RESUMO
Objective: To investigate the role of anterior part of commissural subnucleus of nucleus tractus solitarius (acNTS) injury in insulin-resistant hyperglycemia during chronic restraint stress (CRS). Methods: We produced the CRS models (n = 20, a 7-day restraint followed by a 3-day free moving procedure for 40 days) in rats, and detected the parameters related to glucose metabolism. Results: The CRS induced a moderate (not higher than 11 mmol/L) and irreversible insulin-resistant hyperglycemia in about 1/3 (n = 7) of the individuals. CRS-hyperglycemic rats showed a condensed staining of acNTS neurons, and Caspase-3 immunostaining and TUNEL also showed positive, indicating apoptotic changes of acNTS neurons. After acNTS mechanical damage (n= 6), the blood glucose level rised gradually, which also led to insulin-resistant hyperglycemia. The characteristics of hyperinsulinemia, increased islet volume, and serum corticosterone levels in acNTS mice were consistent with those of CRS mice. Conclusion: The result indicates that during CRS, injury (apoptosis) of glucose-sensitive acNTS neurons causes dysregulation of blood glucose. Restraint stress model has value as a potential application in the study of stress-induced hyperglycemia.