Eighteen preruminating calves obtained at approximately 38 d of age were used to determine whether the ruminant insulin response to propionate is an inherent response or one that is acquired because of ruminal propionate production. A liquid milk replacer diet was fed alone or with isocaloric additions of propionate [50 mmol . (kg BW . 75-1 . d-1] or glucose. Both additions caused a strong insulin response, but the response by propionate-fed calves appeared to be independent of plasma glucose concentrations during the early post-feeding hours. After receiving the experimental diets for 18 d, all calves were given an iv infusion or propionate [.035 mmol propionate . (kg BW . 75-1 . min-1 for 20 min]. All calves demonstrated a plasma insulin rise and glucose decline due to the infusions, but glucose-fed and propionate-fed calves appeared less sensitive to the iv propionate than the calves fed only milk replacer.

The present study examines the interaction of light damage to the retina and streptozotocin (SZ)-induced diabetes in male and female rats during the early development of the disease, when changes occur in the blood-retinal barrier and in pigment cell membranes. Exposure of rats to low illuminance was used to determine the relationship between photically-induced cell death and diabetes. Other groups of animals were exposed to a greater illuminance for shorter time periods (24 hours) in attempts to identify a specific post-treatment day for the effect of diabetes. Blood glucose levels were monitored to indicate the severity of the diabetes. Morphometric analyses and histopathologic observations demonstrated that the outer nuclear layer (ONL, photoreceptor nuclei) was reduced significantly in thickness in female rats exposed to light during a 9 day period after SZ injection, but was unchanged from the control groups when exposed beginning at 12 days after SZ treatment. Removal of the pituitary gland prior to SZ treatment and light exposure resulted in the survival of more photoreceptor cells and prevented the differential in ONL thickness observed between control and diabetic intact animals. Attempts to establish a period of greatest susceptibility of the diabetic retina to photic damage were unsuccessful, but results indicate that prior light history and/or shipment stress might be related to retinal damage from light exposure.

SummaryRats were subjected to the following procedures: No treatment, Stressor (10% NaCl i.p.), Warfarin for 7 days, Stressor followed by Warfarin; and groups were sacrificed at intervals for assessment of spontaneous hemorrhage and of adrenal ascorbic acid concentration. There was no hemorrhage in the no treatment and stressor groups; some hemorrhage in the warfarin group; profound hemorrhage with Warfarin + Stressor. The adrenal ascorbic acid concentration was found to be lower, 8 h and again 5 days after stress, and remained lower in the warfarin + stress animals. Warfarin had no effect on adrenal ascorbic acid level.In another series of experiments in which the stress consisted of an electric current to the cage floor for 6 sec over 15 min, rats were sacrificed daily for determination of serum corticosterone concentration and occurrence of spontaneous hemorrhage. There was a statistically significant increase of serum corticosterone concentration with stress, warfarin and combined warfarin and stress treatments (P< 0.001 for all three variables). There was a significant correlation (r = 0.96 and 0.89, P< 0.01) for serum corticosterone concentration with hemorrhage score and incidence of hemorrhage in stressed rats receiving warfarin, but not in those receiving only warfarin. The results indicate an activation, rather than an exhaustion, of the pituitary-adrenal axis during the combined action of anticoagulant and stress, which results in the development of spontaneous hemorrhage.