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Effects of diabetes on development of small intestinal enzymes of infant rats
D Wen1, S J Henning, R L Hazelwood
1Department of Biology, University of Houston, Texas 77004.
Insights
Streptozotocin (SZ) induced diabetes in rat pups accelerated the maturation of small intestinal sucrase and maltase enzymes. Elevated blood glucose may directly impact disaccharidase development in these models.
Area of Science:
- Developmental biology
- Gastroenterology
- Endocrinology
Background:
- The development of small intestinal enzymes is crucial for nutrient absorption in early life.
- Streptozotocin (SZ) is a diabetogenic agent used to induce experimental diabetes.
Purpose of the Study:
- To investigate the impact of SZ-induced diabetes on the ontogeny of small intestinal enzymes in postnatal rat pups.
- To explore the relationship between hyperglycemia and intestinal enzyme activity.
Main Methods:
- Postnatal rat pups were injected with streptozotocin (SZ) or vehicle control.
- Plasma glucose, insulin, corticosterone, pancreatic insulin, and liver glycogen were measured.
- Activities of sucrase, lactase, maltase, and acid beta-galactosidase in small intestinal segments were analyzed.
Main Results:
- SZ-treated rats exhibited precocious maturation of sucrase and maltase.
- Plasma glucocorticoids remained stable, but pancreatic insulin was significantly reduced.
- Jejunal lactase and ileal acid beta-galactosidase activities were not affected by SZ-induced diabetes.
Conclusions:
- Elevated blood glucose, a consequence of diabetes, may directly stimulate the development of disaccharidases in the small intestine.
- The SZ rat pup model offers a valuable tool for studying the effects of hyperglycemia on intestinal enzymes, independent of insulin level changes.
Abstract:
The effect of streptozotocin (SZ) on the development of small intestinal enzymes in postnatal rat pups was studied. SZ was injected ip on Day 10 and, if necessary, again on Day 12. On Days 15, 18, and 21, one pup from each group (including a vehicle-injected control (C) group) was decapitated under conditions which minimized stress. Plasma glucose, insulin (IRI), and corticosterone were measured, as were pancreatic IRI, liver glycogen, and liver membrane binding of IRI. Small intestinal segments were processed and analyzed for sucrase, lactase, maltase, and ileal acid beta-galactosidase activities. Our results indicate that plasma glucocorticoid levels remained virtually constant in both SZ and C groups, while the ontogenic profiles of sucrase and maltase in SZ rats were shifted toward an earlier appearance and a precocious maturation. Circulating levels of IRI were not reduced significantly by SZ despite the fact that pancreatic IRI was decreased 95%. Jejunal lactase, unlike data reported for diabetic rats, was not affected by SZ diabetes. Also, acid beta-galactosidase was unaltered in the SZ rat pups. It is concluded that possibly the elevated disaccharidases seen in diabetic postnatal rat pups are the direct effect of elevated blood glucose. If so, the SZ rat pup model may be a useful tool with which to study effects of glucose on intestinal enzymes in the absence of changes in plasma insulin.