Exercise augments the modulatory effects of vitamin E on pre-diabetes-induced aortopathy: a potential role of adiponectin.

Background: We tested the hypothesis that vitamin E may protect against pre-diabetes-induced aortic injury (aortopathy), and exercise can augment the action of vitamin E.Material and methods: Rats were either fed with a high fat and fructose diet (HFD) (model group) or a standard laboratory chow (control group) for 15 weeks before being sacrificed. The three protective groups were treated with vitamin E (HFD + Vit E), swimming exercises (HFD + Ex), and vitamin E plus swimming exercises (HFD + VitE + Ex), respectively.Results: Aortopathy was developed in the model group as demonstrated by substantial tissue ultrastructural alterations, which were partially protected by vitamin E and effectively protected with vitamin E plus swim exercise. Also, swimming exercises significantly (p < .05) increased the modulatory effects of vitamin E on dyslipidemia, insulin resistance, blood pressure, oxidative stress, inflammation, leptin, and adiponectin, except coagulation and thrombosis.Conclusions: Swim exercise augments the protective effects of vitamin E in a pre-diabetic animal model.

Suppression of monosodium glutamate-induced acute kidney injury and renal ultrastructural damage in rats by vitamin E / Supresión de lesiones renales agudas inducidas por glutamato monosódico y daño ultraestructural renal en ratas por vitamina E

Food additives and flavour enhancers used in the food industry are potential health risks. We tested the hypothesis that the food additive and flavour enhancer, monosodium glutamate (MSG), which is the sodium salt of glutamic acid can induce ultrastructural alterations to the kidney, and the antioxidant vitamin E can protect against acute kidney injuries induced by a toxic dose of MSG in a rat model of the disease. The model group of rats received a daily dose of MSG (4 gm/kg) for 7 days, whereas the protective groups were either received a 100 mg/kg vitamin E plus MSG or 300 mg/kg vitamin E plus MSG for 7 days. Rats were then sacrificed on day 8. Transmission and light microscopy images revealed substantial kidney damage induced by MSG in the model group as demonstrated by degenerated epithelial cells with Pyknotic nuclei, swollen mitochondria, damaged brush margins, dilated tubules, and widening of Bowman's space with shrinkage and deformity of some glomeruli. Treatment of the model group with vitamin E showed a substantial protection of kidney tissue and renal ultrastructure by 300 mg/kg vitamin E compared to a partial protection by 100 mg/kg vitamin E. In addition, MSG significantly (p<0.05) increased serum levels of urea and creatinine, which were significantly (p<0.05) decreased with vitamin E. However, for serum creatinine, high doses of vitamin E (300 mg/kg) were more effective than lower doses (100 mg/kg) of vitamin E. These results indicate that vitamin E at 300 mg/kg effectively protects against MSG-induced acute kidney injury in rats.

Los aditivos alimentarios y los potenciadores del sabor utilizados en la industria alimentaria son riesgos potenciales para la salud. Probamos la hipótesis de que el aditivo alimentario y el potenciador del sabor, glutamato monosódico (MSG), la sal sódica del ácido glutámico, puede inducir alteraciones ultraestructurales del riñón, y que las propiedades antioxidantes de la vitamina E, pueden proteger contra las lesiones renales inducidas por una dosis tóxica de MSG en un modelo de rata. El grupo modelo de ratas recibió una dosis diaria de MSG (4 g / kg) durante 7 días, mientras que los grupos protectores recibieron una dosis de 100 mg / kg de vitamina E más MSG o 300 mg / kg de vitamina E más MSG durante 7 días. Las ratas se sacrificaron el día 8. Las imágenes de microscopía óptica y de transmisión revelaron un daño renal sustancial inducido por el MSG en el grupo modelo, como lo demuestran las células epiteliales degeneradas con núcleos picnóticos, mitocondrias hinchadas, bordes dañados, túbulos dilatados y ensanchamiento del espacio de Bowman, además de la deformidad de algunos glomérulos. El tratamiento del grupo modelo con vitamina E mostró una protección sustancial del tejido renal y la ultraestructura renal de 300 mg / kg de vitamina E en comparación con una protección parcial de 100 mg / kg de vitamina E. Además, el MSG aumentó significativamente (p <0,05) en el suero los niveles de urea y creatinina, disminuyeron significativamente (p <0,05) con la vitamina E. Sin embargo, para la creatinina sérica, las dosis altas de vitamina E (300 mg / kg) fueron más efectivas que las dosis más bajas (100 mg / kg) de vitamina E. Estos resultados indican que la vitamina E a 300 mg / kg protege eficazmente contra la lesión renal aguda inducida por MSG en ratas.

Vitamin E protects against hepatocyte ultrastructural damage induced by high fat diet in a rat model of pre-diabetes / La vitamina E protege contra el daño ultraestructural de los hepatocitos inducido por la dieta alta en grasas en un modelo de pre-diabetes en ratas

SUMMARY: We sought to investigate the potential protective effect of Vitamin E supplementation against hepatocyte ultrastructural alterations induced by high fat diet (HFD) in a rat model of pre-diabetes. Therefore, rats were either fed with HFD (model group) or a standard laboratory chow (control group) for 12 weeks before being sacrificed. The protective group fed on a HFD and started the treatment with vitamin E (100 mg/kg/day, i.p) from day 1 until being sacrificed at week 12. The harvested liver tissues were examined using transmission electron microscopy (TEM) and blood samples were assayed for biomarkers of liver injury and prediabetes. TEM images showed that HFD induced profound pathological changes to the hepatocyte ultrastructure as demonstrated by degenerated hepatocytes with damaged cytoplasm that have mitochondrial swelling, dilation of endoplasmic reticulum, blebbing of plasma membranes, and cytoplasmic accumulations of lipid droplets and vacuoles, which were substantially but not completely protected with vitamin E. In addition, HFD significantly (p<0.05) augmented biomarkers of liver injury and pre-diabetes such as alanine aminotransferase (ALT), aspartate aminotransferase (AST), tumor necrosis factor-alpha (TNF-α), malondialdehyde (MDA), total cholesterol (TC), triglycerides (TG), and low density lipoprotein cholesterol (LDL-C), which were significantly (p<0.05) reduced with vitamin E except TNF-α and TC. Furthermore, none of these biomarkers were reduced to the control level by vitamin E. We conclude that vitamin E is a partial protective agent against HFD-induced liver injury and pre-diabetes.

RESUMEN: El objetivo de este estudio fue investigar el posible efecto protector de la administración de suplementos de vitamina E contra las alteraciones ultraestructurales de los hepatocitos inducidas por una dieta rica en grasas (DRG) en un modelo de prediabetes en ratas. Antes de ser sacrificadas las ratas fueron alimentadas con DRG (grupo modelo) o un alimento estándar de laboratorio (grupo control) durante 12 semanas. El grupo protector se alimentó con una DRG y comenzó el tratamiento con vitamina E (100 mg/kg/día, i.p) desde el día 1 hasta sacrificarlo en la semana 12. Los tejidos hepáticos recolectados se examinaron mediante microscopía electrónica de transmisión (MET) y se tomaron muestras de sangre y se analizaron los biomarcadores de daño hepático y prediabetes. Las imágenes de MET mostraron que el DRG indujo cambios patológicos profundos en la ultraestructura de los hepatocitos, como lo demuestran los hepatocitos degenerados con citoplasma dañado e hinchazón mitocondrial, dilatación del retículo endoplasmático, formación de ampollas en las membranas plasmáticas y acumulaciones citoplásmicas de gotas de lípidos y vacuolas, los que fueron sustancialmente protegidas con vitamina E. Además, DRG aumentó significativamente (p <0,05) los biomarcadores de daño hepático y prediabetes como alanina aminotransferasa (ALT), aspartato aminotransferasa (AST), factor de necrosis tumoral alfa (TNF-α), malondialdehído (MDA), colesterol total (CT), triglicéridos (TG) y lipoproteína de colesterol de baja densidad (LDL-C), la cual se redujo significativamente (p <0,05) con vitamina E, excepto TNF-α y CT. Ninguno de estos biomarcadores se redujo al nivel de control por la vitamina E. Concluimos que la vitamina E es un agente protector parcial contra la lesión hepática inducida por DRG y la prediabetes.