Effects of hypoxia on the development of intestinal enzymes in neonatal and juvenile rats.

Hypoxia in the neonate is known to alter the activity of hepatic and pancreatic enzymes involved in lipid and carbohydrate metabolism. The purpose of this study was to evaluate the effect of neonatal hypoxia on the activity of intestinal enzymes, and to determine whether the administration of glucocorticoids to neonates can mimic the effects of hypoxia. Hypoxia in neonatal rats (0-7 days) increased protein content, and lactase and maltase activity in the duodenal and the jejunal segments of the small intestine compared with normoxic controls. Hypoxia in juvenile rats (28-35 days) did not change these enzymes. Two weeks after returning hypoxic (0-7 days) pups to normoxia, their body weight remained lower than the age-matched controls. In the group recovering from hypoxia, sucrase, maltase, and leucine aminopeptidase activities were lower in the duodenal and the jejunal segment. Compared with controls, LDH activity was lower only in the jejunal intestine in the group recovering from hypoxia. All enzyme activities returned to control levels 3 weeks after recovery. Neonatal rats treated with dexamethasone had a decrease in body weight, but increases in sucrase and maltase activity in both the duodenal and the jejunal segment. Hypoxia in newborn rats caused a delayed maturation of small intestinal enzymes. Increases in serum glucocorticoids after hypoxic exposure probably do not play a major role in the delayed maturation of the disaccharidase activity in the small intestine.

Glucoamylase activity in infants and children: normal values and relationship to symptoms and histological findings.

BACKGROUND: Starch digestion is dependent on a combination of pancreatic and salivary amylase and the intestinal brush border enzymes glucoamylase and sucrase-isomaltase. Glucoamylase splits successive glucose molecules from the nonreducing end of starch molecules and is particularly important in infants who are relatively deficient in pancreatic amylase. METHODS: The authors measured glucoamylase activity in endoscopic mucosal biopsies submitted for measurement of disaccharidase activity from 214 patients aged 1 month to 20 years. Glucoamylase activity was measured using glucose polymers (polycose) as the substrate. The authors also related enzyme activity to histologic appearance and clinical indication for endoscopy. RESULTS: The most common reasons for biopsy were abdominal pain, gastroesophageal reflux, and vomiting. Disaccharidase activity by age was similar to previous reports. Glucoamylase activity did not differ with age, but was 2 to 3 times the activity reported previously. Glucoamylase activity was significantly depressed in children with the most severe histologic abnormalities. Normal glucoamylase activity (+/-2 SD) was 80.6 +/- 54.8 micromoles of glucose produced per minute per gram of protein. CONCLUSIONS: Glucoamylase activity is 2 to 3 times higher when glucose polymers are used as substrate than when glycogen is used. Severe mucosal disease is associated with reduced glucoamylase activity. Quantitation of glucoamylase activity with glucose polymers is more appropriate in evaluating children since these polymers are commonly used as carbohydrate source in the diet.

Neonatal hypoxia in the rat: effects on exocrine pancreatic development.

BACKGROUND: Glucocorticoids profoundly affect pancreatic development during the suckling period. Increases in circulating glucocorticoids during exposure to hypoxia may alter the normal pattern of pancreatic enzyme development. METHODS: Rats were exposed to hypoxia from birth to 7 days (suckling) or from 28 to 35 days of age (weaned at day 21). RESULTS: Hypoxia in neonatal rats (0-7 days) led to decreased pancreatic weight, and trypsin, lipase, and amylase activity compared with normoxic controls. In contrast, rats exposed to hypoxia from 28 to 35 days of age had decreased lipase activity but no change in other pancreatic parameters. Two weeks after hypoxia (0-7 days) pups were returned to normoxia, and their body weights remained smaller than the age-matched, previously normoxic controls. Pancreatic enzyme activities were decreased in the group recovering from hypoxia compared with controls. Recovery of enzyme activities was observed 3 weeks after hypoxic rats were returned to normoxia. Normoxic pups were given dexamethasone to simulate the hyperglucocorticoid state in hypoxia at 7-day olds. Dexamethasone administration led to decreased body weight, but increased pancreatic weight and enzyme activity compared with normoxic, age-matched controls. CONCLUSIONS: Hypoxia in newborn rats delays the maturation of pancreatic exocrine enzymes. The mechanism is not related to increased serum glucocorticoids.