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

Elemental enteral alimentation (EEA) is an alternative to parenteral nutrition in patients with a functioning gastrointestinal tract and increased caloric requirements or in whom regular oral feeding is impossible or impractical. EEA is given by nasogastric, jejunostomy, or gastrostomy tube. It is useful in cases of short-gut syndrome, pancreatic disease, partial intestinal obstruction, colitis, neuropsychiatric cachexia, trauma, fistula, vascular insult, and renal and liver disease, as well as in patients being prepared for surgery or requiring hyperalimentation after surgery or abdominal irradiation. Strict attention must be paid to fluid and electrolyte status and to blood and urine glucose levels in patients receiving EEA. With use of a nasogastric tube, infection of the middle ear is a possible but uncommon complication.
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PMID:Meeting exceptional nutritional needs. 2. Elemental enteral alimentation. 10 Jul 74

The traditional approach to the care of the gastrointestinal tract in the intensive care unit has been one of neglect. However, recent evidence has linked enteric flora to the generation of clinical sepsis in the absence of other infectious foci. The role of the bowel as an efficient barrier to the invasion of its own flora is addressed in this paper. A variety of insults disrupt the integrity of the barrier function of the gut, allowing the entry of bowel organisms or endotoxins, or both, into the portal and systemic circulatory systems. In animal and early clinical studies, a number of interventions, aimed at altering the enteric flora and enhancing the bowel's barrier function, have been shown to modulate the host's resistance to different insults and may even improve clinical outcome. Such interventions include maintenance of enteral feeding, glutamine supplementation of hyperalimentation solutions and selective bacterial decontamination of the bowel.
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PMID:Care of the gut in the surgical intensive care unit: fact or fashion? 190 91

Although chronic physical activity by humans can raise energy requirements and energy intake severalfold above sedentary levels, whether these increases alter digestive strategy remains unknown. To investigate this possibility, food passage rate (mouth-to-large intestinal lactulose transit) and absorption (xylose) were compared in a cross section of young men chosen to represent a wide range of daily physical activity and food intake. In 20 men (energy intake 1,272-5,342 kcal/day), resting mouth-to-cecum transit was faster in high caloric consumers (r = -0.69, P less than 0.01). In contrast, xylose absorption (n = 26; measured either as urinary xylose excretion or integrated breath H2 production from the sugar) was unrelated to food intake. Dietary fiber intake was uncorrelated with energy intake. This apparent human digestive strategy of rapid transit across the gut absorptive surface, without a sacrifice in absorption, parallels the adaptations made by several animal species similarly faced with increased energy demand at constant fiber intake. We therefore conclude that the hyperphagia of chronic exercise in humans may be linked with significant gastrointestinal adaptations.
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PMID:Rapid orocecal transit in chronically active persons with high energy intake. 205 35

Glutamine has been demonstrated to be an important source of fuel for the gut. The purpose of this study was to evaluate the effect of glutamine-supplemented hyperalimentation on gut immune function. Thirty-six female Fischer rats were randomized into three groups: group 1 (chow) was fed rat chow and water ad libitum, group 2 (total parenteral nutrition) received a standard hyperalimentation formula, and group 3 (total parenteral nutrition-glutamine) received a hyperalimentation solution that contained 2% glutamine. Animals were maintained on their respective diets for 2 weeks and then killed. Mesenteric lymph nodes were harvested for culture, bile was assayed for secretory IgA, and bowel was excised to assay bacterial adherence. Results indicated that glutamine-supplemented total parenteral nutrition protects against bacterial translocation from the gut seen with standard formulas. This effect may be mediated by the secretory IgA immune system.
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PMID:Glutamine-supplemented total parenteral nutrition improves gut immune function. 251 19

The activity of tyrosine hydroxylase (TOH), the rate-limiting enzyme in norepinephrine biosynthesis, was measured in selected sympathetic ganglia to develop a quantitative measure of sympathetic autonomic neuropathy in streptozocin-induced diabetic rats. Surprisingly, TOH activity was elevated twofold in diabetic prevertebral ganglia innervating the alimentary tract (i.e., superior mesenteric, celiac, and inferior mesenteric), which has terminal processes that develop neuroaxonal dystrophy in this model system. TOH activity of paravertebral ganglia (i.e., superior cervical and stellate) with nonalimentary targets was not increased in the same animals. Increased TOH activity in the prevertebral ganglia 1) developed within the 1st wk of diabetes and persisted for 10 mo, 2) did not represent a change in TOH affinity for d-1,6-methyl-5,6,7,8- tetrahydropterine cofactor, 3) was prevented by both nicotinamide pretreatment and early institution of insulin therapy, and 4) did not develop as a result of classical transsynaptic induction. Pair-feeding experiments confirmed that the most likely cause of increased TOH activity in this system was the marked hypertrophy and hyperplasia of the diabetic bowel resulting from compensatory hyperphagia. We conclude that TOH activity does not represent a suitable marker for sympathetic autonomic neuropathy in this experimental system. Rather, the increase appears to be an example of a selective increase in the synthesis of neurotransmitter enzymes, possibly in response to increased trophic support provided by the expanded target, i.e., the hypertrophic gut. The additional synthetic stress imposed on prevertebral neurons by the expansion of the innervation of the alimentary target coupled with the complex diabetic metabolic milieu may contribute to the development and selective distribution of dystrophic axonopathy to the innervation of the alimentary tract.
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PMID:Tyrosine hydroxylase activity in sympathetic nervous system of rats with streptozocin-induced diabetes. 256 57

The aim of this investigation was to study the release of cholecystokinin (CCK) in connection with feeding and lactation and to investigate the involvement of CCK in the regulation of food intake. For this purpose a method based on high performance liquid chromatography and subsequent radioimmunoassay (RIA) for the determination of CCK in plasma was developed. CCK was also determined in the cerebrospinal fluid (CSF) by RIA and is referred to as CCK-like immunoreactivity (CCK-LI). Different molecular forms of CCK in dog and rat plasma have been determined. These were found to differ from those in the CSF, suggesting that the CCK measured in plasma and CSF are derived from different sources, i.e. the gut and brain. CCK was released into plasma in response to feeding in dogs and rats and in response to suckling in lactating animals. The release of CCK is under vagal control. Thus, electrical vagal stimulation of anaesthetized rats increased plasma levels of CCK, and abdominal vagotomy abolished the suckling-induced release of CCK. Lesions of the lateral midbrain, which disrupt the oxytocin-mediated milk-ejection reflex, were also found to block the increase in plasma CCK in response to suckling. Intraperitoneal (i.p.) injection of CCK octapeptide (CCK-8) decreased food intake in food deprived male rats in doses which resulted in plasma concentrations within the physiological range. Intracerebral, but not i.p., injection of a low dose of a CCK antagonist, reversed the effect of peripheral CCK-8 on food intake as did i.p. injection of peripheral CCK A receptor antagonists. Thus, the mechanism by which i.p. CCK-8 inhibits food intake may involve both peripheral and central CCK receptor mechanisms. The concentration of CCK-LI in the CSF decreased after food deprivation and increased after feeding or i.p. CCK-8. Intraperitoneal injection of peripheral CCK antagonists prevented the increase in CCK-LI in the CSF and the inhibitory effect of i.p. CCK-8 on food intake. These data indicate that peripheral CCK receptor mechanisms induce a release of CCK in the brain. During the hyperphagia of lactation, plasma but not CSF levels of CCK were increased in the rat. Food deprivation markedly decreased the concentration of CCK in plasma and CSF; and the levels were restored in CSF, but not in plasma, after 1 h of feeding. Removal of the litter decreased food intake and increased the concentration of CCK in the CSF, but not in plasma. Lactating rats were less sensitive to the inhibitory effect of i.p.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Role of cholecystokinin in feeding and lactation. 260 47

Syrian golden hamsters when allowed free access to food and an exercise wheel will run long distances and develop hyperphagia and accelerated linear body growth with high circulating levels of growth hormone and insulin. Somatostatin, a widely distributed brain-gut neurohormonal peptide, modulates nutrient absorption and may regulate food intake. To examine the role of circulating plasma somatostatin-like immunoreactivity (SRIF-LI; pg/ml) in exercise induced hyperphagia 4 groups of animals were studied; an unrestricted exercise group (279.0 +/- 107.7, n = 10); a sedentary group (121.1 +/- 40.8, n = 8); a restricted exercise group (107.7 +/- 12.4, n = 6); and a restricted no exercise group (115.5 +/- 45.9, n = 9). Thus, the unrestricted exercise group has a significantly elevated SRIF-LI concentration (P less than 0.01) while there was no difference between the other 3 groups. The elevation of plasma SRIF-LI in the unrestricted exercise group may represent a response to modulate increased nutrient entry in this group or may represent an incompletely effective satiety signal.
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PMID:Exercise-induced hyperphagia in the hamster is associated with elevated plasma somatostatin-like immunoreactivity. 288 63

The rapid growth (0.8 +/- 0.3 g/day) of a transplantable insulinoma, which also contained substance P (2.9 +/- 2.3 pmol/g) and gastrin-releasing peptide (3.2 +/- 2.1 pmol/g), resulted in the development of hyperphagia, hyperinsulinaemia and hypoglycaemia in rats (n = 8). After a 14-day growth period, the insulinoma-bearing rats showed an increase (49%; p less than 0.01) in the weight of the small intestine but no significant change in stomach weight compared with control animals. The content (pmol/organ) of somatostatin, substance P, neurokinin A and vasoactive intestinal peptide in the stomachs of the tumour rats was unchanged. A depletion in the content (53% p less than 0.01) and concentration (57%; p less than 0.01) of gastrin-releasing peptide, however, suggested either hypersecretion, possibly mediated through hypoglycaemia-induced vagal stimulation, or inhibition of synthesis. The concentration and content of glucagon-like immunoreactivity (enteroglucagon) in the small intestine of the insulinoma rats increased markedly (47%; p less than 0.01 and 120%; p less than 0.01). This increase is consistent with a proposed role of this peptide as a factor trophic to the intestinal mucosa. No significant changes in the concentrations of somatostatin, substance P, neurokinin A, vasoactive intestinal peptide and gastrin-releasing peptide in the small intestine were observed. However, the increase in gut weight resulted in a greater content of vasoactive intestinal peptide (40%; p less than 0.01) and substance P (37%; p less than 0.05) in the insulinoma rats.
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PMID:Effects of a transplantable insulinoma upon regulatory peptide concentrations in the gastrointestinal tract of the rat. 301 8

The growth of gastrointestinal mucosa can be related to ingestion and digestion of diet, with fasting producing mucosal hypoplasia and hyperphagia producing mucosal hyperplasia. Experiments were designed to determine whether induction of polyamine metabolism following ingestion of a meal was related to mucosal growth. Activity of the enzyme ornithine decarboxylase (ODC) in both jejunum and ileum but not in duodenum was dependent on the presence of food in the gut; ODC activity was more than 200-fold greater in mucosa of fed rats than in fasted rats. Inhibition of ODC with difluoromethylornithine lead to mucosal atrophy in ileum but not in duodenum. Refeeding of fasted rats resulted in significant induction of ODC in duodenal, ileal, and colonic, but not fundic, mucosa. In addition, two hormones, epidermal growth factor and glucagon, were effective inducers of ileal ODC activity. Direct evidence for hormonal involvement in the postprandial rise in mucosal ODC activity was provided by experiments in rats that had undergone ileal bypass surgery. After refeeding of fasted rats mucosal ODC activity was induced in both ileum left in continuity and in the bypassed segment. Refeeding of elemental diets demonstrated that ingestion of carbohydrate alone was sufficient for maximal enzyme induction. Mixed amino acids or glyceryl trioleate were no more effective inducers than nonnutritive solutions of cellulose or saccharin. These data demonstrate that hormones which are released during ingestion and digestion of a meal are the stimuli for induction of mucosal polyamine metabolism, suggesting that food-induced mucosal growth is hormonally mediated.
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PMID:Hormonal regulation of postprandial induction of gastrointestinal ornithine decarboxylase activity. 309 78

In summary, the association between malnutrition and infections, including respiratory infections, seems clear from consistent experience in developing nations. Young children are at the greatest risk, both of severe malnutrition and complicating infections. The cell-mediated immune system is the most affected by protein-calorie malnutrition, but antibody responses are also affected and complement levels are low. Infections with organisms handled by cell-mediated immunity would be the most predictable, but the immunoglobulin responses that are important for opsonization of invading microorganisms may also be impaired. The experience in developing nations has been extrapolated to patients in US hospitals, because hospitalized patients often have one or more abnormal nutritional parameters. However, severe malnutrition of the sort found in children in developing nations is uncommon in hospitalized patients, and the effects of malnutrition on host defenses in adults are likely to be less severe than in children. Whether the degrees of malnutrition that have been described in hospitalized patients produce clinically significant effects on antibacterial defenses in the lungs of adults remains uncertain. Despite the intuitive importance of nutritional support, and the repeated observation that nutritional parameters improve with nutritional support, a number of controlled trials have failed to show a clear improvement in patient outcome with aggressive nutritional therapy, including parenteral hyperalimentation. The results of these studies, together with the risks involved in parenteral alimentation have led some to suggest that "the emperor has no clothes," and that aggressive nutritional support is not worthwhile for most patients. The major problem in interpreting the data is the lack of clear clinical endpoints, and this may obscure potentially important responses to nutritional therapy. Nutritional status is only one of many interacting variables that may affect clinical outcome, particularly in patients in critical care units. Survival usually depends on many factors, particularly the status of major organ systems independent of nutrition, so that survival as an endpoint for nutritional studies is likely to be too insensitive. Prospective studies of the incidence and significance of infections, particularly pneumonia, in malnourished patients and the effects of nutritional therapy are lacking. At present, the prudent approach is to treat infections aggressively in malnourished patients, with antibiotics and drainage if necessary, and to provide nutritional supplementation in all patients via the gut as long as possible.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The relationship between malnutrition and lung infections. 311 82


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