Postprandial state

In contrast to previous in vivo models, this in vitro model provides the possibility of dissociating experimentally two important processes of intestinal absorption cellular uptake and secretion. Under conditions mimicking the postprandial state (taurocholate/oleic acid supplementation), differentiated Caco-2 cells were able to (1) take up carotenoids at the apical sides and incorporate them into CMs and (2) secrete them at the basolateral sides associated with CM fractions. Using this approach, the extent of absorption of P-carotene through Caco-2 cell monolayers after 16 hr of incubation was 11.2%, a value falling within the in vivo range (9 to 22%). ° - Of the total amount of P-carotene secreted, 78% was associated with the two CM fractions and 10% with the VLDL fraction. ... 

Under linear concentration conditions (for a P-C concentration range of 0.12-6pM) at 16h incubation and under cell culture conditions mimicking the in vivo postprandial state, the extent of absorption of all-trans P-C through Caco-2 cell monolayers was 11% a value similar to that reported from different human studies. In humans, the bioavailability of a single dose of P-C... 

Glycogen synthase kinase-3 is itself subject to control by reversible phosphorylation. Stimulation of the liver cell by insulin, the key hormone of the postprandial state,... 

The liver not only extracts glucose from the blood in the postprandial state and stores it as glycogen, but is also able to synthesize glucose from non-carbohydrate sources via gluconeogenesis, therefore the liver is crucial in regulating glucose homeostasis. 

The pharmacokinetic properties of the microemulsion were compared with those of the standard formulation in 39 liver-transplanted patients. AUC and Cmax values were significantly increased, and tmax was decreased following the microemulsion formulation, in both fasted and postprandial state. Differences between the microemulsion and the regular formulation in the fasting state and after high-fat meal, respectively, were +64% and +38% for AUC, +119% and +53% for Cmax, and -21% and —59% for tmax [43]. 

In both species, the postprandial state induced significant changes in the distribution of Hf between LP fractions, with increased proportions of Hf in the TRL fractions in both human and beagle plasma at the expense of a decrease in the proportion of Hf in LDL and HDL fractions. 

In the fed postprandial state, glucose and fructose are removed from the portal venous blood by the hepatocytes. This allows glucose stores to be formed in the liver as an energy reserve, and also prevents any wide fluctuations in plasma osmolality as a result of a hyperglycaemic state. Within the hepatocyte, glucose is converted... 

Chan JW et al (2005) Raman spectroscopic analysis of biochemical changes in individual triglyceride-rich lipoproteins in the pre- and postprandial state. Anal Chem 77(18) 5870-5876... 

Lindenbaum, J. Greater bioavailability of digoxin solution in capsules studies in the postprandial state. Clin. Pharmacol. Ther. 1977, 21, 278-282. 

Kinetics of Bile Acid Metabolism. Using an isotope dilution technique, the bile acid pool in normal adults has been found to average from 2 to 4g. Steady state is reached when hepatic synthesis and fecal loss are in balance. In health, the magnitude of each process is 0.3 to 0.8g/day. There are usually 4 to 10 enterohepatic cycles per day. Because of this recycling mechanism, the jejunal concentration of bile acids is maintained at -5 to lOmmol/L during the postprandial state, much higher than the critical micellar concentration of 2mmol/L. Between meals, with decreased entry of bile acids into the intestine, the intraluminal concentration... 

The early postprandial state is illustrated in Figure 16.4. As described, sugars and amino acids are absorbed and transported by the portal blood to the liver. The portal blood also contains a high level of lactate that is a product of enterocyte metabolism. Most lipid molecules are transported from the small intestine in lymph as... 

Fig. 42.13. Amino acid metabolism in the gut. The pathways of glutamine metabolism in the gut are the same whether it is supplied by the diet (postprandial state) or from the blood (postabsorptive state). Cells of the gut also metabolize aspartate, glutamate, and BCAA. Glucose is converted principally to the carbon skeleton of alanine. a-KG = a-ketoglutarate GDH = glutamate dehydrogenase TA = transaminase.

Glutamine utilization by the gut is diminished by a metabolic acidosis compared with the postabsorptive or postprandial states. During metabolic acidosis, the uptake of glutamine by the kidney is increased, and blood glutamine levels decrease. As a consequence, the gut takes up less glutamine. 

---