Efeitos da suplementação de creatina no fígado em modelo experimental de diabetes induzido por estreptozotocina

Abstract

Diabetes Mellitus (DM) is a group of metabolic diseases whose relevance has increased due to their growing prevalence and associated systemic complications. In recent years, creatine (Cr) has been studied for its potential to attenuate tissue damage caused by oxidative stress and inflammation, as well as its possible effects on glycemic control. This study aimed to evaluate the effect of creatine supplementation on the liver of streptozotocin-induced diabetic rats. Twenty Wistar rats were divided into four experimental groups: (C) control, without diabetes and without creatine supplementation (n=5); (CT) control with creatine supplementation (n=5); (D) diabetics without creatine supplementation (n=5); and (DT) diabetics with creatine supplementation (n=5). Groups D and DT received a single dose of streptozotocin (40 mg/kg), while groups CT and DT received dietary creatine supplementation in the feed for seven weeks. Biometric parameters were analyzed and the livers were collected for histopathological evaluation of inflammation, fibrosis and steatosis, as well as immunohistochemical analysis of superoxide dismutase (SOD-1), in order to verify oxidative stress. The diabetic animals showed an increase in feed and water consumption, as well as a loss of body weight, confirming the induction of DM by streptozotocin. Group D showed a significant increase in the hepatosomatic index compared to the control groups, while group DT showed no significant improvement in this parameter. In the histopathological evaluation, the DT group showed a significant improvement compared to the D group in the findings of hyperemia, steatosis, pyknotic nuclei and fibrosis. Although the literature on the use of creatine in diabetic livers is still limited, similar studies corroborate the positive effects observed. However, the DT group showed no significant changes in inflammation, necrosis and hydropic and ballooning degeneration, indicating that creatine does not act effectively in reversing these parameters. SOD-1 immunolabeling showed a reduction in the diabetic groups compared to the controls, and the DT group showed no significant improvement compared to the D group, suggesting that creatine supplementation does not modulate enzymatic antioxidant activity or mitigate oxidative stress. Creatine can partially attenuate some of the liver changes resulting from diabetes, especially in morphological aspects such as fibrosis and steatosis. However, it has no significant effect on inflammation or oxidative stress. Considering the scarcity of studies on the use of creatine in the diabetic liver, this study makes an important contribution to the field and highlights the need for further research.