Related Experiment Video
Updated: Jan 13, 2026

A Model of Chronic Nutrient Infusion in the Rat
Published on: August 14, 2013
Incretin effect is sufficient for glucose control in developing rats
Insights
Incretin hormones stimulate insulin secretion in developing rat pups, similar to adults. Therapies targeting incretins, like DPP-4 inhibitors and GLP-1 receptor agonists, did not cause hypoglycemia, suggesting their potential safety for treating neonatal hyperglycemia.
Area of Science:
- Neonatal Physiology
- Endocrinology
- Pharmacology
Background:
- Neonatal hyperglycemia is common in preterm infants.
- Treatment requires a low risk of hypoglycemia.
- Incretin-based therapies offer a low hypoglycemia risk in adults.
Purpose of the Study:
- Investigate incretin hormone-enhanced insulin secretion in glucose regulation in rat pups.
- Evaluate the risk of hypoglycemia with incretin-based therapies in developing rats.
Main Methods:
- Oral glucose tolerance tests (OGTT) and intraperitoneal glucose tolerance tests (IPGTT) in 2-week-old Wistar rats.
- Comparison of serum glucose, insulin, and incretin hormone concentrations.
- Administration of a DPP-4 inhibitor (linagliptin) and a GLP-1 receptor agonist (liraglutide).
Main Results:
- The incretin effect was substantial (63%) in rat pups, with higher insulin secretion during OGTT compared to IPGTT.
- Therapeutic doses of linagliptin and liraglutide did not induce hypoglycemia in developing rats.
Conclusions:
- Endogenous incretin hormones stimulate insulin secretion in 2-week-old rats, mirroring adult responses.
- DPP-4 inhibitors and GLP-1 receptor agonists appear safe, without causing hypoglycemia in this model.
- Incretin-based therapies may represent a safe therapeutic strategy for neonatal hyperglycemia in preterm infants.
Abstract:
Hyperglycemia is common in extremely preterm infants, and the treatment of neonatal hyperglycemia should be associated with a low risk of hypoglycemia. Incretin-based therapies are characterized by a low risk of hypoglycemia and are efficacious and safe in adults. We aimed to investigate the extent to which the glucose-lowering effect of incretin hormone-enhanced insulin secretion contributes to glucose regulation in healthy, developing rat pups and to evaluate the associated risk of hypoglycemia. We performed oral glucose tolerance (OGTT) and intraperitoneal glucose tolerance test (IPGTT) in 2-week-old Wistar rats and compared the serum concentrations of glucose, insulin, and incretin hormones. OGTT was associated with significantly higher serum incretin hormone concentrations than IPGTT in the pups, and the serum insulin concentrations were higher during OGTT than during IPGTT (the incretin effect was 63%). Thus, the incretin effects were present and substantial in the rat pups. We next administered two drugs (a dipeptidyl peptidase 4 (DPP-4) inhibitor or a glucagon-like peptide 1 (GLP-1) receptor agonist) with incretin effects and evaluated the risk of adverse hypoglycemic events in normal developing rats. Standard therapeutic doses of linagliptin and liraglutide did not influence the blood glucose concentrations of 2-week-old pups, and no hypoglycemia developed. In conclusion, we have shown that endogenous incretin hormones stimulate insulin secretion in normal 2-week-old rats, as in adults. Furthermore, neither a DPP-4 inhibitor nor a GLP-1 receptor agonist induced hypoglycemia as an adverse effect. Therefore, incretin hormones may be safe therapeutic targets for hyperglycemia in preterm infants.
Related Concept Videos
Glucagon-like Receptor Agonists
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by...
Dipeptidyl Peptidase 4 Inhibitors
Glucose Homeostasis: Pancreatic Islets and Insulin Secretion
Insulin and C-peptide are...
Hormones Regulating Blood Glucose
In addition to accelerating glucose uptake and utilization, insulin has...
Oral Hypoglycemic Agents: Glinides

