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We investigated the effect of neutral lipids, polar lipids, and an emulsified formulation (EMF) on carotenoid bioaccessibility in an in vitro digestion assay of vegetables. These reagents enhanced carotenoid bioaccessibility. Contrary to our previous report, they also exhibited effects on lutein. Bile extracts/pancreatin concentrations also participated in the bioaccessibility. The EMF, which consisted of lower amounts of oil, had the same effect on lutein as rapeseed oil. These reagents also showed effects in the aging model, with more reduced bile extract/pancreatin concentrations, suggesting that lipids and EMF contributed to carotenoid bioaccessibility in bile/pancreatic juice secretions due to aging and disease.

Dietary retinyl esters are hydrolyzed in the intestine by the pancreatic enzyme, pancreatic triglyceride lipase (PTL), and intestinal brush border enzyme, phospholipase B. Recent work on the carboxylester lipase (CEL) knockout mouse suggests that CEL may not be involved in dietary retinyl ester digestion. The possible roles of the pancreatic lipase-related proteins (PLRP) 1 and 2 and other enzymes require further investigation. Unesterified retinol is taken up by the enterocytes, perhaps involving both diffusion and protein-mediated facilitated transport. Once in the cell, retinol is complexed with cellular retinol-binding protein type 2 (CRBP2) and the complex serves as a substrate for reesterification of the retinol by the enzyme lecithin:retinol acyltransferase (LRAT). Retinol not bound to CRBP2 is esterified by acyl-CoA acyltransferase (ARAT). The retinyl esters are incorporated into chylomicrons, intestinal lipoproteins that transport other dietary lipids such as triglycerides, phospholipids, and cholesterol. Chylomicrons containing newly absorbed retinyl esters are then secreted into the lymph.

Cholecystokinin (CCK), a peptide synthesized in the small bowel, is secreted into the blood stream after food intake. Its effects are primarily hormonal but of equal significance is that of a neurotransmitter. Its central role as a digestive peptide is illustrated by the following sequence: Mostly fat and protein of a consumed meal liberate CCK which triggers the contraction of the gallbladder and stimulates secretion of pancreatic enzymes. At the same time CCK slows down gastric emptying leading to an optimal ratio of foodstuff and digestive secreta. Via activation of afferent nerves CCK induces the sensation of saturation and thus limits food intake. Many questions remain open or undefined in this context but two conclusions may be drawn. 1. The significance of Pawlowian neural regulation of digestive functions is supported by new evidence, although hormones may support or modulate these functions. 2. It has become clear that a peptide may assume diverse regulatory functions be it as a hormone or as a neurotransmitter. Dear old concepts have therefore to be revised.

The role of endogenous cholecystokinin (CCK) in the regulation of pancreatic exocrine secretion during the interdigestive period was studied in conscious sheep. Intravenous infusion of proglumide (15, 30 and 60 mumol/kg/min) for 70 min significantly decreased flow rate, protein and amylase output in pancreatic juice by 80% at the maximum dose, as well as atropine (10 micrograms/kg/min), without a significant decrease in plasma concentration of immunoreactive CCK. Intravenous injection of CCK (114 pmol/kg) increased the pancreatic secretion during atropine infusion, but not during proglumide infusion. These results suggest that the regulation of interdigestive pancreatic exocrine secretion in sheep depends greatly on endogenous CCK as well as on the cholinergic mechanism.

We have investigated the role of intestinal fat digestion in fat-induced suppression of gastric acid secretion and gastrin release in the rat. Intraduodenal administration of oleic acid (10%, pH 6.5) and triglyceride (10%, pH 6.5) at a rate of 2 ml/hr resulted in significant suppression of gastric acid secretion and gastrin release stimulated by intragastric perfusion of peptone (0.5%). Diversion of pancreatic juice from the duodenum completely abolished triglyceride-induced inhibition of peptone-stimulated gastric acid secretion and plasma gastrin release, but oleic acid-suppressed gastric acid secretion and gastrin release were unaffected by pancreatic juice diversion. Intraduodenal administration of digested triglyceride, prepared by preincubation with lipase, caused significant suppression of the peptone-induced gastric acid secretion and rise in plasma gastrin levels, even though pancreatic juice was excluded. The results of this study indicate that digestive products of triglyceride by pancreatic juice, especially by lipase, are responsible for the intestinal fat-induced inhibition of gastric acid secretion and gastrin release and that intestinal fat digestion plays a significant role in the mechanism.

Absorption of a slowly digestible peptide, oligo-L-methionine (OM), added to a low casein diet was faster than absorption of OM added to a low soybean protein isolate diet in early stages of feeding in chronic portal-cannulated rats. In the present study, the gastric digestion of 14C-labeled OM in rats fed a casein-based diet was higher than that in rats fed an soybean protein isolate-based diet 30 min and 3 hr after feeding. In rats with chronic bile-pancreatic juice diversion from the proximal small intestine, the higher gastric solubilization of OM in the stomach of the casein group was also observed, but the contents of soluble digest of OM in the stomach were lower than those in the normal rats. The portal absorption of OM in the casein group was higher than in the soybean protein isolate group both 30 min and 4 hr after feeding in the bile-pancreatic juice-diverted rats, and the difference of the portal absorption between the diet groups corresponded to the difference of the amount of solubilized OM in the upper small intestine; this, in turn, depends on pepsin digestion in the stomach. These findings suggest that the difference between the two diet groups in the ability to digest OM in the stomach can at least partly explain the higher portal absorption of OM in the casein group in the early stages of feeding.

Studies in the taste system of mammals indicate that monosodium glutamate (MSG) produces a unique taste sensation termed umami. As a derivative of glutamic acid, MSG is a naturally occurring nutrient in many foods; its commercial use to improve food palatability for humans is well documented. Behavioral studies with experimental animals have revealed that preference for MSG in solutions and selection of MSG-flavored diets can be explained by sensory means with no appreciable effects on preference by postingestive consequences. However, preference for umami-flavored fluids is reduced by feeding rats low-protein diets or low quality protein. MSG-flavored diets, initially unpreferred, were subsequently highly selected. However, the adulteration of diets by MSG either did not or only slightly increased food intake. In light of the significant contribution of MSG to diet taste, apparently as a signal coupled to dietary proteins, physiological studies have been initiated to reveal its role as a stimulator of the cephalic phase of pancreatic exocrine secretion. Modified sham-feeding experiments with dogs have shown that oral stimulation by MSG produced significant stimulation of both pancreatic flow and protein output in conscious dogs.

The apparent digestibility of a diet was studied over a period of 87 days after ligature of the pancreatic duct, in the growing pig. Sham operated pigs were used as controls. Feces and urine collections were made during three periods of 10 days each. Mean daily gain of sham operated pigs was higher (560 g/day) than that of pancreatic duct ligated pigs (421 g/day), throughout the experiment. Within the first period (15-24 days after ligature), the apparent digestibility of nitrogen was most affected (-35.6%) while that of energy decreased by 12.1% as compared to values obtained in sham operated pigs. Nitrogen retention was similar in all pigs. Between the 1st (15-25 days) and the 3rd period (78-87 days) after exclusion of the pancreatic secretion from intestine, the apparent digestibility of nitrogen increased by 20% and that of energy by 6%, which might suggest digestive compensation. At the end of the experiment, weights of empty small intestine and liver were significantly higher in the pancreatic duct ligated pigs. The origin of the digestive compensation is discussed.