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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been easy to demonstrate, both in humans and animals, that the stresses which disturbed either the physiological homeostasis, the behavioural homeostasis or both simultaneously, induced the modifications of the food intake; these disorders often found expression in the inappropriate eating or, less frequently, in temporary anorectic phases. The most relevant hypotheses localized, in the anterior and median hypothalamus (paraventricular nuclei, ventral median nuclei, lateral hypothalamic area), the neurobiological mechanisms which were involved in this stress/eating behaviour relationship. In the brain, both aminergic and peptidergic systems were concerned; the stress-induced hyperphagia required the functionality of the dopamine, dorsal noradrenergic bundle and endogenous opioids of the central nervous system. The dramatic stress-induced anorexia was based upon the reciprocal actions of serotonin, norepinephrine and CRF systems. Other peptides, which some of them belonged to the brain-gut peptide group, could interfere with these mechanisms. The neuropeptides being common in the stress and eating physiological systems, the regulatory mechanisms were most coherent; nevertheless, the precise nervous structures and neurochemical circuits that produced the stress-induced hyperphagia or stress-induced anorexia, remain unknown.
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PMID:[Stress and feeding behavior]. 342 63

On the basis of bibliographic references and new own data, major adaptations of lipid metabolism occurring at late gestation are reviewed. Maternal hypertriglyceridemia at late gestation results from the juxtaposition of several factors: enhanced adipose tissue lipolysis facilitating the availability to the liver of substrates for triglyceride synthesis and contributing to augmented flux of very low density lipoproteins (VLDL) into the circulation; maternal hyperphagia and unmodified gut lipid absorption increasing chylomicron formation from dietary lipid; reduced lipoprotein lipase (LPL) activity in extrahepatic tissues (especially adipose tissue) which does not allow a triglyceride removal proportional to their enhanced production. It is proposed that these changes are also responsible for the altered composition of VLDL in late pregnancy. In conditions of food deprivation the use of glycerol released from adipose tissue as preferential gluconeogenic substrate, and the enhanced maternal ketogenesis warrants the availability of fuels for the fetus. Just prior to parturition the increase in mammary gland LPL activity is responsible for the reduction in circulating triglycerides and prepares the mother for lactation.
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PMID:Lipid metabolism in pregnancy. 355 60

Secretory IgA (S-IgA), an immunoglobulin present in secretions, prevents the adherence of bacteria to mucosal cells and is the principle component of the gut mucosal defense system. The purpose of this study was to determine whether the route of nutrient administration affects S-IgA. Twenty-five female Fisher rats were randomized into three groups. Groups I and II were fed an isonitrogenous, isocaloric standard hyperalimentation solution, Group I intravenously and Group II via a gastrostomy. Group III (control) was fed rat chow and water ad lib. Since bile is one of the principle sources of S-IgA, animals had biliary T-tubes placed for sampling of bile every 4 days. At day 16, Group I animals were fed rat chow and water for an additional 8 days. S-IgA was measured by the ELISA immunoassay. Results indicated at day 16 that the S-IgA level in mg/ml of Group I was 1.1 +/- 0.2, while the S-IgA in Groups II and III was 2.2 +/- 0.6 and 2.2 +/- 0.26, respectively. Furthermore, the S-IgA level in Group I after 8 days of enteral feeding rose to 1.8 +/- 0.4. The difference in S-IgA levels between enterally and parenterally fed rats suggests that an important defense barrier is compromised during parenteral hyperalimentation. Rats fed the same nutrients by gastrostomy maintained S-IgA levels better than rats fed the same nutrients intravenously. The rapid return to normal levels after resumption of enteral feeding suggests that the intraluminal presence of foodstuffs is essential for maintenance of S-IgA.
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PMID:The effect of parenteral nutrition on gastrointestinal immunity. The importance of enteral stimulation. 393 61

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.
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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

BAY g 5421 (acarbose) inhibits carbohydrate digestion in the gut, thereby reducing the rate of glucose absorption. This experiment tested whether long term administration of acarbose to developing Zucker "fatty" (fafa) rats would, by reducing several lipogenic factors, attenuate lipid deposition and reduce the hyperphagia and increased food motivated behavior of these animals. From 7 to 20 weeks of life groups of fatty and lean (FaFa) control rats were fed 0, 20 or 40 mg acarbose/100 g maintenance diet (45% carbohydrate, 35% fat, 20% protein calories), while an additional fatty and lean group were pair-fed to respective 40 mg acarbose groups. Lean groups fed acarbose exhibited dose dependent reductions of body weight, insulin, triglycerides, retroperitoneal and epididymal pad weight, adipocyte size, LPL activity/cell (retroperitoneal pad only), and lipid deposition both in total grams of fat and as a percentage of carcass weight. Fatty groups fed acarbose exhibited dose dependent reductions of insulin, blood glucose, retroperitoneal pad weight, and, at one of the two doses used, significantly lowered body weight, (40 mg), triglycerides (20 mg) and cholesterol (20 mg). However, acarbose-fed fatty groups failed to show significant reductions of adipocyte size, number or LPL activity/cell in retroperitoneal and epididymal fat pads, and maintained their obese body composition, on a percentage basis, at levels not significantly different from that of the 0 mg fatty control group. Acarbose administration led to an initial dose dependent reduction of food intake in both genotypes, which persisted for the lean groups. Fatties fed the 20 mg dose showed a gradual tendency (ns) towards increased daily intake, lever pressed at elevated rates for food pellets, and refed at faster rates following fasting. Fatties fed the 40 mg dose maintained their daily intake at fatty control levels, did not lever press at elevated rates, and showed significantly reduced refeeding following fasting. The 40 mg fatty and both lean acarbose treated groups had decreased sucrose solution preference. Possible bases for these differing effects of the drug on feeding behavior by the groups are considered.
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PMID:Effects of a glucosidase inhibitor (acarbose, BAY g 5421) on the development of obesity and food motivated behavior in Zucker (fafa) rats. 662 10

The importance of gut signals for the short-term and long-term control of ingestion was investigated using rat pups in the natural suckling situation. Pups at 10 days of age were deprived of milk and their dam for 9 hr. Pyloric ligation, vagotomy, and preloading procedures were performed on the pups shortly before testing began. The initial latency to attach to a nipple and the incidence of attachment were recorded during the 2-hr suckling period. Milk intake and the weight of gastric contents were measured following the test. Pregastric stimulation together with natural or artificial gastric filling suppressed ingestion. Acute subdiaphragmatic truncal vagotomy enhanced ingestion under these conditions, and vagotomy alone resulted in controlled hyperphagia concomitant with exaggerated gastric filling. The data suggest that the stomach is one site where milk activates a suppression mechanism for ingestion. This mechanism is mediated primarily by the vagus nerve. The importance of nipple-attachment behavior is discussed in relation to ingestive behavior, and the question of satiety in suckling rats is raised. The chronic effects of truncal vagotomy on rat pups were also investigated, beginning with denervation at 10 days of age. The pups were challenged with deprivation and tested in the natural suckling situation on Day 20. Weaning occurred on Day 22, and the pups were sacrificed on Day 41, followed by measurements of body weight, body length, and gastric contents. The physical and behavioral changes that developed during the chronic phase of vagotomy included (1) permanent gastric distension following the first postsurgical bout of ingestion; (2) reduced intake of milk when the availability of milk was greatest during the suckling test; (3) increased resting behavior regardless of milk letdown conditions during the suckling test; (4) failure to gain weight at a normal rate; and (5) failure to grow at a normal rate. The data indicate that the vagus nerve is necessary for normal internal control of ingestion as well as normal gastric filling and emptying in the suckling rat. The inability of suckling and weanling pups to thrive in the chronic phase of vagotomy indicates that nonvagal internal controls of ingestion and digestion function adequately for survival, but they are not optimal for growth and maintenance of body weight in rats.
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PMID:Effects of gastric filling and vagotomy on ingestion, nipple attachment, and weight gain by suckling rats. 668 66

The malnourishing effects of cancer and its treatments haveprovided a strong clinical incentive for the nutritional support of cancer patients with intravenous hyperalimentation (IVH), but potential enhancement of tumor growth by additional substrate provision has generated concern. Twenty-five patients undergoing surgical treatment for gastrointestinal cancer were studied on one of two preoperative dietary regimens: ad libitum oral diet or intravenous hyperalimentation. Using a stable isotope tracer, N-glycine, in vivo tissue fractional protein synthesis rates were determined from operative specimens of tumor and normal gastrointestinal tissue. Despite substantial advantage in caloric and protein intake, and nitrogen retention, tumors in IVH-fed patients were synthesizing protein no faster (14.2%/day) than those in orally fed patients (15.1/day). Tumor fractional protein synthesis rates (PSRs) correlated (r = + 0.708, P less than 0.005) with the PSR of the tissues from which they arose. IVH maintained gut PSR at the level occurring in the orally fed patients. Parenteral nutritional support in cancer patients does not maintain protein synthesis rates at levels greater than those present with regular oral diets. Although not a direct measure of tumor growth, these data provide preliminary evidence that optimal nutritional support of the cancer patient may be possible without undesirable stimulation of tumor growth.
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PMID:Protein synthesis dynamics in human gastrointestinal malignancies. 676 89

The lining of the intestinal tract is constantly renewed in a brisk but orderly fashion. Further acceleration of cell renewal is elicited by various stimuli, notably surgical shortening of the intestine and hyperphagia, which lead to prompt but persistent increases in mucosal mass. Progressive hypoplasia ensues when the small and large bowel are deprived of their normal contents, either by fasting (with or without parenteral nutrition) or by exclusion from intestinal continuity. All atrophic changes are reversed by refeeding or restoration of the normal anatomical disposition. Intestine responds to mucosal damage by regeneration from the crypts. Pancreatobiliary secretions mediate some of the tropic effects of chyme; systemic influences, both neurovascular and humoral, also play a part in the adaptive response of the gut.
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PMID:Intestinal adaptation: factors that influence morphology. 681 79

Recent reports suggest that pelvic inflammatory disease (PID) is more common among users of the IUD than among those using other forms of contraception and that there is an association between IUD use and pelvic actinomycosis. In 1979 a woman at the University of New Mexico Hospital died from pelvic actinomycosis, the 2nd reported death from this disease associated with the use of an IUD, although her death from pulmonary embolus and Candida endocartidis should more appropriately be considered a complication of intravenous hyperalimentation. At least 25 patients are reported to have had serious pelvic actinomycosis associated with the use of an IUD. No particular type of IUD seems less likely to be associated with actinomycosis. Actinomyces are normally present in the gut and oropharynx, so that inoculation of the vagina with stool or saliva in combination with trauma induced by the foreign body such as an IUD may allow the actinomyces to enter tissues. Actinomyces are easily detected by Papanicolaou-stained cervicovaginal smears and are present in as many as 25% of symptomatic women using IUDs. Culture techniques usually fail in detecting actinomyces, the need for an anaerobic environment or overgrowth by bacteria which invariably accompany actinomyces are the usual causes of failure. Usual signs of IUD-associated actinomycosis are pelvic and lower abdominal or back pain, vaginal discharge, fever, and elevation of leukocyte count which are similar to symptoms of mild PID. Therefore these symptoms demand a Papanicolaou-stained cervicovaginal smear and search for actinomyces. Treatment includes removal of the IUD and administration of penicillin. However at least 1 patient after receiving treatment returned later with actinomycotic tubo-ovarian and subphrenic abscesses. A period of at least 4-6 weeks of therapy is usually recommended. Most patients with pelvic masses underwent hysterectomy and bilateral salpingo-oophorectomy in addition to penicillin and IUD removal; a few were successfully treated with drainage of an intra-abdominal abscess.
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PMID:Pelvic actinomycosis associated with use of intrauterine device: a new challenge for the surgeon. 706 52

We reported recently that ventromedial hypothalamic (VMH) lesions increased the synthesis of DNA in the gastrointestinal tract of rats by the firing of vagus nerve activity, mainly via cholinergic receptor mechanisms. In the present study, we examined whether the mitotic response is due to proliferation of a cell population--mucosal, submucosal, or muscular layer. A monoclonal antibody to proliferating cell nuclear antigen (PCNA) has previously been shown to be capable of identifying proliferating cells. Samples of formalin-fixed gastrointestinal epithelium, taken before and after VMH lesioning, were immunostained with the anti-PCNA monoclonal antibody, and the labeling index (LI) was determined. To discriminate the effect of hyperphagia in VMH lesioned rats, we utilized the method of pair-feeding. Cell proliferation was examined by the PCNA-labeling technique 0, 1, 3, and 7 days after VMH lesioning. The increase in proliferation was confined to cells in the mucosa and did not involve the muscularis and serosa. Studies in control animals showed that the LI was higher in the small intestine than in other gut segments, and higher in the large intestine than in the stomach. The mean PCNA-LI began to increase at 1 day and continued to increase for 3 days, then decreased 7 days following the lesioning. Results indicate that the gastrointestinal mucosa is in a state of hyperproliferation after VMH lesioning.
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PMID:Ventromedial hypothalamic lesions induce the proliferation of gastrointestinal mucosal cells in the rat. 763 Mar 10


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