Abstract
BackgroundOxidative stress (OS) plays an important role in type 2 diabetes (T2D) pathogenesis and its complications. New therapies target natural antioxidants as an alternative and/or supplemental strategy to prevent and control them. Our previous chemical and biological studies highlighted the important antioxidant activities of cherries, among other fruits and vegetables, thus we aimed to determine in vivo effects of 2-month long cherry consumption using a high-fat/high-fructose (HFHF) model of diabetic-rats (Lozano et al. in Nutr Metab 13:15, 2016).MethodsAfter 2 months of HFHF, male Wistar rats were divided into: HFHF and HFHF enriched in cherry (nutritional approach) or standard diet ND (lifestyle measures) and ND plus cherry during 2 months. Metabolic, lipidic, oxidative parameters were quantified. Tissues (liver, pancreas and vessels) OS were assessed and hepatic (steatosis, fibrosis, inflammation) and vascular (endothelial dysfunction) complications were characterized.ResultsT2D was induced after 2 months of HFHF diet, characterized by systemic hyperglycaemia, hyperinsulinemia, glucose intolerance, dyslipidaemia, hyperleptinemia, and oxidative stress associated with endothelial dysfunction and hepatic complications. Cherry consumption for 2 months, in addition to lifestyle measures, in T2D-rats decreased and normalized the systemic disturbances, including oxidative stress complications. Moreover, in the vessel, cherry consumption decreased oxidative stress and increased endothelial nitric oxide (NO) synthase levels, thus increasing NO bioavailability, ensuring vascular homeostasis. In the liver, cherry consumption decreased oxidative stress by inhibiting NADPH oxidase subunit p22phox expression, nuclear factor erythroid-2 related factor 2 (Nrf2) degradation and the formation of reactive oxygen species. It inhibited the activation of sterol regulatory element-binding proteins (1c and 2) and carbohydrate-responsive element-binding protein, and thus decreased steatosis as observed in T2D rats. This led to the improvement of metabolic profiles, together with endothelial and hepatic function improvements.ConclusionCherry consumption normalized vascular function and controlled hepatic complications, thus reduced the risk of diabetic metabolic disorders. These results demonstrate that a nutritional intervention with a focus on OS could prevent and/or delay the onset of vascular and hepatic complications related to T2D.
Highlights
Oxidative stress (OS) plays an important role in type 2 diabetes (T2D) pathogenesis and its complica‐ tions
The liver plays a major role in the regulation of blood glucose levels in close cooperation with the pancreas and other peripheral tissues; several studies have reported an association between non-alcoholic fatty liver disease (NAFLD) and cardiovascular disease-related complications [14]
Cherry consumption improves plasmatic oxidative and metabolic disorders associated to diabetes Firstly, we have demonstrated that cherry consumption decreased oxidative stress in plasma
Summary
Oxidative stress (OS) plays an important role in type 2 diabetes (T2D) pathogenesis and its complica‐ tions. More precisely the internal layer endothelium, are the first sites for the development of complications such as high cholesterol and high blood pressure [15], obesity and visceral fat distribution [16], impaired fasting glucose and hyperglycaemia [17] and, more recently hypoglycaemia [18] and insulin resistance [19]. Under these pathological conditions, the strategic equilibrium between relaxant and contractor factors is lost in favour of pro-mitogenic, pro-aggregation mediators and inflammation, leading to endothelial dysfunction as observed in T2D patients [11, 20]. Diabetic vascular complications lead to further functional deterioration inducing coronary arteriosclerosis, neuropathy, nephropathy... [21], and are associated with cardiovascular and all-cause mortality in patients with diabetes [22]
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