagic) and melancholic (anorexic) depression. Compared to controls, bulimic patients had impaired meal-related CCK secretion, correlated with an impaired sense of postprandial satiety. This defect resolved with tricyclic antidepressant-induced amelioration of bulimic behavior, suggesting that deficient CCK secretion may constitute a fundamental pathophysiologic derangement in this disorder. In contrast to patients with bulimia nervosa, hyperphagic patients with seasonal affective disorder failed to show abnormal meal-related CCK secretion. Preliminary evidence shows robust meal-related CCK secretion in melancholic depression with anorexia. We have also begun to explore the dynamics of CCK secretion into cerebrospinal fluid (CSF) utilizing an indwelling lumbar catheter. From studies in humans, we note that this peptide is secreted into the CSF in large (ng/ml) quantities in an episodic fashion that may bear some relationship to food ingestion. Further study of this parameter in volunteers and patients is now underway.

Topics: Cholecystokinin; Eating; Feeding and Eating Disorders; Humans; Mood Disorders

Historically, nutrients and related metabolic signals were considered to control the onset and offset of meals. Recent research has focused upon the roles of peptides found in the gastrointestinal tract and brain as alternate controllers of these processes. During a meal, the gut secretes a variety of peptides as part of the digestive process. Some of these substances, acting as hormonal or as local signals, may also provide information which is relayed to the central nervous system, causing eating to stop and producing the sense of satiety. When administered to animals or people before a meal, exogenous cholecystokinin (CCK), the most studied of the putative satiety peptides, reduces food intake in a dose-dependent manner. Recent findings support the concept that endogenous CCK acts during meals to limit meal size, and evidence is reviewed suggesting a possible pathophysiological role for CCK in bulimia. Adiposity is also regulated via peptide hormones, especially insulin. Insulin is secreted in direct proportion to adiposity, and blood-borne insulin gains access to brain areas important in the regulation of feeding. The administration of insulin into the brain causes reduced eating and weight loss.

Topics: Adipose Tissue; Animals; Appetite Regulation; Body Mass Index; Cholecystokinin; Feeding and Eating Disorders; Humans; Insulin; Peptides; Rats; Satiation

Topics: Anorexia Nervosa; Bulimia; Catecholamines; Cholecystokinin; Dopamine; Endorphins; Feeding and Eating Disorders; Humans

The relationship of oral behaviors to stress has long been recognized both in humans and in wild animals. In the last decade numerous advances have been made in our understanding of stress-induced feeding predominately because of the development of the simple tail-pinch model of stress induced feeding in rats. Present evidence strongly implicates monoamines and the endogenous opioid peptides as well as other neuropeptides as playing a role in the central regulation of stress-induced eating.

Topics: Animals; Bombesin; Bruxism; Cholecystokinin; Corticotropin-Releasing Hormone; Feeding and Eating Disorders; Feeding Behavior; Food Preferences; Haloperidol; Humans; Hyperphagia; Latency Period, Psychological; Lesch-Nyhan Syndrome; Mastication; Nail Biting; Narcotics; Receptors, Dopamine; Reward; Spiperone; Stress, Physiological; Sucking Behavior

Glucocorticoids have major effects on food intake, demonstrated by the decrease of food intake following adrenalectomy. Satiety signals are relayed to the nucleus of the solitary tract (NTS), which has reciprocal projections with the arcuate nucleus (ARC) and paraventricular nucleus (PVN) of the hypothalamus. We evaluated the effects of glucocorticoids on the activation of hypothalamic and NTS neurons induced by food intake in rats subjected to adrenalectomy (ADX) or sham surgery 7 days before the experiments. One-half of ADX animals received corticosterone (ADX+B) in the drinking water (B: 25 mg/l). Fos/tyrosine hydroxylase (TH), Fos/corticotrophin-releasing factor (CRF) and Fos immunoreactivity were assessed in the NTS, PVN, and ARC, respectively. Food intake and body weight were reduced in the ADX group compared with sham and ADX+B groups. Fos and Fos/TH in the NTS, Fos, and Fos/CRF immunoreactive neurons in the PVN and Fos in the ARC were increased after refeeding, with higher number in the ADX group, compared with sham and ADX+B groups. CCK administration showed no hypophagic effect on ADX group despite a similar increase of Fos/TH immunoreactive neurons in the NTS compared with sham and ADX+B groups, suggesting that CCK alone cannot further increase the anorexigenic effect induced by glucocorticoid deficiency. The present data indicate that glucocorticoid withdrawal reduced food intake, which was associated with higher activation of ARC, CRF neurons of the PVN, and catecholaminergic neurons of the NTS. In the absence of glucocorticoids, satiety signals elicited during a meal lead to an augmented activation of brain stem and hypothalamic pathways.

Topics: Adrenalectomy; Animals; Arcuate Nucleus of Hypothalamus; Behavior, Animal; Body Weight; Catecholamines; Cholecystokinin; Corticosterone; Corticotropin-Releasing Hormone; Disease Models, Animal; Drinking; Eating; Fasting; Feeding and Eating Disorders; Glucocorticoids; Hypothalamus; Male; Neural Pathways; Neurons; Paraventricular Hypothalamic Nucleus; Proto-Oncogene Proteins c-fos; Rats; Rats, Wistar; Satiety Response; Solitary Nucleus; Tyrosine 3-Monooxygenase

Recent data suggest that purging disorder, a recently characterized form of eating disorder not otherwise specified, may be worthy of specific delineation in nosological schemes. However, more data are needed to determine how purging disorder differs from bulimia nervosa.. To examine clinical features and subjective as well as objective physiological responses to a standardized test meal in purging disorder compared with bulimia nervosa and controls.. Study visit 1 included psychological assessments with structured clinical interviews and questionnaires. Study visit 2 included assessment of test-meal responses.. Participants recruited from the community completed test-meal studies in a General Clinical Research Center.. Women with DSM-IV bulimia nervosa-purging subtype (n = 37) and purging disorder (n = 20) and non-eating disorder controls (n = 33) with a body mass index (calculated as weight in kilograms divided by height in meters squared) between 18.5 and 26.5 who were free of psychotropic medications.. Assessments of eating disorder severity, postprandial cholecystokinin response, and subjective responses to test meals.. Eating abnormalities were significantly elevated in participants with purging disorder and bulimia nervosa compared with controls but did not differ between eating disorder groups. Participants with purging disorder demonstrated significantly greater postprandial cholecystokinin release compared with participants with bulimia nervosa (t(76.44) = 2.51; P = .01) and did not differ significantly from controls (t(75.93) = 0.03; P = .98). Participants with purging disorder reported significantly greater postprandial fullness and gastrointestinal distress compared with participants with bulimia nervosa and controls.. Purging disorder is a clinically significant disorder of eating that appears to be distinct from bulimia nervosa on subjective and physiological responses to a test meal. Findings support further consideration of purging disorder for inclusion in the classification of eating disorders. Future studies on the psychobiology of purging disorder are needed to understand the propensity to purge in the absence of binge eating.

Topics: Adult; Appetite; Body Mass Index; Bulimia Nervosa; Cholecystokinin; Control Groups; Diagnosis, Differential; Diagnostic and Statistical Manual of Mental Disorders; Eating; Feeding and Eating Disorders; Female; Humans; Hunger; Personality Inventory; Postprandial Period; Psychiatric Status Rating Scales; Satiation; Severity of Illness Index; Surveys and Questionnaires; Vomiting

Gastrointestinal inflammation reduces food intake but the biological mechanisms explaining suppressed feeding during inflammation are unknown. We have used a model of upper gut infection (Trichinella spiralis in the mouse) to study the effect of inflammation on food intake, and explored the role of a key enteroendocrine cell (EEC) in the regulation of feeding by the immune response.. Food intake of NIH mice infected with the intestinal nematode Trichinella spiralis was measured. Duodenal cholecystokinin (CCK) cells were counted. Plasma CCK was measured. Infected mice were treated with a specific CCK1 receptor antagonist, and food intake reassessed. The influence of the immune response on food intake and CCK was mechanistically examined by treating mice with CD4 or mast cell neutralising antibodies. The role of the T helper 2 response was further explored in mice genetically deficient for interleukin (IL)-4, IL-13, or IL-4Ralpha (receptor alpha subunit).. Food intake of infected mice was significantly reduced at the temporal peak of intestinal inflammation. CCK expressing EEC were upregulated in infected mice, and plasma CCK levels were increased. A CCK1 receptor antagonist restored the food intake of infected mice to a significant degree. Furthermore, suppression of food intake was completely abolished in the absence of CD4+ T lymphocytes or IL-4Ralpha.. The data show for the first time that intestinal inflammation results in reduced food intake due to upregulation of CCK. Moreover, following infection, food intake and CCK expressing cells are under the specific control of CD4+ T-cells, via release of IL-4 and IL-13.

Topics: Animals; Cell Count; Cholecystokinin; Cytokines; Disease Models, Animal; Duodenum; Eating; Enteroendocrine Cells; Feeding and Eating Disorders; Immunohistochemistry; Interleukins; Intestine, Small; Mast Cells; Mice; Mice, Inbred BALB C; Mice, Inbred Strains; Receptors, Cholecystokinin; Th2 Cells; Trichinella spiralis; Trichinellosis

Eating disorders (EDs) have a highly heterogeneous etiology and multiple genetic factors might contribute to their pathogenesis. Ghrelin, a novel growth hormone-releasing peptide, enhances appetite and increases food intake, and human ghrelin plasma levels are inversely correlated with body mass index. In the present study, we examined the 171T/C polymorphism of the ghrelin receptor (growth hormone secretagogue receptor, GHSR) gene in patients diagnosed with EDs, because the subjects having ghrelin gene polymorphism (Leu72Met) was not detected in a Japanese population, previously. In addition, beta3 adrenergic receptor gene polymorphism (Try64Arg) and cholecystokinin (CCK)-A receptor (R) gene polymorphism (-81A/G, -128G/T), which are both associated with obesity, were investigated. The subjects consisted of 228 Japanese patients with EDs [96 anorexia nervosa (AN), 116 bulimia nervosa (BN) and 16 not otherwise specified (NOS)]. The age- and gender-matched control group consisted of 284 unrelated Japanese subjects. The frequency of the CC type of the GHSR gene was significantly higher in BN subjects than in control subjects (chi(2) = 4.47, p = 0.035, odds ratio = 2.05, Bonferroni correction: p = 0.070), while the frequency in AN subjects was not different from that in controls. The distribution of neither beta3 adrenergic receptor gene nor CCK-AR polymorphism differed between EDs and control subjects. Therefore, the CC type of GHSR gene polymorphism (171T/C) is a risk factor for BN, but not for AN.

Topics: Adult; Aged; Body Mass Index; Bulimia Nervosa; Cholecystokinin; DNA; Feeding and Eating Disorders; Female; Genotype; Humans; Japan; Male; Middle Aged; Panic Disorder; Polymorphism, Single Nucleotide; Receptors, Adrenergic, beta-3; Receptors, Cholecystokinin; Receptors, G-Protein-Coupled; Receptors, Ghrelin; Reverse Transcriptase Polymerase Chain Reaction; Risk Factors

Topics: Cholecystokinin; Feeding and Eating Disorders; Humans; Infant; Infant, Newborn

The selective dopamine D-1 receptor antagonist SCH 23390 (30 micrograms/kg, SC) significantly reduced palatable food consumption by nondeprived rats in a 30-min test period. Prior administration of the selective CCK-A receptor antagonist devazepide (MK 329; L-364,718) blocked the hypophagic effect of SCH 23390. In contrast, prior administration of the selective CCK-B/gastrin receptor antagonist L-365,260 had no effect. Devazepide did not antagonize a matched hypophagic effect produced by the dopamine D-2 receptor antagonist raclopride (0.1 mg/kg, SC). These data direct attention to possible dopamine-cholecystokinin interactions in relation to the control of ingestional responses, and, more specifically, indicate possible functional relationships between D-1 and CCK-A receptor mechanisms.

Topics: Animals; Benzazepines; Benzodiazepinones; Cholecystokinin; Devazepide; Dopamine; Dopamine Antagonists; Feeding and Eating Disorders; Male; Phenylurea Compounds; Rats; Receptors, Cholecystokinin; Receptors, Dopamine; Receptors, Dopamine D1

In these experiments we examined the effects on gastric motility of cholecystokinin, LiCl, hypertonic NaCl solution, gastric distension, and intraduodenal glucose loads, five dissimilar treatments known to reduce food intake in rats. In addition, we investigated whether any observed effects were dependent on the afferent vagus nerve by pretreating subjects with the neurotoxin capsaicin. Each of the five treatments virtually eliminated the gastric contractions seen after rats had consumed a large meal of chow; these effects were rapid in onset and continued for up to 30 min. The inhibitory effects of cholecystokinin and gastric distension were eliminated by pretreatment with capsaicin, whereas the effects of the other treatments were attenuated only slightly or not at all. Because most of these treatments have been shown to stimulate pituitary oxytocin secretion in rats as well as to inhibit food intake and gastric motility, these results are consistent with the hypothesis that the hypothalamic paraventricular nucleus is a site at which information is integrated in the coordinated control of food intake, gastric function, and neuroendocrine secretion.

Topics: Animals; Anorexia; Capsaicin; Chlorides; Cholecystokinin; Eating; Feeding and Eating Disorders; Gastrointestinal Motility; Glucose; Lithium; Lithium Chloride; Male; Oxytocin; Paraventricular Hypothalamic Nucleus; Rats; Rats, Inbred Strains; Saline Solution, Hypertonic

The existence of a relationship between cholecystokinin (CCK)-induced satiety and the serotoninergic system was evaluated. The food intake of 3-h-fasted male rats was studied after treatment with the COOH-terminal octapeptide of CCK (CCK-8) alone or in combination with one of two blockers of serotonin (5-HT) receptors, metergoline (MET; 1.0 or 0.06 mg/kg), active in both the periphery and brain, or xylamidine tosylate (XYL; 1.5 mg/kg), active only in the periphery. CCK-8 reduced food intake in the 30 min after food presentation by 37% at 2 micrograms/kg, 68% at 4 micrograms/kg, and 80% at 8 micrograms/kg compared with controls. Both doses of MET attenuated CCK-8-induced satiety, increasing food intake of rats treated with all doses of CCK-8 to control values. Food intake was significantly increased over base line by the 1.0-mg/kg dose of MET alone but unaffected by the 0.06-mg/kg dose of MET alone. XYL had no effect either given alone or in combination with CCK-8. These results indicate that the inhibitory action of CCK-8 on food intake is dependent on intact functioning of the serotoninergic system, probably at central sites.

Topics: Amidines; Animals; Anorexia; Cholecystokinin; Dose-Response Relationship, Drug; Eating; Feeding and Eating Disorders; Fenfluramine; Male; Metergoline; Rats; Serotonin

The syndrome of cancer anorexia includes early satiety in man and a reduction in the duration of feeding in experimental animals. These aberrations suggest dysfunction of peripheral and/or central nervous system satiety mechanisms in tumor-bearing individuals. Since the gut peptide, cholecystokinin (CCK), has been implicated as a potent satiety cue in man and animals, plasma and brain concentrations of CCK were measured by radioimmunoassay in anorectic tumor-bearing rats. Plasma concentrations of immunoreactive CCK were not significantly altered in either an acute Walker 256 carcinosarcoma or more chronic methylcholanthrene-induced sarcoma animal model of cancer anorexia. However, levels of immunoreactive CCK were significantly reduced in the hypothalamus and cerebral cortex of animals bearing the methylcholanthrene sarcoma during both mild and severe anorexia. These data demonstrate that elevations in immunoreactive CCK are not a major factor in the etiology of cancer anorexia. If brain CCK is involved in satiety, tumor-bearing rats may be attempting to compensate for their anorexia by down-regulating CCK production.

Topics: Animals; Anorexia; Brain; Carcinoma 256, Walker; Cerebral Cortex; Cholecystokinin; Eating; Feeding and Eating Disorders; Female; Humans; Hypothalamus; Rats; Rats, Inbred F344; Rats, Inbred Strains; Sarcoma, Experimental

Cholecystokinin (CCK) secreted from the duodenum during feeding has been shown to elicit satiety and stimulate growth of the pancreas in addition to affecting gastrointestinal function. In previous experiments hyperphagic Zucker obese rats were less sensitive to the effects of CCK on satiety and had a smaller pancreas than normal-weight rats. In the present experiments with hyperphagic lactating Zucker rats, the food intake response to exogenously administered CCK and the size and composition of the pancreas were measured. Food intakes after a 2-h fast were not decreased by 4.0 or 8.0 micrograms/kg CCK-8 during wk 1, 2, or 3 of lactation. However, in the same rats 2 wk after pups were weaned, 4.0 and 8.0 micrograms/kg CCK-8 decreased food intake 32% (2.1 +/- 0.4 vs. 3.1 +/- 0.3 g, paired t = 2.33, P less than 0.03) and 52% (1.5 +/- 0.2 vs. 3.1 +/- 0.5 g, paired t = 3.48, P less than 0.006). On day 18 of lactation, pancreas weight was increased 41% (1.38 +/- 0.05 vs. 0.98 +/- 0.02 g, paired t = 2.68, P less than 0.02) and contents of DNA, RNA, and protein were increased 57, 57, and 73%, respectively. Thus, hyperphagia in lactating female rats was associated with 1) decreased sensitivity to the satiety effect of CCK similar to that in hyperphagic obese rats and 2) hypertrophy of the pancreas in contrast to decreased pancreas size in obese rats.

Topics: Animals; Cholecystokinin; DNA; Dose-Response Relationship, Drug; Eating; Feeding and Eating Disorders; Female; Humans; Hyperphagia; Lactation; Organ Size; Pancreas; Peptide Fragments; Pregnancy; Proteins; Rats; Rats, Zucker; RNA; Sincalide

Cholecystokinin decreased food intake more effectively in obese mice than in wild-type mice. Following a 23-h fast and 10 min after an ip injection of 0, 30, 60 or 90 U/kg. CCK in physiological saline, eating, drinking and rearing rates were measured for a period of 20 min. Thirty units affected neither group, 60 U slowed the eating rate of obese mice significantly, and 90 U that of both groups, particularly the obese mice (P less than 0.001). Drinking and rearing rates remained unchanged. Obese mice were not hyperphagic under the conditions of the experiment and showed an increase in the latency period which preceded eating, compared with wild-type mice. The enhanced responsiveness to CCK, both in and out of the hyperphagic state, may be associated with low endogenous levels of satiety hormones in the obese mouse.

Topics: Animals; Cholecystokinin; Drinking Behavior; Feeding and Eating Disorders; Feeding Behavior; Female; Humans; Hyperphagia; Mice; Mice, Obese

Topics: Animals; Anorexia; Cholecystokinin; Feeding and Eating Disorders; Female; Humans; Intestinal Diseases, Parasitic; Intestine, Small; Sheep; Sheep Diseases; Trichostrongyloidiasis; Trichostrongylosis