Possible transcriptional mechanisms involved in the protective effects of intermittent fasting and exercise on streptozotocin-induced liver damage in diabetic rats

Derangements of liver transcriptional factors and enzymes have important implications in diabetes related complications. Hence, this study which consists of two experimental phases was aimed at evaluating the possible underlying molecular mechanisms of intermittent fasting (IF), exercise. starvation and honey in streptozotocin (STZ)-mediated liver damage in diabetic rats. In the non-diabetic phase, rats were exposed to an oral regimen of distilled water (0.5mL/Kg), intermittent fasting, exercise, starvation, and honey at 1g/Kg body weight for four (4) weeks while in the diabetic phase, after STZ injections, interventions with IF, exercise, starvation and honey treatment began for four (4) weeks prior to liver biochemical evaluation. The IF and exercise greatly decreased liver transcription factor (resistin, SREBP-Ic), inflammatory cytokines/enzyme (TNF-α, IL-6, IL-1β, MPO) as well as oxidative and nitregic stress with correspondent increase in liver PPAR-γ, IL-10, SOD, CAT and GSH in diabetic rats unlike starvation and honey regimen relative to diabetic controls. More so, IF and exercise greatly increased liver glycogen synthase and decreased glycogen phosphorylase in diabetics rats, whereas starvation and honey regimen had no effect relative to diabetic control. Intermittent fasting and exercise strategically reduced STZ-induced liver metabolic disorder through modulation of liver transcriptional factors and inhibition of pro-inflammatory cytokines, oxido-nitrergic and adipokine signaling pathway. This abstract was presented at the American Physiology Summit 2025 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.