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Published on: November 2, 2015
Effects of hypoxia on the development of intestinal enzymes in neonatal and juvenile rats
Ping C Lee1, Mark Struve, Hershel Raff
1Departments of Pediatrics, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, USA. pclee@mail.mcw.edu
Insights
Neonatal hypoxia delays small intestinal enzyme maturation in rats, affecting carbohydrate and protein metabolism. Glucocorticoid treatment partially mimics these effects but doesn't fully explain the delayed enzyme activity.
Area of Science:
- Biochemistry
- Developmental Biology
- Pediatric Research
Background:
- Neonatal hypoxia impacts hepatic and pancreatic enzyme activity.
- Intestinal enzyme maturation is crucial for nutrient absorption in newborns.
Purpose of the Study:
- To investigate the effects of neonatal hypoxia on small intestinal enzyme activity.
- To determine if glucocorticoids mimic hypoxia-induced changes in intestinal enzymes.
Main Methods:
- Hypoxia exposure in neonatal (0-7 days) and juvenile (28-35 days) rats.
- Measurement of intestinal protein content and enzyme activities (lactase, maltase, sucrase, leucine aminopeptidase, LDH).
- Dexamethasone administration to neonatal rats.
Main Results:
- Neonatal hypoxia increased protein, lactase, and maltase in the duodenum and jejunum.
- Hypoxia in juvenile rats showed no significant enzyme changes.
- Post-hypoxia recovery showed reduced sucrase, maltase, and leucine aminopeptidase activity.
- Dexamethasone treatment decreased body weight but increased sucrase and maltase activity.
- Enzyme activities normalized 3 weeks after recovery from hypoxia.
Conclusions:
- Neonatal hypoxia causes a delay in small intestinal enzyme maturation.
- Glucocorticoids may partially mimic hypoxia's effects on disaccharidase activity.
- The observed enzyme changes are temporary, with full recovery within weeks.
Abstract:
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.
