INT2884
From wiki-pain
|
|
|
|
|
Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Whilst we have shown previously that plasma CCK and PYY levels are increased in critically ill patients [28-30] and that CCK and PYY are known to slow GE, the present study is the first to directly demonstrate a relationship between GE and plasma concentrations of CCK and PYY in critical illness. | |||||||||||||||
| |||||||||||||||
|
However, the concept of heightened hormonal release from a similar nutrient load in critically ill patients, particularly those with impaired motility [28,29], is also illustrated in the present study by the finding that the overall increase in plasma CCK and PYY in patients with delayed GE was similar to those with normal GE. | |||||||||||||||
| |||||||||||||||
|
The major observations are that, during critical illness, (a) GE was inversely related to both fasting and postprandial plasma CCK and PYY concentrations but (b) the postprandial increases in plasma CCK and PYY were also directly related to GE. | |||||||||||||||
| |||||||||||||||
|
As observed in lean [1,2,4,7,11,12] and obese [47] healthy subjects, the present study demonstrates a weak but direct relationship between the rate of GE and postprandial increases in plasma CCK and PYY in critically ill patients. | |||||||||||||||
| |||||||||||||||
|
ProCCK mRNA levels were increased 1.5-2.5 times by dbcAMP, noradrenaline and isoproterenol when compared with controls. | |||||||||||||||
| |||||||||||||||
|
The presence of such a feedback mechanism in chronic pancreatitis patients with exocrine enzyme deficiency possibly leads to an increase in cholecystokinin plasma levels. | |||||||||||||||
| |||||||||||||||
|
The variably low levels of enzyme activity observed during the administration of Vivonex HN suggest only minimal stimulation of cholecystokinin. | |||||||||||||||
| |||||||||||||||
|
Intraduodenal infusion of long chain triglycerides induces satiation, fullness and nausea, reduces gastric tone, and increases plasma levels of cholecystokinin (CCK), gastric inhibitory polypeptide, neurotension, and pancreatic polypeptide. | |||||||||||||||
| |||||||||||||||
|
Intraduodenal infusion of long chain triglycerides induces satiation, fullness and nausea, reduces gastric tone, and increases plasma levels of cholecystokinin (CCK), gastric inhibitory polypeptide, neurotension, and pancreatic polypeptide. | |||||||||||||||
| |||||||||||||||
|
In feed-intolerant patients, there was a trend for a greater magnitude of elevation in both PYY (AUC (0180 min): 2,743 ± 589 versus 1,526 ± 335 pmol/l.min; P = 0.09) and CCK (AUC (0180 min): 258 ± 43 versus 148 ± 35 pmol/l.min; P = 0.07) concentrations compared with feed-tolerant patients. | |||||||||||||||
| |||||||||||||||
|
In both groups, there was an increase in the absolute plasma CCK concentration after 20 minutes of duodenal nutrient infusion. | |||||||||||||||
| |||||||||||||||
|
This is followed by a review of work providing evidence in animal models (and suggestive evidence in humans) for the importance of CCK and opioid neuropeptides in affecting infant emotion regulation and the impact of touch-based interventions, in particular in the context of infant-mother attraction, contact, separation, and attachment. | |||||||||||||||
| |||||||||||||||
|
The patients with steatorrhea had a significantly (P less than 0.001) lower integrated plasma CCK response to the meal (177 +/- 23 pM.150 min) than the healthy subjects (468 +/- 41 pM.150 min), while patients with chronic pancreatitis without steatorrhea had an intermediate integrated postprandial CCK secretion (327 +/- 101 pM.150 min). | |||||||||||||||
| |||||||||||||||
|
Plasma concentrations of the satiety hormone cholecystokinin (CCK) increase with ageing. | |||||||||||||||
| |||||||||||||||
|
CCK antagonists have been shown to increase GE and energy intake in humans [17-19]. | |||||||||||||||
| |||||||||||||||
|
Although the majority of our patients received acid suppression therapy and therefore may have had increased serum gastrin levels, the cross-reactivity between gastrin and CCK is less than 2% [46] and is unlikely to contribute to the elevated CCK concentrations. | |||||||||||||||
| |||||||||||||||
|
In the fasted state, there is an increase in plasma concentrations of hormones that slow GE, such as CCK and PYY, and a decrease in hormones that may accelerate GE, such as ghrelin [28-30]. | |||||||||||||||
| |||||||||||||||
|
Levels of proCCK and proenkephalin A mRNA were determined by Northern blot analysis with proCCK- and proenkephalin A-specific cRNA hybridization probes 9 h after drug treatments. | |||||||||||||||
| |||||||||||||||
|
Fourteen patients with a cystic duct syndrome (CDS) underwent cholecystokinin (CCK) cholescintigraphy. | |||||||||||||||
| |||||||||||||||
|
Integrated response of plasma CCK was significantly lower in patients with chronic pancreatitis and DM than in the two other groups. | |||||||||||||||
| |||||||||||||||
|
General Comments
This test has worked.