Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0392674 (exhaustion)
 13,658 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Secretion of trypsin, chymotrypsin, lipase and amylase was measured in male rats under urethane anaesthesia using a method of continuous perfusion of the duodenum. Prolonged infusion of cholecystokinin-pancreozymin (CCK-PZ) over a period lasting 200-360 min was administered either alone or together with a submaximal dose of secretin (1 unit/100 g - 10 min). Infusion of CCK-PZ was carried out using maximal doses (1--1.5 unit/100 g - 10 min) with and without secretin. Supramaximal doses of CCK-PZ (2 and 4 units/100 g - 10 min) were used only in combination with secretin. In all experiments secretion of enzymes showed a triphasic pattern including an initial peak followed by a plateau secretion after 10--20 min (phase 1), a decreasing second phase and finally base-line secretion (phase 3), thus demonstrating exhaustion of enzyme output from the gland with time. With increasing and supramaximal dose of CCK-PZ the cumulative output of enzymes from start to baseline secretion decreased progressively. Under the same conditions the levels of peak and plateau secretion were lower, the duration of plateau secretion was longer and the decreasing phase of secretion was shortened. These features indicate inhibition of secretion with increasing supramaximal doses of CCK-PZ infusion. Whereas the proteolytic enzymes and lipase reacted in a parallel way always amylase secretion was sustained on a higher level, implicating an alternative pathway for secretion.
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PMID:Effect of prolonged infusion of maximal and supramaximal doses of pancreozymin on pancreatic enzyme secretion in the rat--exhaustion or inhibition? 94 24

We examined the possible physiologic effects of intravenous (IV) amino acids (AAs) and long-chain triacylglycerols (LCTs) on gallbladder (GB) motility and release of cholecystokinin (CCK) on humans. GB contraction was studied in normal volunteers after administration of a fatty meal and IV infusion of AA and LCT. The GB contraction volume was calculated with ultrasound. Cholecystokinin-8 (CCK-8) and cholecystokinin-33/39 (CCK-33/39) were measured by radio-immunoassay. Administration of a fatty meal resulted in GB contraction by 60% of its basal volume and was accompanied by an increase in the serum levels of both CCK-8 and CCK-33/39. Administration of IV AA and LCT resulted in GB contraction by 17 and 37%, respectively, of its basal volume. The latter contractions were accompanied by increased levels of CCK-8 only. We conclude that IV administration of AA and LCT can result in human GB contraction and induce the release of only CCK-8. Continuous IV administration of AA and LCT for greater than 2h causes exhaustion of CCK-8 release, so that the GB returns to its initial volume.
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PMID:Gallbladder contraction after administration of intravenous amino acids and long-chain triacylglycerols in humans. 180 71

Recently, we demonstrated that hypercalcemia causes marked stimulation of feline exocrine pancreatic secretion, and that this effect is absent when a large dose of cholecystokinin (CCK) is infused prior to induction of hypercalcemia. To investigate this effect in more detail, anesthetized cats were given calcium i.v. after preadministration of CCK or urecholine (a cholinergic agonist) at specific doses, or of saline as a control. We found that the hypercalcemia-induced stimulation of pancreatic protein secretion was abolished after preadministration of CCK at large doses. After the prestimulus dose was decreased or the calcium dose was increased, however, the pancreatic secretory response to hypercalcemia was preserved. In contrast, the response to a submaximal dose of CCK was unchanged after prestimulation with a large dose of CCK. Similar results were obtained when urecholine instead of CCK was used as prestimulus. These findings indicate that loss of pancreatic responsiveness to hypercalcemia following prestimulation with CCK is dependent on doses of both prestimulus and calcium used, and that it is not specific for prestimulation with CCK but also inducible by cholinergic agonists. They further suggest that this phenomenon is not due to exhaustion of pancreatic secretory capacity, but may reflect decreased sensitivity to the hypercalcemic stimulus instead.
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PMID:Stimulatory effect of hypercalcemia on pancreatic secretion is prevented by pretreatment with cholecystokinin and cholinergic agonists. 356 41

The purpose of the present investigation was to determine the independent effects of hypoxia and physical exercise on peripheral cholecystokinin (CCK) metabolism in humans. Thirty-two physically active men were randomly assigned in a double-blind manner to either a normoxic (N; n = 14) or hypoxic (H; n = 18) group. During the acute study, subjects in the H group only participated in two tests, separated by 48 h, which involved a cycling test to exhaustion in normobaric normoxia and normobaric hypoxia (inspired O(2) fraction = 0.21 and 0.16, respectively). In the intermittent study, N and H groups cycle-trained for 4 wk at the same relative exercise intensity in both normoxia and hypoxia. Acute normoxic exercise consistently raised plasma CCK during both studies by 290-723%, which correlated with increases in the plasma ratio of free tryptophan to branched chain amino acids (r = 0.58-0.71, P < 0.05). In contrast, acute hypoxic exercise decreased CCK by 7.0 +/- 5.5 pmol/l, which correlated with the decrease in arterial oxygen saturation (r = 0.56, P < 0.05). In the intermittent study, plasma CCK response at rest and after normoxic exercise was not altered after physical training, despite a slight decrease in adiposity. We conclude that peripheral CCK metabolism 1) is more sensitive to acute changes than chronic changes in energy expenditure and 2) is potentially associated with acute changes in tissue PO(2) and metabolic precursors of cerebral serotoninergic activity.
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PMID:Physical exercise and normobaric hypoxia: independent modulators of peripheral cholecystokinin metabolism in man. 1113 99

Leptin, an ob gene product of adipocytes, plays a key role in the control of food intake and energy expenditure but little is known about leptin response to strenuous exercise in fasted and fed subjects or before and after blood donation. This study was designed to determine the immediate effects of strenuous exercise in healthy volunteers under fasting or fed conditions and before and one day after blood donation (450 ml) on plasma levels of leptin and gut hormones [gastrin, cholecystokinin (CCK), pancreatic polypeptide (PP) and insulin], as well as on "stress" hormones (cortisol, catecholamines and growth hormone. Two groups (A and B) of healthy non-smoking male volunteers were studied. All subjects performed incremental exercise tests until exhaustion (up to maximal oxygen uptake--VO2max), followed by 2 h of rest session. Group A perfomed the tests on a treadmill, while group B on a cycloergometer. In group A, one exercise was performed under fasting conditions and the second following ingestion of a standard liquid meal. In group B, one exercise test was performed as a control test and the second 24 h after blood donation (450 ml). Blood samples were withdrawn 5 min before the start of the test, at the VO2max, and 2 h after finishing the exercise. No significant change in plasma teptin were observed both immediately and 2 h after the exercise in fasted subjects, but after the meal the plasma leptin at VO2max and 2 h after the test was significantly higher, while after blood donation was significantly reduced. The postprandial rise in plasma leptin was accompanied by a marked increment in gut hormones; gastrin, CCK and PP and stress hormones such as norepinephrine, cortisol and GH. These hormonal changes could contribute to the postprandial rise in plasma leptin concentrations, while the fall of leptin after blood donation could be attributed to the inadequate response of stress hormones and autonomic nervous system to exhausting exercise. We conclude that strenuous physical exercise; 1) fails to affect plasma leptin level but when performed after meal but not after blood withdrawal it results in an increase and fall in plasma leptin, and 2) the release of gut hormones (gastrin, CCK and PP) and stress hormones (norepinephrine, cortisol, GH) increase immediately after exercise independently of feeding or blood donation and 3) following blood donation the strenuous exercise resulted in a marked reduction in the plasma leptin, cortisol and GH concentrations, possibly due to the impairment in the autonomic nervous control of these hormones.
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PMID:Leptin, gastrointestinal and stress hormones in response to exercise in fasted or fed subjects and before or after blood donation. 1132 13