Previously, we demonstrated that dexamethasone (Dex) administration at a dose of 1 mg/kg 24 hours before an ulcerogenic stimulus, exerts a proulcerogenic effect accompanied by impairments in carbohydrate metabolism (Filaretova et al, 2009, 2014). The present study examines how different housing conditions – standard conditions (SC), social isolation (SI), and environmental enrichment (EE) – influence Dex-induced impairments in carbohydrate metabolism and hematological parameters. The experiments were performed on male Sprague–Dawley rats during the winter season. Beginning at 30 days of age, the pups were housed for 6 weeks under SC, or SI, or EE conditions. Dex (1 mg/kg, i.p.) or its vehicle (control) was administered 24 hours prior to the glucose tolerance test (GTT). During the GTT, blood glucose levels were measured before the glucose load (baseline, 0 min; 2 g/kg, i.p.) and at 30, 60, 120, and 180 minutes afterward in rats fasted for 24 hours. Following the GTT, indomethacin (IM) was administered at an ulcerogenic dose (35 mg/kg, s.c.). Four hours after IM administration, the rats were decapitated, their stomachs were collected to assess the erosion area, and blood samples were obtained to evaluate hematological parameters, including calculation of the neutrophil-to-lymphocyte ratio (NLR), an indicator of pathological processes. Administration of glucose in the GTT led to an increase in blood glucose levels, reaching a maximum (peak) at 30 minutes in all control rats (SC, SI, EE) that had received the Dex vehicle. The lowest peak of the glycemic curve was observed in control SI rats compared with the peaks in control EE and SC rats. Beginning at 60 minutes, glucose levels gradually declined in all control groups, returning to baseline (0 min) only in the control EE rats. Pretreatment with Dex prior to the GTT caused a significant increase in baseline glucose levels in rats of all groups. In SC rats, Dex reduced the peak of the glycemic curve compared with their respective controls. In contrast, in EE rats the peak remained unchanged under Dex treatment and was significantly higher than in SC rats. Dex also did not modify the low peak observed in SI rats, which remained as low as in the corresponding control group. The Dex-induced impairment of carbohydrate metabolism was accompanied by a marked increase in the NLR in the blood in all groups (SC, SI, EE); however, this increase was less pronounced in EE rats. Summary & Conclusion. A faster normalization of blood glucose levels following the glucose load, along with the absence of a Dex-induced reduction in the glycemic peak in EE rats, compared with SC and SI rats, suggests an enhanced resistance of EE animals to Dex-induced disturbances in carbohydrate metabolism. This greater resilience is further supported by the comparatively lower NLR observed in EE rats. Altogether, these findings demonstrate that EE, as a non-invasive intervention, can mitigate Dex-induced impairments in carbohydrate metabolism and hematological parameters, indicating its potential for preventing the adverse effects of glucocorticoid treatment. Supported by State Program 47 SP “Scientific and Technological Development of the Russian Federation” (2019-2030), 0134-2019-0001. This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.
Filaretova et al. (Fri,) studied this question.