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Studies have shown that the microbiota along the gastrointestinal tract (GIT) plays an important role when it comes to the maintenance of its proper functions. Many studies exist that have analyzed the composition of the bacterial community in the different regions of the GIT of humans and model animals. Microbial imbalance leads to several systemic disorders, including cardiovascular and renal disease. The imbalance between the production of reactive oxygen species (ROS) and their elimination by antioxidants leads to oxidative stress. Oxidative stress plays an important role in a variety of physiological processes, as well as disease. The continuous formation of ROS in the GIT is the result of the interaction between intestinal mucosa, symbiotic bacteria and dietary factors. It has also been proven that ROS play a role in the pathogenesis of several GI disorders, including IBD. We hypothesized that the levels of advanced glycation end products (AGEs) would be the highest in the ileum, caecum or colon, where the microbiota mostly consist of butyrate producing bacteria, Bacterioides, Clostridium, Ruminococcus or Bifidobacterium, which derive energy through carbohydrate fermentation. We also assumed that advanced oxidation protein products (AOPP) mostly act in the segments, where bacteria reside and which are responsible for the amino acid fermentation, such as caecum or colon. Lipid hydroxyperoxides are generated during digestion in the stomach, which contains absorbed oxygen and has a low pH. According to this we hypothesized that the highest concentration of thiobarbituric acid reacting substances (TBARS) could be in the stomach, which, however, has not been confirmed. Because Lactobacilli are able to produce catalase, an endogenous antioxidant, and are abundant in the small intestine, we hypothesized that antioxidant capacity (measured by ferric reducing ability) would be the highest here. The highest levels of AGEs were found in the caecum. The highest level of TBARS was found in the jejunum of the rats. The assessment of our hypothesis also revealed high levels of AOPP in the caecum. It has been shown that AOPP contributes to the progression of IBD. The ferric reducing ability of tissue was the lowest in the colon of the experimental animals, which is in accordance with previous studies that show that rat colon has a lower total antioxidant capacity than the small bowel. In summary, we offer some insight into the differences between the oxidative status along the GIT of rats and some advice concerning supportive antioxidant therapy of gastrointestinal diseases., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

Simple Summary: Type 2 diabetes mellitus (T2DM) is a global health burden that adversely affects various organs, including the brain, leading to neurodegeneration. Recent research emphasizes the cerebellum's role in studying the interactions between T2DM, obesity, aging, and brain energy metabolism. This study focused on the cerebellum of Zucker diabetic fatty (ZDF) rats, a model that mirrors the diversity of T2DM in humans. The primary objective was to measure oxidative stress markers and kinetic properties of sodium–potassium ATPase (Na,K-ATPase) in relation to T2DM severity (not documented yet). Na,K-ATPase is an active transport mechanism crucial for maintaining unequal cation distributions across the plasma membrane, and its activity has been shown to be altered by diabetes in various organs. While oxidative stress is well established in the pathogenesis of diabetes, this study confirmed systemic oxidative and carbonyl damage in ZDF rats and provided new evidence of such damage in cerebellar tissue. However, no differences were found in cerebellar oxidative stress markers based on T2DM severity. Additionally, Na,K-ATPase activity was higher in the cerebellum of ZDF rats compared with controls, suggesting the presence of compensatory mechanisms in this brain region in aged ZDF animals. However, further research is needed to confirm and elucidate this phenomenon. Type 2 diabetes mellitus has been referred to as being closely related to oxidative stress, which may affect brain functions and brain glucose metabolism due to its high metabolic activity and lipid-rich content. Na,K-ATPase is an essential enzyme maintaining intracellular homeostasis, with properties that can sensitively mirror various pathophysiological conditions such as diabetes. The goal of this study was to determine oxidative stress markers as well as Na,K-ATPase activities in the cerebellum of Zucker diabetic fatty (ZDF) rats depending on diabetes severity. The following groups of male rats were used: Wistar, ZDF Lean (fa/+), and ZDF (fa/fa) rats, arbitrarily divided according to glycemia into ZDF obese (ZO, less severe diabetes) and ZDF diabetic (ZOD, advanced diabetes) groups. In addition to basic biometry and biochemistry, oxidative stress markers were assessed in plasma and cerebellar tissues. The Na, K-ATPase enzyme activity was measured at varying ATP substrate concentrations. The results indicate significant differences in basic biometric and biochemical parameters within all the studied groups. Furthermore, oxidative damage was greater in the cerebellum of both ZDF (fa/fa) groups compared with the controls. Interestingly, Na,K-ATPase enzyme activity was highest to lowest in the following order: ZOD > ZO > Wistar > ZDF lean rats. In conclusion, an increase in systemic oxidative stress resulting from diabetic conditions has a significant impact on the cerebellar tissue independently of diabetes severity. The increased cerebellar Na,K-ATPase activity may reflect compensatory mechanisms in aged ZDF (fa/fa) animals, rather than indicating cerebellar neurodegeneration: a phenomenon that warrants further investigation. [ABSTRACT FROM AUTHOR]