Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Feeding is often influenced by competitive needs or by environmental factors. Nevertheless, in physiological conditions hunger is elicited by depletion of macronutrients. The first question is what specific signals cause food intake? Recent data suggest that the signal comes not from exclusive depletion of carbohydrates or of anyone type of the major macronutrients but from overall decreased cellular power production (hypoischymetric signal). Locomotion free metabolic rate has been shown to decrease preceding hunger and to increase in order to determine satiety. Satiation, which occurs largely before ingested nutrients can cross the intestinal barrier and replete the inner milieu, obeys a specific mechanism. Following the stimulation by ingestion of the oro-gastro-intestinal receptors metabolic hormones such as glucagon and insulin are released and enhance metabolism of endogenous reserves. The so-induced endogenous "meal" brings about an anticipatory hypermetabolism which inhibits further ingestion. Post-absorptive satiety subsequently will replace the pre-absorptive state of satiation. The long term regulation of body weight is more subtle. When the actual body weight exceeds its defended value, responsiveness towards signals of hunger diminishes. This hyporesponsiveness seems to be a consequent of an enlargement of the microscopic fat depot at the level of hypothalamic receptive structures which parallels the peripheral increase of the macroscopic fat depot. Thus, hunger promoting signals become less effective and feeding decreases. A symmetrical process takes place in case of body weight loss which results in central hyperresponsiveness to hunger related stimuli and thus facilitates feeding and body weight recovery.
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PMID:[Physiology of food intake and regulation of body weight]. 304 93

Glucose and related pancreatic hormones play a major role in the metabolism of monogastric mammals yet their influence on hunger and/or satiety is, as yet, poorly understood. Glucose, insulin and glucagon rise during a meal and gradually decline to baseline levels shortly after a meal. A sudden drop in plasma glucose as well as insulin have been reported just prior to the onset of a meal but the functional significance of this is not yet clear. Systemic injections of glucose have no acute satiety effects but intraduodenal and intrahepatic infusions reduce food intake and free-feeding and deprived animals respectively. Treatments which decrease cellular glucose utilization directly (2-DG) or indirectly (insulin) increase food intake while exogenous glucagon (which produces hyperglycemia) decreases it. There is considerable evidence that some or all of these effects may be due to a direct central action of glucose, 2-DG, insulin, and glucagon on brain mechanisms concerned with the regulation of hunger and satiety although influences on peripheral "glucoreceptors" have been demonstrated as well. The functional significance of glucoprivic feeding is, however, questioned. The feeding response to 2-DG and related compounds is capricious, and its temporal course does not parallel the hyperglycemic reaction which presumably reflects cellular glucopenia. Moreover, numerous brain lesions which increase, decrease, or have no effect on ad lib intake and often have no effect on the response to deprivation have been shown to severely impair or abolish feeding responses to systemic injections of 2-DG that produce severe central as well as peripheral glucopenia. Feeding responses to insulin are intact after most of these lesions, suggesting that this hormone may influence food intake in a fundamentally different fashion. The mechanism of insulin action is not understood--the classic feeding response is obtained only with doses that are pharmacological when compared to normal plasma levels and there is increasing evidence that lower doses may have opposite, inhibitory effects on food intake and body weight. Relatively small doses of glucagon decrease food intake (although opposite facilitatory effects have been reported after even smaller doses) but the effect does not appear to be due to hepatic mobilization of glucose as initially assumed. Decreases in food intake after intracranial injections of very small doses suggest a direct central action.
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PMID:The role of glucose, insulin and glucagon in the regulation of food intake and body weight. 309 17

The neurotoxin capsaicin has been shown to selectively interfere with unmyelinated sensory fibers, as well as leading to depletions of substance P and other peptides. Meal pattern analysis was performed both before and after treatment with capsaicin in twelve adult male Sprague-Dawley rats. Capsaicin treatment only briefly altered feeding patterns. No long term effect on body weight was noted. These same animals were then tested for the appetite suppressing effects of IP injections of glucagon (125 micrograms/kg) and epinephrine (30 micrograms/kg). Capsaicin treated rats decreased their intake of sweetened condensed milk during a 30 minute test in response to glucagon and epinephrine. Controls failed to suppress intake in response to glucagon, but drank less milk after epinephrine than did capsaicin treated rats. Efficacy of capsaicin treatment was obtained using similarly treated animals subject to histological evaluation within 2 days of capsaicin treatment. These results suggest that peripherally generated information relayed to the CNS via small-diameter sensory neurons is not a necessary component of the normal hunger/satiety sequence, nor body weight regulation.
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PMID:Capsaicin and its effects upon meal patterns, and glucagon and epinephrine suppression of food intake. 365 50

In order to ascertain direct central anorectic actions of mazindol (MZD), subtle changes in meal patterns and endogenous feeding related chemical substances were examined in rats following intra-third ventricle injection of 0.03 mumole MZD. In ad lib feeding, MZD decreased meal size and prolonged postprandial intermeal interval during a 4 hr period starting 2 hr after injection. The magnitude of anorectic actions of MZD was depressed by hunger. Although the action of MZD is short in duration, long duration anorexia was achieved by chronic infusion for 8 days. Infusion of MZD starting at 5:50 p.m. decreased plasma insulin, leaving glucose and glucagon unaffected, although no change in plasma glucose or insulin was observed following injection at 11:30 a.m. These findings, together with other reports, can be explained by MZD's direct effects on the hypothalamic hunger and satiation centers.
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PMID:Changes in meal pattern and endogenous feeding related substances following mazindol administration. 638 20

1. To assess the influence of counterregulatory hormones, independently of neuroglycopaenia, on higher cerebral (cognitive) function, 'hypoglycaemic' warning symptoms and glucose kinetics, 10 healthy subjects participated in two hyperinsulinaemic (2 m-units min-1 kg-1) glucose clamp studies. After 100 min of euglycaemia (plasma glucose level 5 mmol/l), the plasma glucose level was either (a) maintained at 5 mmol/l for 120 min by glucose infusion with concomitant replacement of counterregulatory hormones (continuous infusions of glucagon, adrenaline, noradrenaline, cortisol and growth hormone) to mimic the hormonal milieu normally associated with hypoglycaemia (hormone infusion study) or (b) lowered to 2.8 mmol/l for 120 min (hypoglycaemia study). Assessments were made of cognitive function (P300 auditory evoked responses), symptoms (visual analogue scales) and glucose kinetics (3-[3H]glucose). 2. Hypoglycaemia was associated with an increase in all symptoms (facial flushing, palpitations, tingling, trembling, sweating, hunger, light-headedness and sleepiness, P < 0.01) and all subjects were aware that blood glucose levels had fallen. P300 evoked potential latency increased from 280 +/- 6 to 312 +/- 5 ms (mean +/- SEM, P < 0.01). In contrast, P300 latency and several individual symptoms (hunger, facial flushing, sweating and light-headedness) did not change from baseline during the hormone infusion study (P < 0.05 versus hypoglycaemia). Hepatic glucose production was lower (1.5 +/- 0.4 versus 2.3 +/- 0.3 mg min-1 kg-1, P < 0.05) and peripheral glucose uptake was higher (7.4 +/- 1.0 versus 5.6 +/- 0.6 mg min-1 kg-1, P < 0.01) during infusion of the hormones compared with during hypoglycaemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of counterregulatory hormones, independently of hypoglycaemia, on cognitive function, warning symptoms and glucose kinetics. 840 88

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

The effects of four equienergetic breakfasts with varying fiber and macronutrient contents on hunger and satiety ratings, on subsequent lunch intake, and on postprandial carbohydrate and fat metabolism were investigated in normal weight male subjects in two experiments, in which lunch was offered at a predetermined time (Experiment 1) or in which the subjects were free to choose when to eat lunch (Experiment 2). Consumption of either a commercially available high fiber cereal (HFC, 10% fiber), a medium fiber cereal (MFC, 7% fiber), a low fiber cereal (LFC, 3% fiber), or a standard continental breakfast (0% fiber) on nonconsecutive days did not differentially affect hunger and satiety ratings, the size or microstructure of the subsequent lunch, and the breakfast to lunch intermeal interval (in Experiment 2). Plasma concentrations of glucose, lactate, and insulin increased more after the LFC breakfast than after the other breakfast varieties. A reactive postprandial hypoglycaemia occurred after the LFC breakfast, shortly before lunch. The plasma concentrations of fat metabolites (triglycerides, free fatty acids, beta-hydroxybutyrate) and of glucagon were not differentially affected by the breakfast varieties. The results are consistent with the assumption that energy content of a meal is the major determinant of subsequent energy intake in man and the fiber content and macronutrient composition have only a modulating effect.
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PMID:Breakfasts with different fiber and macronutrient contents do not differentially affect timing, size or microstructure of the subsequent lunch. 900 Mar 33

The sweet taste of nonnutritive sweeteners has been reported to increase hunger and food intake through the mechanism of cephalic-phase insulin release (CPIR). We investigated the effect of oral sensation of sweetness on CPIR and other indexes associated with glucose metabolism using nutritive and nonnutritive sweetened tablets as stimuli. At lunchtime, 12 normal-weight men sucked for 5 min a sucrose, an aspartame-polydextrose, or an unsweetened polydextrose tablet (3 g) with no added flavor. The three stimuli were administered in a counterbalanced order, each on a separate day at 1-wk intervals. Blood was drawn continuously for 45 min before and 25 min after the beginning of sucking and samples were collected at 1-min intervals. Spontaneous oscillations in glucose, insulin, and glucagon concentrations were assessed as were increments (slopes) of fatty acid concentrations during the baseline period. The nature of the baseline (oscillations: glucose, insulin, and glucagon; and slopes: fatty acids) was taken into account in the analyses of postexposure events. No CPIR and no significant effect on plasma glucagon or fatty acid concentrations were observed after the three stimuli. However, there was a significant decrease in plasma glucose and insulin after all three stimuli. Only the consumption of the sucrose tablet was followed by a postabsorptive increase in plasma glucose and insulin concentrations starting 17 and 19 min, respectively, after the beginning of sucking. In conclusion, this study suggested that oral stimulation provided by sweet nonflavored tablets is not sufficient for inducing CPIR.
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PMID:Cephalic phase responses to sweet taste. 906 23

Accumulating evidence suggest that a good way to compare the satiety power of meals with different compositions or energy contents is to measure the onset latency of the next meal when freely requested by subjects deprived of any time cues. This study was performed in normal-weight young men (aged 19-24 y) isolated from time cues. At sessions 1 and 2, we studied the effects of two high-carbohydrate pasta lunchs with either 50 g low-energy butter substitute (lunch A) or 50 g butter (lunch B) on hunger ratings, on the latency of the dinner request, and on energy and nutrient intakes at the offered ad libitum dinner. Sessions 3 and 4 were designed to examine the effects of the two lunchs on the postlunch and predinner profiles of plasma glucose, insulin, glucagon, and lipids; consequences on the metabolic and hormonal responses to the fixed dinner offered on request also were tested. The addition of 1588 kJ butter to the pasta lunch compared with the addition of 67 kJ butter substitute had no effect on hunger ratings but significantly delayed the onset of dinner by approximately 38 min; however, neither energy intake nor nutrient intakes were different. The high-fat lunch led to a slightly different postlunch plasma glucose concentration profile but, as expected, to higher plasma triacylglycerol and fatty acid concentrations. The high-fat lunch also led to postdinner glucose intolerance with normal insulin and high fatty acid concentrations that may help explain the partial and delayed adjustment in energy intake after a high-fat meal as reported by some studies.
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PMID:Satiety power of dietary fat: a new appraisal. 912 70

The gut peptide glucagon-like peptide 1(7-36) amide (GLP-1) is released into the circulation after food intake. GLP-1 has been shown to have an incretin effect and inhibits gastrointestinal motility in humans. In rats, intracerebral administration of GLP-1 results in reduced food intake. Obese humans have been found to have an attenuated plasma GLP-1 response to a mixed meal. To approximate the physiologic state, GLP-1 or saline was administered intravenously and randomly at the beginning of a test meal served on a universal eating monitor to 6 obese subjects to test our hypothesis that GLP-1 influences termination of food intake (and thus food intake during a meal) and feelings of satiety in humans. As a marker for gastric emptying, 1.5 g acetaminophen was given at the start of the meal. Blood samples for analysis of acetaminophen, insulin, glucose, glucagon, and C-peptide were obtained. Hunger, fullness, and food choice were assessed with visual analogue scales and food-choice questionnaires. GLP-1 infusion resulted in a prolonged period of reduced feelings of hunger, desire to eat, and prospective consumption after the meal. The rate of gastric emptying was slower during infusion of GLP-1. Postprandial blood glucose concentrations were reduced during the GLP-1 infusion, but the amount of energy consumed, eating rate, and plasma concentrations of insulin, glucagon, and C-peptide were unchanged. GLP-1 given exogenously at the start of a meal did not seem to affect meal termination or the amount of food eaten. However, postprandial feelings of hunger decreased, suggesting that exogenous GLP-1 may influence feelings of hunger and satiety in humans.
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PMID:Glucagon-like peptide 1 increases the period of postprandial satiety and slows gastric emptying in obese men. 973 26


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