Physiology

The physiology of the gastrointestinal absorption of (and the energy retrieved from) the glucose molecule along the length of the gastrointestinal tract in its various forms is discussed in the following sections, together with the influence of other dietary factors (Figure 2).

Absorption

In its simplest form, glucose ingested by mouth is rendered isotonic in the stomach by the gastric juices and expelled through the pylorus into the duodenum, where active transport takes place at the brush border by way of a sodium-linked glucose transporter. The absorbed glucose that is taken up by way of the portal vein suppresses hepatic glucose output but does not markedly alter the glucose balance across the liver. The major part of the absorbed glucose is taken up by muscle and also adipose tissue under the action of insulin. Similarly, sucrose, maltose, and lactose are both split and absorbed at the brush border by the brush border enzymes sucrase-isomaltase, maltase, and lactase. Although sucrose deficiency is exceedingly rare, hypolactasia is common in adult life in most of the world's populations, with the exception of those of northern European origin. Thus, unlike sucrose malabsorption, small-intestinal lactose malabsorption is common, with significant amounts of lactose entering

Glucose, maltose dextrins and amylopectin

High amylose starch (RS2) Retrograded starches (RS3)

'Entrapped starch' (RS1)

Intact granules (Soluble fiber, antinutrients, enzyme inhibitors)

Stomach

Stomach

Small intestine

Colon

High amylose starch (RS2) Retrograded starches (RS3)

'Entrapped starch' (RS1)

Intact granules (Soluble fiber, antinutrients, enzyme inhibitors)

Glucose

SCFA

Figure 2 Effect of different forms of glucose on glucose absorption and short-chain fatty acid (SCFA) production and uptake from the gut.

the colon, resulting in gas production, short-chain fatty acid (SCFA) synthesis, and, in some instances, diarrhea.

On the other hand, purified, fully hydrated, cooked amylopectin starch commences digestion in the mouth under the action of salivary amylase. Enzyme activity ceases under the acidic conditions of the stomach and resumes in the duodenum under the action of pancreatic amylase. Amylolytic digestion in both mouth and stomach results predominantly in the production of free glucose, maltose, maltotriose, and the a-limit dextrins of greater polymeric length. The free glucose is taken up by the brush border glucose transporter, and the uptake of maltose and maltotriose is effected by brush border enzymes, notably the sucrase-isomaltase complex.

In both situations, absorption in the small intestine is considered to be complete.

However, foods as eaten do not usually comprise pure glucose and pure amylopectin starch as their carbohydrate components. Many factors influence small-intestinal absorption in terms of both rate and amount (Table 2). Some of these factors were previously discussed in connection with amylose and resistant starch.

Food Components

Insoluble fiber may form a coat around starchy foods, limiting the penetration of enzymes and thus reducing the rate and amount digested. Viscous soluble fibers may also reduce the rate of

Table 2 Factors influencing glycemia and gastrointestinal events

Factors influencing the availability of carbohydrate

Physiological effect

Glycemia

Stomach, gastric emptying

Small intestine, absorption rate

Motility Colon

Baterial fermentation

Fecal bulk

Food components

Fiber

Soluble (viscous) -

Insoluble 0 ?

Macronutrients

Protein-starch interaction -

Fat-starch interaction -

Starches

Amylopectin +

Amylose -

Sugars and glucose polymers

Glucose ++

Maltose ++

Maltodextrins ++ Antinutrients

Phytates -

Tanins -

Saponins ?

Lectins -

Amylase inhibitors -

Alpha-glucosidase inhibitors -

Food processing

Cooking

Starch gelatinisation +

Starch regtrogradation -

Parboiling (e.g., rice) -Particle size Milling

Crushing +

Flaking +

Extruding +

+, increase, promote; -, inhibit, reduce; 0, no effect; ?, uncertain.

absorption through prolonging gastric emptying and by acting as a barrier to diffusion in the small intestine. Starch-protein interactions (as seen with gluten in wheat products) and starch-fat interactions have been shown to reduce the rate of digestion, and fat is known to slow gastric emptying. A number of the so-called 'antinutrients' present in foods, notably lectins, phytates, and tannins, have been shown to reduce the digestibility of foods. For example, it is considered that phytate, by binding calcium ions that catalyse starch digestion by amy-lase, reduces the rate of small-intestinal starch digestion.

Food processing may influence the rate of digestion by removing or reducing the level and activity of inhibitory food components. It may also modify the structure of the food or its components to make the food more available to digestive enzyme attack. Examples are cooking, resulting in starch gelatiniza-tion, and reducing the particle size (and hence increasing the surface area available to digestive enzymes) by milling, crushing, or flaking. On the other hand, processing may also reduce digestibility by parboiling, cooking with retrogradation of the starch, and extrusion, as in the production of pasta, producing a more compact physical structure.

Increasing the frequency of meals and reducing their size spreads the nutrient load over time and hence prolongs the time spent in the absorptive state. It is perhaps the 'clearest' model of slowing the rate of absorption and is referred to again to explain the metabolic consequences of reducing the absorption rate.

Finally, enzyme inhibitors of carbohydrate absorption have been developed for pharmacological use in the treatment of diabetes, and these work by reducing the rate of carbohydrate uptake from the small intestine. One example of this class of substances is acarbose, an a-glycoside hydrolase inhibitor that has antiamylase and anti-sucrase-isomaltase activity and thus inhibits both intralumi-nal and brush border carbohydrate digestion and absorption of starch, sucrose, and maltose.

Possible Effects of Prolonging Absorption Time of Carbohydrate

The question remains as to what physiological effects are produced when carbohydrate is absorbed more slowly (Table 3). Studies have demonstrated the effectiveness of carbohydrate-absorption enzyme inhibitors in treating diabetes but also in preventing the development of diabetes in high-risk subjects treated with acarbose over a 3-year period. A further way to reduce the rate of absorption of

Table 3 Possible effects of prolonging absorption time of carbohydrates

Flatter postprandial glucose profile Lower mean insulin levels postprandially and throughout the day

Reduced gastric inhibitory polypeptide response Reduced 24-h urinary C peptide output Prolonged suppression of plasma free fatty acids Reduced urinary catecholamine output Lower fasting and postprandial serum total and LDL

cholesterol levels Reduced hepatic cholesterol synthesis Lower serum apolipoprotein B levels Lower serum uric acid levels Increased urinary uric acid excretion carbohydrate without altering its composition is to change the rate of ingestion of carbohydrate substrates.

A number of effects appear to be beneficial when glucose is sipped slowly rather than drunk as a bolus or when starchy meals are eaten more frequently but in smaller amounts. Studies by Ellis in the 1930s first demonstrated a reduction in insulin requirements in patients with diabetes when glucose and insulin were administered in small, frequent doses. Since then, a range of metabolic benefits have been ascribed to increased meal frequency (the 'nibbling versus gorging' phenomenon). Early studies reported lower total cholesterol levels with increased meal frequency. Subsequent studies showed low-density lipoprotein (LDL) cholesterol reduction in subjects eating 3 meals a day compared to those eating from 6 to as many as 17 meals daily for periods of 2-8 weeks. An extreme model of slowing absorption, in which 17 meals daily were fed, demonstrated lower levels of apolipoprotein B in addition to total and LDL cholesterol. Population studies also indicated that total cholesterol levels were lower in those who ate more meals daily. Studies using stable isotopes showed that cholesterol synthesis was reduced at greater meal frequencies. Furthermore, mevalonic acid excretion (a water-soluble marker of cholesterol synthesis) suggested that the change in cholesterol levels was also related to the change in urinary mevalonic acid output. Since insulin is known to stimulate HMG-CoA reductase activity, a rate-limiting enzyme in cholesterol synthesis, the depressed cholesterol synthesis was attributed to the lower insulin levels observed. In addition, the reduction in serum cholesterol levels on 'nibbling' may have resulted from increased bile acid losses due to more frequent bile acid cycling through the gut following increased meal frequency.

Studies of non-insulin-dependent diabetes have shown depressed glucose and insulin levels during the day with increased meal frequency. In non-diabetic subjects, the major effect of reducing the absorption rate (by sipping glucose over 3h instead of taking the same amount of glucose as a bolus within 5 minutes) was to reduce insulin secretion. In addition, insulin suppression of free fatty acids and branched-chain amino acid levels was prolonged, and following glucose challenge no counter-regulatory response was observed.

Finally, serum uric acid, an independent risk factor for coronary heart disease, was reduced and increased urinary uric acid excretion was seen with increased food frequency. As with the reduction in serum cholesterol levels, the effects of lower insulin levels were used to explain these differences. It was suggested that insulin promoted renal reabsorption of uric acid, as demonstrated in the context of sodium reabsorption and hypertension in hyperinsu-linemic states.

Further effects of food frequency on diabetes have been assessed. It has been suggested that increased food frequency may limit obesity by reducing adipose tissue enzyme levels. Acute studies in humans failed to show an increased thermogenic response with increased meal frequency. Nevertheless, when satiety was assessed in acute studies, fluctuations in satiety were less over the whole day; long-term studies have yet to be undertaken. Concern still remains that 'snacking' may increase body weight in susceptible individuals. Despite these concerns, the demonstration that increased meal frequency can improve certain aspects of lipid and carbohydrate metabolism makes it a valuable model for other methods of 'spreading the nutrient load' (e.g., reducing the rate of glucose absorption).

Colonic Function

A portion of the starch, together with dietary fiber including cellulose and /3-glucan, enters the colon and is fermented by the colonic microflora with the growth of the fecal biomass and the production of SCFA, hydrogen, and methane. The extent to which this occurs varies from individual to individual and is based on the nature of the resistant starch and the source of the cellulose (e.g., vegetable cellulose is more readily fermented than cereal cellulose). Although some individuals may have starch in their feces, the majority of subjects show little or no fecal starch. Furthermore, all the /3-glucan is broken down by bacterial action in the colon. A large proportion of the cellulose escapes colonic bacterial fermentation and contributes directly to fecal bulk. Thus, a significant proportion of glucose molecules are not absorbed in the small intestine but enter the colon and are salvaged after conversion to SCFAs. The SCFAs are rapidly absorbed and contribute to the host's energy metabolism. They are usually produced in the ratio of 60% acetate, 20% propionate, and 20% butyrate, but the relative ratios of these three fatty acids vary depending on the substrate and the rate of fermentation. Of the three SCFAs, only acetate appears in the peripheral circulation to any significant extent. Propio-nate is of interest since it is gluconeogenic and has been suggested to inhibit hepatic cholesterol synthesis. It is largely extracted by the liver at first pass. Butyrate, on the other hand, is taken up and used by colonocytes. The slower the fermentation, the higher the butyrate levels. Starches have been claimed to increase colonic butyrate and in some instances propionate production, and butyrate is said to have antineoplastic properties.

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