BIOCHEMISTRY: A TEXTBOOK FOR MEDICAL UNIVERSITIES - E. S. Severin - 2004

CHAPTER 7. CARBOHYDRATE METABOLISM

IV. Disorders of Carbohydrate Digestion and Absorption

The Pathogenesis of Carbohydrate Digestion and absorption disorders generally stems from two primary causes:

✵ defects in Enzymes involved in the intestinal Hydrolysis of CARBOHYDRATES;

✵ impaired absorption of carbohydrate digestion products into the Cells of the intestinal mucosa.

In both cases, osmotic diarrhea occurs, triggered by unhydrolyzed Disaccharides or unabsorbed Monosaccharides. These unutilized carbohydrates reach the distal PARTS OF THE intestine, altering the Osmotic Pressure of the intestinal contents. Furthermore, the carbohydrates remaining in the intestinal lumen are partially broken down by microorganisms, producing organic acids and gases. Together, these factors lead to an influx of Water into the intestine, an increase in the volume of intestinal contents, enhanced peristalsis, cramps, pain, and flatulence.

The term "malabsorption" refers specifically to the inadequate absorption of digested carbohydrate products. However, because the clinical manifestations of impaired digestion and impaired absorption are similar, the term "malabsorption" is commonly used to describe both types of disorders.

A. Impairment of carbohydrate DIGESTION IN THE intestine

Digestive disorders can be associated either with insufficient activity of specific disaccharidases or with a deficiency of an entire enzymatic complex, such as the sucrase-isomaltase complex.

Both hereditary and acquired forms of enzyme deficiency are known. Symptoms of congenital forms manifest quite early—for instance, after the first feedings of breast milk (in lactase deficiency), or following the transition to formula feeding or the Introduction of sugar and starch into the diet (in deficiency of α-amylase or specific disaccharidases). If inadequately treated, congenital forms of the pathology are accompanied by chronic dysbio-

sis and delayed physical development in the child.

Acquired forms of the pathology can occur in association with intestinal diseases such as gastritis, colitis, and enteritis. Notably, a decrease in lactase activity is particularly pronounced in these cases. As previously mentioned, intestinal lactase activity is normally lower than that of other disaccharidases, meaning that any reduction in its activity becomes clinically apparent to the body first.

Lactase deficiency in adults can also have another cause: an age-related decline in the expression of the lactase Gene. It has already been noted that lactase activity in healthy adults is significantly lower than in infants. Therefore, a further reduction in lactase activity from an already low baseline level can manifest in some individuals as milk intolerance. Individuals of African and Asian descent are most frequently carriers of lactase deficiency. The average prevalence of this condition ranges from 7 to 12% in European countries, reaches 80% in China, and is as high as 97% in certain regions of Africa. Such patterns in the distribution of lactase deficiency are attributed to historical dietary traditions and the absence of dairy farming in these respective regions. Examples and causes of disaccharide digestion disorders are summarized in Table 7-2.

Class="center">Table 7-2. Disorders of disaccharide digestion

Rare forms of carbohydrate digestion disorders also exist. For instance, hereditary trehalase deficiency is known, which manifests as dyspepsia following the consumption of mushrooms containing trehalose.

In certain cases, malabsorption may be caused by multiple factors. For example, following gastric surgery, possible complications include impaired mixing of food with digestive juices, reduced secretion of these juices, accelerated transit of food through the intestine, and bacterial colonization of the cecum and blind loop.

B. Impairments of monosaccharide absorption

Absorption disorders may result from a defect in any component (protein or enzyme) involved in the transport system of monosaccharides across the membrane. Pathologies associated with a defect in the sodium-dependent glucose cotransporter protein have been described.

Carbohydrate tolerance tests are used to diagnose various digestive disorders. Intestinal disaccharidase deficiency can be diagnosed by administering a specific disaccharide followed by the measurement of Blood glucose concentrations. To increase sensitivity, this test is performed by first administering the disaccharide (50 g) and subsequently an equivalent amount of its constituent monosaccharides (25 g of each). Following the load, blood glucose concentration normally increases by approximately 50% relative to baseline. In pathological states, only minimal hyperglycemia is observed.

If the monosaccharide tolerance test is accompanied by an adequate increase in its blood concentration, whereas the disaccharide tolerance test fails to elicit a normal response, this strongly points to a defect in intestinal disaccharidase rather than in the transport system.

Lactase deficiency can be assessed by measuring breath hydrogen levels (the hydrogen breath test). Hydrogen is produced As a result of the action of bacterial enzymes on lactose.