Evaluation of sucrose-enriched diet consumption in the development of risk factors associated to type 2 diabetes, atherosclerosis and non-alcoholic fatty liver disease in a murine model

Overconsumption of sucrose, the main contributor of the total added sugar intake in the world, has been associated with negative metabolic effects related to non-communicable diseases. However, this relationship continues to be a controversial topic and further studies are needed. The aim of this st...

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Published inInternational journal of environmental health research Vol. 31; no. 6; pp. 651 - 669
Main Authors Plazas Guerrero, Carolina Gabriela, Acosta Cota, Selene De Jesús, Castro Sánchez, Francisco Humberto, Vergara Jiménez, Marcela De Jesús, Ríos Burgueño, Efrén Rafael, Sarmiento Sánchez, Juan Ignacio, Picos Corrales, Lorenzo Antonio, Osuna Martínez, Ulises
Format Journal Article
LanguageEnglish
Published England Taylor & Francis 01.09.2021
Taylor & Francis LLC
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Summary:Overconsumption of sucrose, the main contributor of the total added sugar intake in the world, has been associated with negative metabolic effects related to non-communicable diseases. However, this relationship continues to be a controversial topic and further studies are needed. The aim of this study was to evaluate the sucrose-enriched diet consumption in the development of risk factors associated with type 2 diabetes, atherosclerosis and non-alcoholic fatty liver disease in a murine model. Sucrose-enriched diet-fed rats showed a decrease in food, lipids and protein intake as well as in serum total cholesterol levels, an increase in carbohydrates intake, glucose, insulin, triglycerides, VLDL-c and HDL-c levels and a greater degree of insulin resistance, steatosis and non-alcoholic steatohepatitis. Our results show that sucrose-enriched diet consumption during 25 weeks contribute to the development of risk factors associated with type 2 diabetes, atherosclerosis and non-alcoholic fatty liver disease in male Wistar rats.
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ISSN:0960-3123
1369-1619
DOI:10.1080/09603123.2019.1680817