Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The strengths of taste aversion induced by sulphated cholecystokinin 26-33 (CCK-8; 1,2,4 and 8 micrograms/kg IP) and lithium chloride (LiCl; 7.5, 15, 30 and 60 mg/kg IP) were determined in order to assess the relative aversiveness of the two compounds. All doses of LiCl induced strong aversion, but only the highest dose of CCK-8 induced aversion, which was mild. Effects of CCK-8 and LiCl on food intake were then compared in the hour (hr) following 8 hr of food deprivation; rats were on this food deprivation schedule for a relatively long time (78 days) throughout testing. All doses of CCK-8 reduced food intake significantly. Most doses of LiCl either did not affect or significantly increased food intake. Although 60 mg/kg LiCl did not affect food intake when administered 15 or 30 min before food presentation, it significantly increased food intake when administered 1, 2 or 3 hr before food presentation. Overeating of solid food may be an illness-induced behavior. Although a very high dose of LiCl (120 mg/kg) decreased food intake markedly, the rats were obviously distressed, not satiated. Failure of CCK-8 to affect feeding behavior like LiCl is indirect evidence that the reduction of food intake by CCK-8 is not merely the result of aversiveness, but is an extremely potent and specific behavioral effect.
 ...
PMID:Cholecystokinin octapeptide and lithium produce different effects on feeding and taste aversion learning. 301 Mar 48

We studied the effect of early postoperative enteral hyperalimentation on the nutritional state and hormones in digestive organs in twenty patients who underwent resection of thoracic esophageal carcinoma and reconstruction of new esophagus. Following results were obtained. 1. Although enteral hyperalimentation was started in the early postoperative period (postoperative 3 day), the incidence of complications including diarrhea was decreased dramatically and satisfactory nutritional effect was obtained due to the development of many excellent chemically defined enteral nutrients. 2. Gut hormones including CCK showed the same response as in the preoperative period to the loading of enteral nutrients. And that, it is suggested that the response of CCK is affected by the lipid content in the nutrients and that this response was effective to prevent the postoperative biliary stasis. 3. Enteral nutrition made it possible to self-regulate water absorption from digestive organs, to control body fluid volume and to prevent over hydration or hypovolemia to comparison with parenteral nutrition.
 ...
PMID:[Nutritional management following resection of esophageal cancer--effect of early postoperative enteral hyperalimentation]. 314 65

There is increasing evidence that peptides in the brain are important in the control of food intake. Administration of opioid and CCK peptides have elicited hunger and satiety, respectively. To evaluate the interaction of these peptides and their role in the central nervous system, concentrations of met-enkephalin were measured in the hypothalamus of rats following peripheral administration of CCK; in addition, effects of feeding and fasting and obesity were studied. In CCK- vs. saline-injected rats met-enkephalin concentrations were decreased in the paraventricular nucleus (PVN), suprachiasmatic nucleus (SC), supraoptic nucleus (SON), dorsomedial hypothalamus (DMH) and ventromedial hypothalamus (VMH). In fed compared with fasted rats met-enkephalin concentrations were higher in the anterior hypothalamus (AH) and lower in the SC; in obese compared with lean rats, concentrations were higher in the AH, PVN, SC, SON, DMH, lateral hypothalamus and VMH. These results show that peripheral injections of CCK can decrease concentrations of met-enkephalin in the brain and suggest a mechanism by which these peptides may interact to influence behavior. In addition, the findings support the hypothesis that the hyperphagia which is typical of obese rats may be due to increased concentrations of met-enkephalin.
 ...
PMID:Changes in brain met-enkephalin concentrations with peripheral CCK injections in Zucker rats. 371 42

During lactation food intake increases greatly without an accompanying large increase in body weight; therefore, this physiological state is an excellent example of non-obese hyperphagia. In the present study, we found that cholecystokinin (CCK-8) decreased food intake in lactating and virgin female rats. However, female rats were more resistant to the effect of CCK on eating following weaning of the pups. Bombesin (BB) suppressed food intake in virgin female rats and in lactating rats during early and mid lactation. Rats were resistant to its satiating effect during late lactation and during the postweaning period. Calcitonin potently suppressed food intake in virgin, lactating and postweaning rats. The present findings suggest that CCK and bombesin decrease food intake more effectively in virgin female rats and during earlier phases of lactation than during late lactation or postweaning.
 ...
PMID:The effect of cholecystokinin, bombesin and calcitonin on food intake in virgin, lactating and postweaning female rats. 379 39

The effect of feeding an alpha-amylase inhibitor (BAY e 4609, 700 mg/100 g food) for 20 or 90 days on the enzymes of the exocrine pancreas of the rat was investigated. The amylase inhibitor-fed rats gained significantly less weight despite a higher food intake than control rats on a standard diet. Fecal weight increased threefold. Pancreatic wet weight, pancreatic DNA, protein and insulin concentrations were not influenced. The amylase content of the pancreas was significantly diminished compared with controls. The trypsin level increased and the changes in the amount of lipase were not significant. Also in response to an infusion of 15 or 60 IU CCK/kg/h combined with 0.5 clinical units of secretin/kg/h amylase secretion was significantly diminished after both feeding periods compared with controls, while trypsin output increased as did the output of lipase to a lesser extent. The enzyme pattern of the pancreatic juice reverted to normal when the animals consumed the control diet again. Gut weight and length increased significantly in the experimental animals. It is concluded that the changes in the pancreatic enzymes are induced by altered food intake. The amylase inhibitor prevents the digestion of starch and by this carbohydrate absorption. As a consequence, hyperphagia develops resulting in an increased protein and fat intake. Unlike trypsin a negative feedback regulation does not exist between alpha-amylase concentration in the gut and pancreatic enzyme secretion.
 ...
PMID:Influence of short- and long-term feeding of an alpha-amylase inhibitor (BAY e 4609) on the exocrine pancreas of the rat. 616 90

The ability of nanomolar concentrations of guanine, but not adenine, nucleotides to inhibit specific 125I-Bolton-Hunter CCK binding to ligated rat vagus nerve demonstrated that vagal CCK binding sites were linked to G-proteins during axonal transport. The GTP analogue, GTP[S], reduced specific binding to both anterogradely and retrogradely transported binding sites by more than 90% at 1 microM. Transport of these putative receptor-G-protein complexes was examined under conditions of food deprivation or physiological hyperphagia induced by either lactation or genetic obesity. None of the physiological or imposed manipulations of food intake had any effect on the axonal transport of CCK binding sites. Transection of the cervical vagus resulted in an accumulation of binding sites at the lesion site that was indistinguishable from that seen following ligation for the same period.
 ...
PMID:G-protein coupling of vagal CCK binding sites and comparisons of transport rates. 768 78

Galanin (GAL), a 29 aminoacid peptide, is widely distributed in the central nervous system and especially in the hypothalamus. It strongly stimulates food intake when it is injected in the paraventricular nucleus (PVN) of normal rats. The obese Zucker rat with a well-established hyperphagia is characterized by a general dysregulation of some important neuropeptides involved in the regulation of feeding behavior e.g. neurotensin, NPY or CCK and the aim of this study was to measure GAL in different microdissected brain areas in lean (Fa/Fa) and obese (fa/fa) male Zucker rats. As feeding status may modulate the central peptide concentrations, it was measured in ad libitum fed rats and in 48-h fasted rats of both genotypes. GAL was measured by a specific radioimmunoassay in the arcuate nuclei (ARC) and parvocellular (PVNp) and magnocellular (PVNm) parts of the PVN as well as in the median eminence (ME), median preoptic area (MPOA), supraoptic (SON) and dorsomedian (DMN) nuclei. Two-way analysis of variance revealed a very significant effect of genotype in the PVNp (P < 0.001), SON (P < 0.001) and in the ME (P < 0.02). No significant variations at all were noted in the ARC, PVNm, MPOA and DMN. GAL concentrations were more than doubled in the PVNp and SON of ad lib obese rats when compared to the ad lib lean rats (P < 0.005). On the other hand, in the ME where GAL concentration was about 4-fold greater than in the other areas, there was a 20 to 30% decrease in GAL concentrations in the obese rat (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Galanin in the hypothalamus of fed and fasted lean and obese Zucker rats. 769 1

Otsuka Long-Evans Tokushima Fatty (OLETF) rats develop obesity, hyperglycemia, and non-insulin-dependent diabetes mellitus and do not express cholecystokinin A (CCK-A) receptors, the receptor subtype mediating the satiety actions of CCK. In short-term feeding tests, male OLETF rats were completely resistant to exogenous CCK, and their response to bombesin was attenuated. Comparisons of liquid meal consumption in OLETF and control Long-Evans Tokushima (LETO) rats demonstrated that 1) OLETF rats had greater intakes during 30-min scheduled daytime meals and significantly larger and fewer spontaneous night-time meals and 2) although the initial rates of licking were the same, OLETF rats maintained the initial rate longer and the rate at which their licking declined was slower. In 24-h solid food access tests, OLETF rats consumed significantly more pellets than LETO controls, and this increase was attributable to significant increases in meal size. Together, these data are consistent with the interpretation that the lack of CCK-A receptors in OLETF rats results in a satiety deficit leading to increases in meal size, overall hyperphagia, and obesity.
 ...
PMID:Disordered food intake and obesity in rats lacking cholecystokinin A receptors. 953 Feb 26

Adult Otsuka Long-Evans Tokushima fatty (OLETF) rats lack functional cholecystokinin A (CCK-A) receptors, are diabetic, hyperphagic, and obese, and have patterns of ingestion consistent with a satiety deficit secondary to CCK insensitivity. Because dietary fat potently stimulates CCK release, we examined how dietary fat modulates feeding in adult male OLETF rats and their lean [Long-Evans Tokushima (LETO)] controls. High-fat feeding produced sustained overconsumption of high-fat diet (30% corn oil in powdered chow) over a 3-wk period in OLETF but not LETO rats. We then assessed the ability of gastric gavage (5 ml, 1-2 kcal/ml x 15 s) or duodenal preloads (1 kcal/ml, 0.44 ml/min x 10 min) of liquid carbohydrate (glucose), protein (peptone), or fat (Intralipid) to suppress subsequent 30-min 12.5% glucose intake in both strains. In OLETF rats, gastric and duodenal fat preloads were significantly less effective in suppressing subsequent intake than were equicaloric peptone or glucose. These results demonstrate that OLETF rats fail to compensate for fat calories and suggest that their hyperphagia and obesity may stem from a reduced ability to process nutrient-elicited gastrointestinal satiety signals.
 ...
PMID:Decreased responsiveness to dietary fat in Otsuka Long-Evans Tokushima fatty rats lacking CCK-A receptors. 1051 56

The Koletsky ("corpulent) obese rat is homozygous for an autosomal recessive mutation of the leptin receptor (Lepr) that results in hyperphagia, obesity, and hyperlipidemia. Unlike the Lepr mutation that characterizes the fatty Zucker rat (Lepr(fa)), the Koletsky mutation (Lepr(fak)) is null. Because the Lepr(fak) mutation is null, exogenous leptin should have no effect on body weight or food intake in fa(k)/fa(k) rats. We confirmed that prediction: murine leptin, administered into the third ventricle for 5 consecutive days, did not affect daily food intake or body weight in fa(k)/fa(k) rats but produced dose-related inhibitions of food intake and body weight in +/+ and +/fa(k) rats. Although fa(k)/fa(k) rats did not respond to leptin, their response to CCK-8 (4 microg/kg ip) injected before 30-min test meals of 10% sucrose was not different from that of +/+ or +/fa(k) rats. These results demonstrate that the fa(k)/fa(k) rat is a good model in which to analyze the controls of food intake, energy expenditure, and energy storage in the absence of leptin effects.
 ...
PMID:Effects of leptin and cholecystokinin in rats with a null mutation of the leptin receptor Lepr(fak). 1084 19


1 2 3 4 Next >>