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Query: HUMANGGP:036187 (gut)
 73,132 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two groups each of young and old animals were fed nutritonally adequate liquid diet. One group of each served for control, while in the other one 36% of the total caloric intake was supplied by ethanol in place of part of the fat and carbohydrate. The young animals became rapidly adapted to the alcohol containing diet, while the aged animals refused to eat it even at the expense of transient hunger and thirst. Alcohol treatment resulted in body weight loss and the appearance of slight ST segment abnormalities in the ECG. Histological study of the myocardium revealed no pathological finding. Alcohol reduced the blood pressure, TPR, gut and skin fractions of the cardiac output, myocardial nutritive blood flow, and vascular resistance of the carcass in both groups, whereas it increased the relative weight of the heart. There was a greater decrease of blood pressure and a greater increase in the relative weight of the heart in the old than in young alcohol treated animals. Chronic exposure to alcohol results in a redistribution of circulation which is detrimental to cardiac function. This alcohol induced redistribution affects the cardiovascular system of old animals more severely.
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PMID:Effect of chronic exposure to alcohol on the circulation of rats of different ages. 57 97

Regulation of food intake is commonly treated as a negative feedback-loop. Hunger and/or appetite lead man and animals to ingest food. The subsequent meal-contingent activation of pre- and postabsorptive mechanisms then leads to satiety. The activation of oral and gastrointestinal chemo- and mechanoreceptors is important on the preabsorptive site. The gastrointestinal hormone cholecystokinin may also have a physiological satiety effect. Preabsorptive satiety mechanisms are influenced by the rate of gastrointestinal transit. The pancreatic hormone glucagon, which is released during meal taking, and various metabolites contribute to the postabsorptive regulation of food intake through activation of hepatic chemoreceptors, which are connected to the brain via predominantly vagal afferents. In addition, glucoreceptors in the brain, in particular in the nucleus of the solitary tract, contribute to food intake regulation by monitoring blood glucose concentration or, more specifically, glucose utilization. The nucleus of the solitary tract, which relays vagal afferents from gut and liver and also gustatory afferents, projects to the hypothalamus and to other forebrain structures. In this neural network the informations from the periphery are integrated by various neurotransmitters and neuropeptides, but the exact role of the substances involved is not fully understood yet. Body weight and, hence, body fat presumably affects feeding through modulation of a postabsorptive mechanism.
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PMID:[Regulation of food intake]. 220 33

Release of the brain-gut peptide cholecystokinin (CCK) is stimulated by intragastric instillation of ethanol, and peripheral administration of CCK inhibits ethanol consumption. To assess the temporal specificity of the inhibitory effect of CCK on alcohol intake, water-deprived rats were given 5% ethanol at 20, 10 or 0 min after intraperitoneal injections of CCK octapeptide. Delaying access to ethanol for 20 min prevented a significant effect of CCK on intake. CCK's temporally constrained inhibitory action on alcohol consumption is consistent with an ethanol satiation effect. To test the motivational specificity of CCK's effect on fluid intake, rats were allowed a 2-bottle choice of 2% ethanol and water after CCK injections. Ethanol solution intake was suppressed by CCK, and total water intake was unaffected. The putative alcohol satiation action of CCK is appropriately specific to ethanol solution in free-choice tests. Hungry, but not fluid-deprived rats that were either ethanol experienced or naive received a 2-bottle choice of 4% ethanol or water after CCK or saline injections. CCK again specifically inhibited ethanol intake, but this effect required prior ethanol experience. Doses of CCK and naloxone, an opioid receptor blocker, combined to inhibit ethanol intake in an infra-dose-additive manner in water-deprived rats. CCK may act endogenously, in part on opioid receptor-mediated processes, as a preabsorptive satiety signal of ethanol. The full expression of this action appears to depend on prior conditioning of nutritive expectancy of the postingestive effects of alcohol.
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PMID:Cholecystokinin and satiation with alcohol. 281 43

Studies of brain monoamines and neuropeptides have provided extensive evidence in support of their role in the control of normal eating behavior. In this process, the medial and lateral portions of the hypothalamus, working in conjunction with forebrain and hindbrain sites and with peripheral autonomic-endocrine systems, have a critical responsibility in balancing signals for hunger and satiety. Via its rich and biologically active neurotransmitter substances, the hypothalamus monitors and integrates the complex sensory and metabolic input concerning the nutritional status of the organism and transduces this information into appropriate quantitative and qualitative adjustments in food intake. The specific neurotransmitters for which there is the most extensive evidence for a physiological function include the eating-stimulatory substances norepinephrine (alpha 2), opioid peptides, pancreatic polypeptides, growth hormone-releasing factor, and gamma-aminobutyric acid; the eating-inhibitory substances dopamine, epinephrine, serotonin, cholecystokinin, neurotensin, calcitonin, glucagon, and corticotropin-releasing factor; and possibly other gut-brain peptides. From biochemical, pharmacological, and anatomical studies, hypotheses have been generated to explain the role of these various monoamines and neuropeptides in controlling total energy intake, in determining the amount and pattern of macronutrient selection, and in maintaining normal energy and nutrient stores under fluctuating conditions within the external environment.
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PMID:Brain monoamines and peptides: role in the control of eating behavior. 286 77

Studies of brain monoamines and neuropeptides have provided extensive evidence in support of their role in the control of food intake, meal patterns and appetite for specific macronutrients. In this process, the medial and lateral portions of the hypothalamus have a critical responsibility in balancing signals for hunger and satiety. Via its rich and biologically active neurotransmitter substances, the hypothalamus monitors and integrates the complex sensory and metabolic input concerning the nutritional status of the organism and transduces this information into appropriate quantitative and qualitative adjustments in food intake. The specific neurotransmitters for which there is the most extensive evidence for a physiological function include the eating-stimulatory substances norepinephrine, opioid peptides, pancreatic polypeptides, galanin and gamma-aminobutyric acid; and the eating-inhibitory substances dopamine, epinephrine, serotonin and several gut-brain peptides. From biochemical, pharmacological and anatomical studies, hypotheses have been generated to explain the role of these various monoamines and neuropeptides in controlling total energy intake, in determining the amount and pattern of macronutrient selection, and in maintaining normal energy and nutrient stores under dynamic conditions within the external environment.
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PMID:[Central neurotransmitters and control of specific appetite for the macronutrients]. 290 20

Profitable livestock production from forages largely depends on efficiency of converting forages into products. Efficient grazing management systems require an understanding of the roles of system components. However, experimentation should be conducted with regard to the system as a whole rather than on the systems components in isolation. This may necessitate development of computer models. The short-term intake of forage by grazing animals is controlled both by the structure of the forage and by effects of the ingested forage on gut fill as moderated by the hunger-satiety complex. Intake can be defined as the product of bite size, rate of biting and grazing time. Measurement of these variables is facilitated by the use of esophageally fistulated animals and automatic recording devices. Bite size has the greatest influence on intake, with rate of biting and grazing time being compensatory variables. Sward structure influences bite size to varying degrees. In temperate grass swards, leaf surface height appears to be the dominant influence on bite size. But in tropical grass swards, leaf density and leaf:stem ratio have a greater influence on bite size than does leaf surface height. Alternative techniques to conventional grazing trials are described. Diversity of environments and forages in the U.S. requires further research into the development of grazing systems. In the future, small-scale trials and computer simulation techniques likely will be used to a greater extent.
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PMID:Researching the plant-animal interface: the investigation of ingestive behavior in grazing animals. 304 96

The relationship between the subjective state of hunger and objective food intake was investigated using a diary self-report method. Thirty-one adult humans were paid to record in a diary, for 7 consecutive days, everything that they either ate or drank, the time that they ingested it, and how hungry they were on a seven point scale. The diary entries were encoded and entered into a computer. Meals were identified according to 5 different definitions and meal compositions, estimated stomach contents, and intermeal intervals calculated. Univariate and multiple linear regression predictions of self-reported hunger and meal size were calculated from these data. Self-reported hunger was found to be related negatively to the energy content and the proportion of protein in the stomach at the time of meal ingestion. Meal size was also found to be related to these same factors and also positively to self-rated hunger. These results suggest that protein has a unique satiating property beyond its contribution to total food energy. When self-rated hunger and the premeal stomach contents were all used in a multiple regression prediction of meal size the premeal stomach contents influence became nonsignificant leaving subjective hunger as the only significant predictor of meal size. These results suggest that subjective hunger represents an intermediary step in the cause-effect sequence between gut filling and cessation of meal ingestion.
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PMID:Subjective hunger relationships with meal patterns in the spontaneous feeding behavior of humans: evidence for a causal connection. 321 51

1. Possible links between metabolism and satiation were investigated using volunteer subjects given test meals based on milk solids. Satisfaction was rated by the subjects on a six-point scale and the course of metabolism was followed by measurement of the respiratory quotient (RQ). 2. The time-course of satiation was the same for a high-carbohydrate, a high-fat and a high-protein meal, in spite of the very different time-course of metabolism. The degree of satiation was reduced by added sodium chloride, without affecting the RQ rise. On the other hand, calcium chloride produced a suppression of the RQ rise without altering the satiation. 3. It is proposed that the results indicate that the primary receptors responsible for post-prandial satiation lie within the gut wall and that there is probably a number of receptor types. Likely candidates for these receptors are the gut hormone-secreting cells. 4. Although very-low-protein meals produce less satiation than meals containing 220 g protein/kg dry weight, there is no additional satiation obtained by increasing the protein level further. This is not inconsistent with the possibility of a protein hunger separate from an energy hunger.
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PMID:The effect of meal composition on the degree of satiation following a test meal and possible mechanisms involved. 321 15

Feeding problems, anorexia and vomiting are common in infants and children with chronic renal failure (CRF), and play a major role in the growth failure often found in this condition. However, the gastroenterological and nutritional aspects of CRF in children have received little attention, hence therapeutic interventions are usually empirical and often ineffective. Gastritis, duodenitis and peptic ulcer are often found in adults with CRF on regular haemodialysis and following renal transplantation. Despite persistent hypergastrinaemia, gastric acid secretion is decreased rather than increased in most of these patients, and active peptic disease appears to be promoted by the removal of the acid output inhibition (neutralisation of gastric acid by ammonia) that follows active treatment. Helicobacter pylori, on the other hand, does not seem to play a significant role in the pathogenesis of peptic disease in CRF. Gastro-oesophageal reflux has been found in about 70% of infants and children with CRF suffering from vomiting and feeding problems, and thus appears to be a major problem in these patients. In a number of symptomatic patients with CRF, gastric dysrhythmias and delayed gastric emptying have also been found; hence there appears to be a complex disorder of gastrointestinal motility in CRF. Serum levels of several polypeptide hormones involved in the modulation of gastrointestinal motility [e.g. gastrin, cholecystokinin (CCK), neurotensin] and the regulation of hunger and satiety (e.g. glucagon, CCK) are significantly raised as a consequence of renal insufficiency, and can be reverted to normal by renal transplantation. Furthermore, several other humoral abnormalities (e.g. hypercalcaemia, hypokalaemia, acidosis, etc.) are not uncommon in CRF. By directly affecting the smooth muscle of the gut or stimulating particular areas within the central nervous system, all these humoral alterations may well play a major role in the gastrointestinal dysmotility, anorexia, nausea and vomiting in patients with CRF. Specific pharmacological and nutritional interventions should thus be considered for the treatment of vomiting and feeding problems in CRF.
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PMID:Gastrointestinal function in chronic renal failure. 874 22

Animal studies suggest that aging is associated with anorexia and disordered gastrointestinal transit. To determine whether there is a relationship between the effects of aging on appetite and gastrointestinal transit in humans, 19 young (age 23-50 yr) and 14 elderly (age 70-84 yr) normal volunteers underwent measurements of 1) desire to eat, hunger, and fullness (visual analog scales); 2) gastric emptying (scintigraphy); 3) orocecal transit (breath hydrogen); 4) total gut transit (radiopaque markers); and 5) autonomic nerve function (cardiovascular reflexes). We found that, postprandially, elderly subjects had less desire to eat (P < 0.05) and less hunger (P < 0.05), but not a significantly greater fullness than younger subjects. Gastric emptying (50% emptying time) for solid (182 +/- 26 vs. 127 +/- 13 min, P < 0.05) and liquid (47 +/- 4 vs. 35 +/- 3 min, P < 0.05) meal components was slower in elderly subjects. Postprandial hunger was inversely related (r = -0.39, P < 0.05) to solid gastric emptying. There were no significant differences in orocecal and total gut transit times between the two groups. Autonomic nerve function was abnormal in 11 elderly but none of the young subjects (P < 0.01). We conclude that aging is associated with 1) diminished desire to eat and hunger, 2) slowing of solid and liquid gastric emptying, 3 no change in orocecal and total gut transit, and 4) autonomic nerve dysfunction. The slowing of gastric emptying may contribute to anorexia in aging subjects.
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PMID:Evidence for the anorexia of aging: gastrointestinal transit and hunger in healthy elderly vs. young adults. 903 15


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