Affiliation:
1. Department of Pediatrics Milwaukee Wisconsin U.S.A.
2. Department of Pharmacology and Toxicology Milwaukee Wisconsin U.S.A.
3. Department of Medicine Medical College of Wisconsin Milwaukee Wisconsin U.S.A.
4. Endocrine Research Laboratory St. Luke's Medical Center Milwaukee Wisconsin U.S.A.
Abstract
ABSTRACTBackgroundGlucocorticoids 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.MethodsRats were exposed to hypoxia from birth to 7 days (suckling) or from 28 to 35 days of age (weaned at day 21).ResultsHypoxia 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.ConclusionsHypoxia in newborn rats delays the maturation of pancreatic exocrine enzymes. The mechanism is not related to increased serum glucocorticoids.