Glucose and the two lesser dietary monosaccharides, fructose and galactose, enter the circulation through the intestinal mucosa. The speed with which glucose can be absorbed is limited by the rate of transfer from the intestine but rarely exceeds 50 g (0.28 mol) per hour. This comparatively massive influx of glucose into a pool of less than 20 g ordinarily produces a remarkably small perturbation in blood glucose because the rate of removal from the glucose pool increases to match glucose input.
In healthy people, arterial blood glucose concentrations generally return to fasting levels within 2 h of eating a carbohydrate-rich meal and before all of it has been absorbed. This remarkable feat of homeo-stasis is achieved through the prompt and appropriate release of insulin into the circulation. This is a consequence of stimulation of pancreatic B cells (the source of insulin) by a rising arterial blood glucose concentration augmented by the insulinotropic hormones, GIP and GLP-1, released by endocrine cells in the intestinal mucosa. Nervous impulses originating in the brain in response to anticipation of eating (the cephalic phase) and from the mouth, gut wall, and portal vein may also play a role.
Under the influence of the rise in plasma insulin so produced and a simultaneous reduction in glucagon secretion, the liver reduces its rate of glucose input into the pool and increases its rate of extraction. Peripheral insulin-sensitive tissues, such as connective tissue, skin, fat, and especially striatal muscle, also start removing glucose. As a result of these duel actions, arterial blood glucose concentration decreases and the stimulus to insulin secretion declines until all of the food has been absorbed.
Ordinarily, the rates of change of glucose inflow from the gut into the glucose pool and the outflow of glucose into the tissues are so well aligned that arterial blood glucose levels rarely fall below fasting levels after a meal, and then only temporarily. Venous blood glucose levels do so more often. The somewhat unnatural conditions resulting from ingestion of large amounts of a glucose solution on an empty stomach may produce a 'reactive hypogly-cemia' due to persistence of insulin action after plasma insulin has fallen to basal levels and all of the glucose has been absorbed from the gut. Such a reactive hypoglycemia may be, but rarely is, sufficiently severe to produce (neuroglycopenic) symptoms even in perfectly healthy individuals.
The exact disposition of glucose absorbed from the gut after a carbohydrate-rich meal by healthy subjects varies widely from individual to individual, and it depends on the size, composition, and physical nature of the meal. Within 4 h of ingestion, approximately 70% of a 70-g oral glucose load given in solution is removed by peripheral tissues, where most of it is used to generate energy by oxidation to carbon dioxide and water or turned into metabolites. The remaining 30% is removed by the liver during its passage from the gut to the periphery and converted into glycogen, triglycerides, and other metabolites.
Volunteers given a meal consisting of glucose (1 g per kilogram bodyweight) as a 45% solution on an empty stomach reduced their normal basal release of glucose from preformed glycogen in the liver from 9gh-1 to approximately 2.2 gh-1 (i.e., approximately 75%). This persists for the period (3 or 4h) during which glucose is absorbed from the gut. In other words, although there is a small net uptake of glucose by the liver following a carbohydrate-rich meal, the liberation of glucose from preformed glycogen does not cease completely. Glycogenolysis and gluconeogenesis take place simultaneously but at different rates, depending on whether glucose is being absorbed as well as on the amount and nature of the hormones released by the pancreas and intestine in response to the presence of food.
Before being absorbed, sucrose is cleaved into glucose and fructose, and lactose is cleaved into glucose and galactose. Galactose shares a transporter mechanism with glucose, whereas fructose uses a less efficient one of its own. Fructose and galactose, and a percentage of absorbed glucose, are removed on their first pass through the liver and converted into glycogen. This provides a store of carbohydrate that is released as glucose into the body pool when absorption from the gut is no longer occurring and gluconeogenesis has not yet become fully reestablished.
Starches and their partial hydrolytic products are converted enzymatically into glucose in the gut lumen and mucosal brush border at a rate that depends on their composition and physical form. Some starches are absorbed as rapidly as preformed glucose, whereas others are absorbed much more slowly. This is reflected in the rate and magnitude of the increase in blood glucose concentration that follows their ingestion and is referred to as the glycemic index.
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