[The effects of electric stress on pancreatic B cell function in rats fed a high fat diet (I). Glucose tolerance and glucose-induced insulin release from the perfused pancreas (author's transl)].

The synergistic effects of dietary obesity produced by the feeding of a high fat diet and stress induced by electric shocks on glucose tolerance and glucose-induced insulin release from the perfused pancreas were investigated. Male Wistar rats weighing 90 approximately 100 g were fed ad libitum for 12 weeks either a control (50% Starch; C) or a high fat diet (40% Butter; F). Some of the rats on both diets received 100 electric shocks of 1 sec. duration in the stress session for 1 hour per day for the last 3 weeks of the experimental period. Low stress (LS) groups were shocked at a fixed time (Inter Shock Interval: 36 sec.). High stress (HS) groups were shocked at random (ISI: mean = 36 sec, 9 approximately 108 sec. variable). Non-stress (NS) groups were not given any shocks. Rats were killed at 24 hours after the final stress session. Under NS conditions, rats in the F-NS group gained a significant amount of weight and had normal levels of fasting plasma glucose and insulin but an impaired glucose tolerance (k = 3.49). Insulin release from the perfused pancreas in the F-NS group showed a delay in the initiation of release by the stimulation of glucose (16.7 mM), but the total amounts of insulin released did not differ from that in the C-NS group. On the other hand, the levels of plasma 11-OHCS in the fed state were much more highly elevated in the HS group than in the LS group, which was not influenced by the high fat diet. The fasting levels of plasma glucose in the F-HS group (121 +/- 7 mg/100 microliter) were significantly higher than those in the C-HS group (101 +/- 7 mg/100 microliter) in spite of a normal insulin concentration in plasma. In contrast to the normal glucose tolerance in the C-HS group (k = 5.14), glucose tolerance in the F-HS group (k = 3.04) was impaired. Insulin release from the perfused pancreas in response to glucose in both diet group was not significantly altered under LS conditions. In the C-HS group, however, the total amount of insulin released in the second phase was enhanced to 165% of that in the C-NC group. Conversely, in the F-HS group the total amount of insulin released in the first phase was significantly decreased to 40% of that in the F-NS group. These findings indicate that the elevation of plasma 11-OHCS levels provoked by shocks at random rather than in a fixed time schedule is caused by the difficulty in predicting shocks, and a chronic stress induced by electric shocks at random further impairs glucose tolerance and suppresses glucose-induced insulin release in rats fed a high fat diet.