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Neonatal hypoxia in the rat: effects on exocrine pancreatic development
Ping C Lee1, Mark Struve, Suzan M Lewis
1Department of Pediatrics, Medical College of Wisconsin, Milwaukee 53226, USA. pcl@mail.mcw.edu
Insights
Neonatal hypoxia in rats impairs pancreatic enzyme development, delaying maturation. This effect is not caused by increased glucocorticoids, suggesting other mechanisms are involved in pancreatic enzyme regulation.
Area of Science:
- Developmental Biology
- Physiology
- Endocrinology
Background:
- Glucocorticoids significantly influence pancreatic development in suckling mammals.
- Elevated glucocorticoids during hypoxia may disrupt normal pancreatic enzyme development patterns.
Purpose of the Study:
- To investigate the impact of hypoxia on pancreatic development and enzyme activity in neonatal and weaned rats.
- To determine if increased glucocorticoids mediate the effects of hypoxia on pancreatic enzyme maturation.
Main Methods:
- Rat pups were exposed to hypoxia from birth to 7 days (neonatal) or from 28 to 35 days (weaned).
- Pancreatic weight and activities of trypsin, lipase, and amylase were measured.
- Dexamethasone was administered to normoxic pups to simulate hyperglucocorticoid states.
Main Results:
- Neonatal hypoxia (0-7 days) decreased pancreatic weight and enzyme activity (trypsin, lipase, amylase).
- Hypoxia in weaned rats (28-35 days) only decreased lipase activity.
- Dexamethasone administration increased pancreatic weight and enzyme activity, contrasting with hypoxia effects.
Conclusions:
- Hypoxia during the neonatal period delays the maturation of pancreatic exocrine enzymes in rats.
- The observed delay in pancreatic enzyme maturation due to neonatal hypoxia is not mediated by increased serum glucocorticoids.
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.