Digestion of Starch by Salivary Amylase
The role of salivary amylase in the digestion of starches remains controversial. In the absence of pancreatic amylase, the key enzyme for starch digestion, salivary amylase may well represent a potential compensatory alternate pathway for the digestion of amylose, amylopectin, and glycogen.
Clinically significant depression of pancreatic amylase occurs in chronic pancreatitis, pancreatic resection, pancreatic neoplasm, cystic fibrosis, and other causes of pancreatic insufficiency. Quantitation of salivary amylase in these diseases has yet to be performed. It is also unclear whether the presence of starch in a meal protects salivary amylase from inactivation by the acidic gastric environment.
In the first six months of life, pancreatic amylase is very low or absent. Despite this physiologic pancreatic amylase deficiency, young infants seem to tolerate moderate amounts of starches in the diet
(1). Fi,rthermore, during acute diarrhea in infancy, soluble polymers of glucose derived from corn are well tolerated. The use of polymers of glucose have the advantage of providing the infant with potential mucosal injury with a carbohydrate source that can be readily absorbed and has a high caloric density with low osmolality (2). It seems, therefore, that salivary amylase and glucoamylase of the small intestinal brush border can compensate for physiologic amylase deficiency in infancy, even during diarrheal episodes.
In this issue of Digestive Diseases and Sciences,
Fried, Abramson, and Meyer (3) utilized a selective salivary isoamylase inhibitor (4, 5) to quantitate the amount of salivary amylase in postprandial jejunal fluid. This is a comparatively simple method using a wheat isolate that inhibits 88% of salivary amylase and 27% of pancreatic amylase. Standard curves of amylase inhibitor activity were constructed by mixing known concentrations of pure salivary and
Address for reprint requests: Dr. E. Lebenthal, Children's
Hospital.of
Clinically significant depression of pancreatic amylase occurs in chronic pancreatitis, pancreatic resection, pancreatic neoplasm, cystic fibrosis, and other causes of pancreatic insufficiency. Quantitation of salivary amylase in these diseases has yet to be performed. It is also unclear whether the presence of starch in a meal protects salivary amylase from inactivation by the acidic gastric environment.
In the first six months of life, pancreatic amylase is very low or absent. Despite this physiologic pancreatic amylase deficiency, young infants seem to tolerate moderate amounts of starches in the diet
(1). Fi,rthermore, during acute diarrhea in infancy, soluble polymers of glucose derived from corn are well tolerated. The use of polymers of glucose have the advantage of providing the infant with potential mucosal injury with a carbohydrate source that can be readily absorbed and has a high caloric density with low osmolality (2). It seems, therefore, that salivary amylase and glucoamylase of the small intestinal brush border can compensate for physiologic amylase deficiency in infancy, even during diarrheal episodes.
In this issue of Digestive Diseases and Sciences,
Fried, Abramson, and Meyer (3) utilized a selective salivary isoamylase inhibitor (4, 5) to quantitate the amount of salivary amylase in postprandial jejunal fluid. This is a comparatively simple method using a wheat isolate that inhibits 88% of salivary amylase and 27% of pancreatic amylase. Standard curves of amylase inhibitor activity were constructed by mixing known concentrations of pure salivary and
Address for reprint requests: Dr. E. Lebenthal, Children's
Hospital.of