Effects of Redox Disturbances on Intestinal Contractile Reactivity in Rats Fed with a Hypercaloric Diet. (25th October 2018)

• Record Type: Journal Article
• Authors: de Souza, Iara L. L.; Ferreira, Elba dos S.; Diniz, Anderson F. A.; Carvalho, Maria Thaynan de L.; Queiroga, Fernando R.; Toscano, Lydiane T.; Silva, Alexandre S.; da Silva, Patrícia M.; Cavalcante, Fabiana de A.; da Silva, Bagnólia A.
• Other Names: Franco Jeferson L. Academic Editor.
• Is Part Of: Oxidative medicine and cellular longevity. Volume 2018(2018)
• Publication Date: 2018-10-25
• Subjects: Oxidative stress -- Periodicals; Cells -- Aging -- Periodicals; Cells -- Aging; Oxidative stress; Oxidative Stress -- Periodicals; Cell Aging -- Periodicals; Periodicals; 611.0181
• DOI: 10.1155/2018/6364821
• Languages: English
• ISSNs: 1942-0900

Abstract

Abstract : Few studies have associated the effects of changes in caloric intake and redox disturbances in the gastrointestinal tract. Therefore, the present study aimed at evaluating the hypercaloric diet consumption influence on the contractile reactivity of intestinal smooth muscle, morphology, and oxidative stress of rat ileum. Wistar rats were randomly divided into groups that received a standard diet and fed with a hypercaloric diet for 8 weeks. Animals were euthanized, and the ileum was isolated to isotonic contraction monitoring. Morphology was evaluated by histological staining and oxidative stress by quantification of malondialdehyde levels and total antioxidant activity. Cumulative concentration-response curves to KCl and carbachol were attenuated in rats fed with a hypercaloric diet compared to those that received a standard diet. In addition, an increase in caloric intake promotes a rise in the thickness of the longitudinal smooth muscle layer of rat ileum and tissue malondialdehyde levels, characterizing lipid peroxidation, as well as a decrease in the antioxidant activity. Thus, it was concluded that the consumption of a hypercaloric diet impairs rat intestinal contractility due to mechanisms involving modifications in the intestinal smooth muscle architecture triggered by redox disturbances.