Pattern of Stress-Induced Hyperglycemia according to Type of Diabetes: A Predator Stress Model

Abstract

BackgroundWe aimed to quantify stress-induced hyperglycemia and differentiate the glucose response between normal animals and those with diabetes. We also examined the pattern in glucose fluctuation induced by stress according to type of diabetes.MethodsTo load psychological stress on animal models, we used a predator stress model by exposing rats to a cat for 60 minutes and measured glucose level from the beginning to the end of the test to monitor glucose fluctuation. We induced type 1 diabetes model (T1D) for ten Sprague-Dawley rats using streptozotocin and used five Otsuka Long-Evans Tokushima Fatty rats as obese type 2 diabetes model (OT2D) and 10 Goto-Kakizaki rats as nonobese type 2 diabetes model (NOT2D). We performed the stress loading test in both the normal and diabetic states and compared patterns of glucose fluctuation among the three models. We classified the pattern of glucose fluctuation into A, B, and C types according to speed of change in glucose level.ResultsIncrease in glucose, total amount of hyperglycemic exposure, time of stress-induced hyperglycemia, and speed of glucose increase were significantly increased in all models compared to the normal state. While the early increase in glucose after exposure to stress was higher in T1D and NOT2D, it was slower in OT2D. The rate of speed of the decrease in glucose level was highest in NOT2D and lowest in OT2D.ConclusionThe diabetic state was more vulnerable to stress compared to the normal state in all models, and the pattern of glucose fluctuation differed among the three types of diabetes. The study provides basic evidence for stress-induced hyperglycemia patterns and characteristics used for the management of diabetes patients.

Stress Hyperglycemia as First Sign of Asymptomatic Type 1 Diabetes: An Instructive Case and Literature Review

“…To elucidate the pattern of glucose uctuation under psychiatric stress, T1DM animal models under a predator stress circumstance showed the SH was characterized as "fast and slow" pattern, in which blood glucose rapidly increased and slowly decreased thereafter 14 . Although we cannot fully extrapolate the animal results to humans, blood glucose levels of the present case indeed rapidly increased from 174 mg/dl to 400 mg/dL within 2 hours (9th -11th hours after admission), maintained peak levels above 400 mg/dL for 5 hours (11th -15th hours after admission) and then decreased slowly to 89 mg/dL (Fig.…”

Genetic determinants of obesity heterogeneity in type II diabetes

“…Glucagon, epinephrine and cortisol as stress hormones cause hyperglycemia through stimulation of gluconeogenesis and glycogenolysis in liver, inhibition of insulin secretion and interruption of glucose absorption in muscle [ 55 – 57 ]. It has been documented that epinephrine stimulates glucagon to produce glucose in stress situation, whereas cortisol maintains elevated glucose by epinephrine and glucagon in post-stress phase [ 58 , 59 ].…”

Genetic Determinants of Obesity Heterogeneity in Type II Diabetes

“…Glucagon, epinephrine and cortisol as stress hormones cause hyperglycemia through stimulation of gluconeogenesis and glycogenolysis in liver, inhibition of insulin secretion and interruption of glucose absorption in muscle [52]- [54]. It has been documented that epinephrine stimulates glucagon to produce glucose in stress situation, whereas cortisol maintains elevated glucose by epinephrine and glucagon in post-stress phase [55], [56].…”