Nutrition and gastrointestinal function

Barbara Schneeman

In healthy individuals, the nutrients available from foods that the body needs for metabolism are provided by the process of digestion and absorption in the gastrointestinal tract. Consequently, the gastrointestinal tract is important both in terms of maintaining the nutritional status of the gut as well as providing nutrients to maintain nutritional status and homeostasis of the whole organism. Because the gastrointestinal tract is the first organ system to respond to the composition of the diet and thus mediates variations in dietary composition, an understanding of gastrointestinal response may provide some insight about the impact of diet composition on overall metabolic response by the whole organism.

Figure 1 illustrates some of the important interactions within the gut that demonstrate its critical role in nutrition and health of the total organism. The gastrointestinal (GI) tract itself has a very high nutrient need based on the high turnover of epithelial cells along the villi and the daily synthesis and secretion of protein for digestive enzymes. Protein turnover in the GI tract is estimated to account for about 20% of total body protein turnover, although the GI tract is typically less than 5 % of total tissue mass in the body. The intestinal organs are able to derive part of their nutrient needs from the nutrients present in the lumen during digestion. In fact the hormones released during the gastric and intestinal phases of digestion to stimulate secretion and motility also have trophic effects which ensure cell and enzyme renewal during the postprandial phase (Johnson, 1988).

The importance of the luminal presence of nutrients to maintain the gastrointestinal tract can be clearly demonstrated by comparing enteral and parenteral feeding. Atrophy of intestinal tissue occurs when luminal nutrients are not present to support growth (Lo and Walker, 1989; Weser, 1989). In rats fed intravenously the weight of intestinal mucosa is about two-thirds of the weight of those fed intragastrically (Ney et al., 1986). Because of its high nutrient needs, GI function can be severely compromised during malnutrition. The potential consequences of malnutrition on GI function include

* Atrophy of the mucosal surfaces

* Decreased pancreatic digestive enzyme function

* Increased microbial action in the colon due to the greater presence of undigested substrates

* Impairment of the immune functions of the GI tract.

With the loss of digestive and absorptive capacity in the malnourished state, it is difficult for the GI tract to function effectively to provide nutrients to other tissues, and it is critical that the gut’s capacity be restored during renourishment (U.S. DHHS, 1988).


The gastrointestinal response to diet is mediated by neural and hormonal stimuli (Fig. 2). An important part of the neural stimulation of GI function occurs during the cephalic phase of digestion, when food is seen and smelled. This response essentially prepares the GI tract for the presence of food. Neural stimulation, primarily mediated by the vagus nerve, elicits acid and pepsin secretion in the stomach, gallbladder contraction and secretion of enzyme-rich fluid from the pancreas. Neural reflexes are also involved in mediating motility of both the small and large intestines.

In addition to the innervation of the gut, the GI tract contains various hormones and regulatory peptides that can be released by the presence of food and elicit responses from organs in the gut. The gut is one of the richest endocrine organs in the body. Insulin and glucagon are examples of hormones that are released from the gastrointestinal tract whose peripheral effects on organs other than those of the GI tract have been well studied. The potential effects of other gut hormones on nongastrointestinal tissues has not been well-characterized. The distribution of hormones and regulatory peptides along the gut is regional (Table 1).

The release of these hormones is mediated by protein or amino acids, fat and carbohydrate. For example, protein is a potent stimulant of gastrin, cholecystokinin (CCK), and gastric inhibitory peptide (GIP) release; fat is a stimulant of CCK, secretin and GIP release as well as enteroglucagon, neurotensin, and peptide YY release; and carbohydrate is known to regulate release of GIP as well as the endocrine hormones, insulin and glucagon. The functions of these gut hormones and dietary stimulants of their release have recently been reviewed (Go, 1989). In terms of evoking the hormonal and neural mechanisms in the gut to ensure secretion of digestive juices in response to consumption of food, it is clear that dietary protein, fat, and to a lesser extent carbohydrates are mediators of gastrointestinal response Fig. 3). This immediate, acute response is essential to facilitate the digestive and absorptive process; however, these mechanisms also play a role in the longer term adaptive response in the composition of digestive secretions in response to chronic exposure to dietary components. In reviewing this area three important themes, which will be illustrated further, are evident: 1) the importance of certain dietary components in stimulating the gastrointestinal response to food; 2) the adaptive response of the gastrointestinal tract to dietary factors; and 3) the physiology of the gastrointestinal tract has important consequences for the metabolism of nutrients.

The pancreas contains a range of hydrolytic enzymes that digest the macromolecules which are ingested in the diet. These enzymes include proteases (e.g., trypsinogen, chymotrypsinogen, proelastase, procarboxypeptidases), [alpha]-amylase, lipase, colipase, phospholipase and cholesterol esterase. The proteases, and possibly the lipid digestive enzymes, are secreted from the pancreas in an inactive form and are activated in the small intestine by the action of enterokinase or trypsin. The secretion of an enzymerich fluid from the pancreas can be stimulated by the hormones gastrin, released from the stomach, and CCK, which is released from the duodenum. Thus during the cephalic and gastric phases of digestion pancreatic secretion is initiated, and while nutrients are in the small intestine, CCK has an important role in sustaining sufficient enzyme secretion for digestion to occur.

Earlier work demonstrated in a rat model that pancreatic enzyme secretion is regulated by negative feedback from the level of active pancreatic protease present in the duodenum. Dietary constituents stimulate enzyme secretion from the pancreas by interruption of this feedback. Consequently the trypsin inhibitors in soybeans as well as dietary proteins are potent stimulants of pancreatic enzyme secretion because of their interaction with the pancreatic proteases. The ability of dietary protein to stimulate pancreatic protein secretion can be significantly enhanced by low levels of residual trypsin inhibitor activity (Berger and Schneeman, 1986). For example, soy protein isolate and egg albumen are more potent stimulants of enzyme secretion than casein due to their higher content of trypsin inhibitor. This difference in pancreatic response to dietary proteins is mediated by differences in the release of GI hormones (Liddle et al., 1984). Likewise the secretion of digestive enzymes other than the proteases differs, potentially affecting carbohydrate and lipid digestion and absorption, and these dietary proteins stimulate changes in the composition of enzymes within the pancreatic tissue (Richter and Schneeman, 1987). Experimental evidence indicates that the pattern of enzyme activity in the pancreatic tissue adapts to chronic consumption of dietary proteins and enzyme inhibitors in a manner that is reflective of the acute stimulatory ability of these dietary components. Hence, chronic consumption of a diet containing trypsin inhibitor or that is high in protein leads to increased pancreatic protease activity. This adaptation is mediated through CCK which promotes enzyme synthesis and pancreatic growth as well as secretion. Besides adapting to the protein and trypsin inhibitor content of the diet, the pancreas has been shown to adapt to a high fat, low carbohydrate diet by increasing the activity of lipase and decreasing the activity of amylase (Sabb et al., 1986). The exact mechanism for this adaptation is not known but may be mediated by the absorption of lipid and carbohydrate digestion products rather than release of a specific hormone. The loss of enzyme capacity and ability to adapt pancreatic enzyme activity to dietary composition may contribute to age-related changes in energy utilization (Bartos and Groh, 1969; Greenberg and Holt, 1986; unpublished observations).

Studies in humans have indicated that digests of proteins and fatty acids are stimulants of pancreatic enzyme secretion. Trypsin inhibitors have been shown to be potent stimulants of enzyme secretion, additionally, pancreatic enzyme secretion in humans is regulated by a feedback mechanism analogous to that which occurs in the rat (Toskes, 1986). Two consequences of understanding that regulation of secretion and potential enlargement of the pancreas may occur through similar mechanisms in the rat and the human have been 1) the use a pancreatic enzyme supplements in the treatment of pain associated with severe pancreatitis (Toskes, 1986), and 2) concern about the implications of studies in rats which have indicated that certain soy preparations that contain trypsin inhibitor promote formation of nodules in pancreatic tissue and the formation of tumors when an initiator is present (Gumbmann et al., 1986). When the protein content of the diet is adequate, rats are less likely to develop nodules spontaneously when fed soy protein isolate (Richter and Schneeman, 1987). Green et al. (1986) have proposed that when dietary protein intake is high, enzyme synthesis in pancreatic tissue can increase to compensate for the increased secretion of enzymes, whereas if protein intake is low, enzyme synthesis may be inadequate and thus CCK release remains high, eventually leading to hyperplastic regions in the pancreas.

It has long been known that dietary proteins and fats are potent stimulants of gastrointestinal function, but until recently the carbohydrate portion of the diet, whether the digestible carbohydrates (starch and sugars) or the nondigestible polysaccharides associated with dietary fiber, have been viewed as somewhat neutral. However, it is now known that glucose is a potent releaser of GIP, which augments insulin release. We are only beginning to understand the important role that nondigestible carbohydrates can have on the functions of the GI tract. Certain sources of dietary fiber, such as pectins and gums, have been associated with slower digestion and absorption of carbohydrates and fats due to their ability to interfere with digestive enzyme activity, to increase the viscosity and volume of the intestinal contents, and by binding micellar components (Schneeman, 1990). Studies to examine the effect of dietary fiber on the morphology and structure of the intestines have demonstrated that the presence of fiber leads to adaptive changes in the gut (Cassidy et al., 1981). In a long-term feeding study, we have observed that the weight and length of the small intestine is greater in rats fed psyllium husk than in those fed a low fiber diet, and that supplementing the diet with wheat bran appears to protect small intestinal villi from damage. Dietary fiber and undegraded starch are the primary sources of fermentable substrate for the microflora in the large intestine (Cummings, 1986). The activity of this microflora is clearly important for maintaining the health of the large intestine, but, in addition, the products of fermentation, such as the short chain fatty acids can be absorbed and potentially affect hepatic or peripheral metabolism of lipids and carbo-hydrates. The research currently under way on dietary fiber is of particular importance for understanding the role of the gastrointestinal tract in determining metabolic responses to dietary composition because the fiber must mediate its effects on lipid or carbohydrate metabolism via its effects on gastrointestinal function.


A relatively new area of interest with respect to the potential importance of the gastrointestinal tract in mediating metabolic response to dietary composition concerns the alimentary lipemic response to consumption of a meal. Most individuals spend 12 hours or more in an alimentary or postprandial state and, during this time, dynamic remodeling of lipoprotein particles occurs. After the first meal of the day, the typical pattern of meal eating is likely to sustain a lipemic state throughout the day since the peak in triglyceride response is typically at 3 to 4 hours after the meal (Redard et al., 1990). The increase in plasma triglycerides after a meal is derived from both intestinal and hepatic sources as indicated by increase in the concentration of apolipoprotein (apo) B100 and B48 in triglyceride-rich lipoproteins (TRL) (Cohn et al., 1989; 1991). Apo B48 is derived from secretion of chylomicrons from the small intestine, whereas apo B100 is predominately associated with TRL made in the liver. Although plasma cholesterol concentrations do not change significantly during the alimentary period (Cohn et al., 1988; 1989; 1991), the movement of cholesterol among lipoprotein particles is stimulated. When conditions favor the movement of cholesterol to chylomicrons or B48-containing TRL during alimentary lipemia, this metabolic state may provide an opportunity to remove cholesterol from peripheral tissues (Castro and Fielding, 1985; Fielding et al., 1989). Thus, an exciting new area of investigation concerns the potential effect of dietary components such as fiber, fatty acid composition and total dietary fat content on the generation and clearance of TRL after a meal.

In conclusion, the diet of healthy individuals is typically varied and complex. The gastrointestinal tract is capable of responding and adapting to variations in diet composition. The pattern of nutrient appearance in the blood as well as the chemical and neural signals released by the gut during the alimentary period are likely to be important in regulating the metabolism of nutrients from the diet. Further work is needed to understand this relationship and its importance for understanding the effect of diet composition on health.


Bartos V, Groh J. The effect of repeated stimulation of the pancreas on the pancreatic secretion in young and aged men. Gerontol Clin 1969;11: 56-62.

Berger J, Schneeman BO. Stimulation of bile-pancreatic zinc, protein and carboxypeptidase secretion in response to various proteins in the rat. J Nutr 1986;116:265-72.

Cassidy MM, Lightfoot FG, Grau LE, Story JA, Kritchevsky D, Vahouny GV. Effect of chronic intake of dietary fibers on the ultrastructural topography of rat jejunum and colon: a scanning electron microscopy study. Am J Clin Nutr 1981; 34:218-28.

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Cohn JS, McNamara JR, Cohn SD, Ordovas JM, Schaefer EJ. Plasma apolipoprotein changes in the triglyceride-rich lipoprotein fraction of human subjects fed a fat-rich meal. J Lipid Res 1988; 29:925-36.

Cohn JS, McNamara JR, Krasinski SD, Russell RM, Schaefer EJ. Role of triglyceride-rich lipoproteins from the liver and intestine in the etiology of postprandial peaks in plasma triglyceride concentration. Metabolism 1989;38:484-90.

Cummings JH. The effect of dietary fiber on fecal weight and composition. In: Spiller GA, ed. Handbook of dietary fiber in human nutrition. Boca Raton, FL: CRC Press, 1986:211-80.

Fielding PE, Jackson EM, Fielding CJ. Chronic dietary fat and cholesterol inhibit the normal postprandial stimulation of plasma cholesterol metabolism. J Lipid Res 1989;30:1211-7.

Go VLW. Role of gastrointestinal hormones in adaptation. In: Halsted CH, Rucker RB, eds. Nutrition and origins of disease. Bristol-Myers Nutrition Symposia. New York: Academic Press, 1989;7: 321-331.

Green GM, Levan VH, Liddle RA. Interaction of dietary protein and trypsin inhibitor on plasma cholecystokinin and pancreatic growth in rats. Adv Exp Biol Med 1986;199:123-32.

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Gumbmann MR, Spangler WL, Dugan GM, Rackis JJ. Safety of trypsin inhibitors in the diet: Effects on the rat pancreas of long-term feeding of soy flour and soy protein isolate. Adv Exp Biol Med 1986;199:33-79.

Johnson LR. Regulation of gastrointestinal mucosal growth. Physiol Rev 1988;68:456-502.

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Lo CW, Walker WA. Changes in the gastrointestinal tract during enteral and parenteral feeding. Nutr Rev 1989;47:193-8.

Ney DM, Lefevre M, Schneeman BO. Alteration in lipoprotein composition with intravenous compared to intragastric fat-free feeding in the rat. J Nutr 1986;116:2106-20.

Redard CL, Davis PA, Schneeman BO. Dietary fiber and gender: effect on postprandial lipemia. Am J Clin Nutr 1990;52:837-45.

Richter BD, Schneeman BO. Pancreatic response to long-term feeding of soy protein isolate, casein, or egg-white in rats. J Nutr 1987;117:247-52.

Sabb JE, Godfrey PM, Brannon PM Adaptive response of rat pancreatic lipase to dietary fat: Effects of amount and type of fat. J Nutr 1986; 116:892-9.

Schneeman BO. Macronutrient absorption. In: Kritchevsky D, Bonfield C, Anderson JW, eds. Dietary Fiber. New York, Plenum Press, 1990: 157-166.

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Weser E. Intestinal adaptation to parenteral nutrition. In: Halsted Ch, Rucker RB. Nutrition and origins of disease Bristol-Myers Nutrition Symposia. New York: Academic Press, 1989;7: 343-56.

Dr. Schneeman is currently Professor, Departments of Nutrition, Food Science and Technology and Internal Medicine, University of California, Davis. Her research has focused on the influence of dietary factors on the rate and site of nutrient absorption and the adaptation of the gastrointestinal tract to dietary factors. She is Associate Editor of the Journal of Nutrition. She is a member of the American Institute of Nutrition, the Institute of Food Technology, the Society for Experimental Biology and Medicine and many advisory committees, and has published extensively in professional journals.

Table 1

Regional Distribution of

Gastrointestinal Hormones

Stomach Gastrin

Duodenum (upper Cholecystokinin

small intestine) (CCK)


Gastric inhibitory

pepti de (GIP)


Distal intestine Neurotensin


Peptide YY

Pancreas Insulin


Pancreatic polypeptide


Peptide G

COPYRIGHT 1993 Lippincott/Williams & Wilkins

COPYRIGHT 2004 Gale Group

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