Disease relevance of Postprandial Period

• CONCLUSIONS: Glucose fluctuations during postprandial periods and, more generally, during glucose swings exhibited a more specific triggering effect on oxidative stress than chronic sustained hyperglycemia [1].
• 1. A total serum bile acid particularly in the postprandial periods is more sensitive than either BSP or ICG for the detection of minimal liver disease and will become a useful screening method [2].

High impact information on Postprandial Period

• CONCLUSIONS--Recommended over-the-counter doses of famotidine and calcium carbonate tablets have different pharmacokinetic profiles when taken in the postprandial period [3].
• METHODS: LES pressure, esophageal pressures, esophageal pH, and crural diaphragm electromyogram were recorded simultaneously in the postprandial period for 30 minutes before and two 30-minute periods after the injection of atropine [4].
• BACKGROUND & AIMS: EM523, a motilin agonist, is intended to be used as a gastroprokinetic during the postprandial period, but the mechanism(s) by which EM523 stimulates postprandial contractions in the stomach has not been studied before [5].
• Our data suggest that individuals who ingest moderate amounts of caffeine may develop hypoglycemic symptoms if plasma glucose levels fall into the "low-normal" range, as might occur in the late postprandial period after ingestion of a large carbohydrate load [6].
• We hypothesized that postprandial glycemic excursions could be normalized in type 1 diabetes by suppressing glucagon with pramlintide acetate in the immediate postprandial period and supplementing glucagon in the late postprandial period [7].

Biological context of Postprandial Period

• The aim of this post hoc analysis was to assess the effects of pramlintide, an amylin analog shown to reduce postprandial glucose excursions in patients with diabetes, on markers of oxidative stress in the postprandial period [8].
• In the postprandial period (0730-2030 h), the areas under the curve (AUC) for circulating triglyceride and total cholesterol were significantly higher in hypopituitary than control women (P = 0.0089 and P = 0.0016, respectively) [9].
• In humans, pramlintide slows gastric emptying and suppresses glucagon secretion during the prandial/postprandial period to slow and reduce the entry of glucose into the circulation [10].
• Coordinated release of acylation stimulating protein (ASP) and triacylglycerol clearance by human adipose tissue in vivo in the postprandial period [11].
• Whole-body plasma noradrenaline spillover and thermogenesis during the 120 min postprandial period were 37% and 36% higher after the single meal as compared with the multiple meals, although this was not statistically significant [12].

Anatomical context of Postprandial Period

• This shift in glycine taurine ratio shows, that the relative increase in concentrations of glycine conjugates exceeds the relative increase in concentrations of taurine conjugates in the early postprandial period, and supports the view that there is significant absorption of glycine conjugated bile acids from the proximal small intestine [13].
• These results suggest that ethanol may reduce cardiovascular risk by modulating vascular muscle cell growth during the postprandial period [14].
• Leucine excess under conditions of low or compensated aminoacidemia does not change skeletal muscle and whole-body protein synthesis in suckling lambs during postprandial period [15].
• CONCLUSIONS: This study showed no significant pharmacodynamic effect of tegaserod on gallbladder contractility or on CBD and CHD diameters as a surrogate marker of sphincter of Oddi function during both the interdigestive (fasting) and the digestive (postprandial) periods in healthy female subjects and female patients with IBS-C [16].
• In the presence of metoprolol, gastric acid content was significantly increased during the late postprandial period producing a corresponding increase in acid load delivered to the duodenum. beta 1-adrenoceptor blockade appears to prolong the gastric secretory response to food without altering gastric emptying [17].

Associations of Postprandial Period with chemical compounds

• Concomitant administration of caffeine (250 mg, 30 minutes before breakfast), however, maintained the beneficial effect of dihydroergotamine during the postprandial period [18].
• CR did not differ significantly when values in the fasting state were compared with those in the postprandial periods and was therefore unaffected by plasma C-peptide concentration [19].
• In the dosis used cisapride was found to increase lower oesophageal sphincter pressure in the interdigestive and in the late postprandial state, but to have no effect in the early postprandial period [20].
• Vitamin A was added to the test meal in all subjects to trace the metabolism of the chylomicron (Sf greater than 1000) and non-chylomicron (Sf less than 1000) fractions in the postprandial period [21].
• RESULTS: During the four hour postprandial period, 5-HT concentrations were significantly higher in patients with IBS than in healthy volunteers at 0.5 hours (p < 0.05), 2 hours (p < 0.05) and 2.5 hours (p < 0.05) [22].

Gene context of Postprandial Period

• Furthermore, in type IIB subjects, CETP-mediated total CE flux over the 8 h postprandial period from HDL to potentially atherogenic TRL was significantly enhanced, and notably to VLDL-1 (32-fold elevation; P < 0.005), relative to control subjects [23].
• Furthermore, there was a positive correlation between changes in EGG-3 cpm amplitude and those in serum immunoreactive hPP levels during the postprandial periods (r = 0.55, p < 0.001) [24].
• Circulating levels of glucose, insulin, glucagon, glucose insulinotrophic peptide (GIP) and GLP-1 were measured over a 9-h postprandial period [25].
• It is concluded that in dumpers pancreatic glucagon is augmented in the early postprandial period, probably through stimulation by catecholamines [26].
• Our study demonstrates that, during the postprandial period, motilin antral receptors can be stimulated only with doses of motilin exceeding the physiological plasma concentrations, and that the motor effect obtained did not mimic the usual postprandial motility pattern [27].

Analytical, diagnostic and therapeutic context of Postprandial Period

• During the fasting and postprandial periods, serum insulin, glucose, triacylglycerol, and nonesterified fatty acid concentrations were measured, and rates of DNL were quantified via intravenous infusion of [1-(13)C] sodium acetate and mass isotopomer distribution analysis [28].
• The therapeutic effects of positioning and state of alertness were evaluated in 79 patients with gastroesophageal reflux (GER) and 49 nonreflux patients by extended esophageal pH monitoring during the two-hour postprandial period [29].
• The effect of local intra-arterial infusions of somatostatin on small bowel motility in the postprandial period and during an intravenous pentagastrin infusion was studied in five dogs [30].

References