Lupin protein isolate improves insulin sensitivity and steatohepatitis in vivo and modulates the expression of the Fasn, Gys2, and Gsk3b genes

Food Science & Nutrition

Pedro Macedonio García‐López¹  José Alfredo Domínguez‐Rosales²  Irma Catalina Soto‐Luna²  Carmen Magdalena Gurrola‐Díaz²  Tereso Jovany Guzmán²  Belinda Vargas‐Guerrero² 

[1] Departamento de Botánica y Zoología Centro Universitario de Ciencias Biológicas y Agropecuarias Universidad de Guadalajara Zapopan Mexico;Instituto de Investigación en Enfermedades Crónico‐Degenerativas Instituto Transdisciplinar de Investigación e Innovación en Salud Departamento de Biología Molecular y Genómica Centro Universitario de Ciencias de la Salud Universidad de Guadalajara Guadalajara Mexico;

关键词: carbohydrate metabolism;    fatty liver;    high‐fat diet;    insulin resistance;    lipid metabolism;   

DOI  :  10.1002/fsn3.2206

来源: DOAJ

【 摘 要 】

Abstract Although studies on lupin protein isolate (LPI) have indicated the presence of a preventive effect on insulin resistance (IR) and lipid disturbances, their influence on established pathological traits has received little attention. Here, we evaluated the in vivo effects of LPI on IR and steatohepatitis as well as its influence on genes involved in lipid and carbohydrate metabolism. We first induced IR and steatohepatitis in rats by maintaining them on a high‐fat diet for 5 weeks. Thereafter, we administered LPI to the rats daily for 3 weeks. LPI improved insulin sensitivity (AUC: 6,777 ± 232 vs. 4,971 ± 379, p < .05, pre‐ vs. post‐treatment values) and reduced glucose and triglyceride levels by one‐third. In addition, LPI‐treated rats exhibited attenuated steatohepatitis. At the molecular level, LPI treatment reduced liver Fasn gene expression substantially but increased Gys2 and Gsk3b levels. We concluded that the hypolipidemic and hypoglycemic activities of LPI may be caused by reduced liver lipogenesis and modulation of insulin sensitization mechanisms.

【 授权许可】

Unknown