RT Journal Article
T1 Mechanistically different effects of fat and sugar on insulin resistance, hypertension, and gut microbiota in rats.
A1 Ramos-Romero, Sara
A1 Hereu, Mercè
A1 Atienza, Lidia
A1 Casas, Josefina
A1 Jáuregui, Olga
A1 Amézqueta, Susana
A1 Dasilva, Gabriel
A1 Medina, Isabel
A1 Nogués, Maria Rosa
A1 Romeu, Marta
A1 Torres, Josep Lluís
K1 diabetes
K1 hypertension
K1 microbiota
K1 obesity
AB Insulin resistance (IR) and impaired glucose tolerance (IGT) are the first manifestations of diet-induced metabolic alterations leading to Type 2 diabetes, while hypertension is the deadliest risk factor of cardiovascular disease. The roles of dietary fat and fructose in the development of IR, IGT, and hypertension are controversial. We tested the long-term effects of an excess of fat or sucrose (fructose/glucose) on healthy male Wistar-Kyoto (WKY) rats. Fat affects IR and IGT earlier than fructose through low-grade systemic inflammation evidenced by liver inflammatory infiltration, increased levels of plasma IL-6, PGE2, and reduced levels of protective short-chain fatty acids without triggering hypertension. Increased populations of gut Enterobacteriales and Escherichia coli may contribute to systemic inflammation through the generation of lipopolysaccharides. Unlike fat, fructose induces increased levels of diacylglycerols (lipid mediators of IR) in the liver, urine F2-isoprostanes (markers of systemic oxidative stress), and uric acid, and triggers hypertension. Elevated populations of Enterobacteriales and E. coli were only detected in rats given an excess of fructose at the end of the study. Dietary fat and fructose trigger IR and IGT in clearly differentiated ways in WKY rats: early low-grade inflammation and late direct lipid toxicity, respectively; gut microbiota plays a role mainly in fat-induced IR, and hypertension is independent of inflammation-mediated IR. The results provide evidence that suggests that the combination of fat and sugar is potentially more harmful than fat or sugar alone when taken in excess.
YR 2018
FD 2018-01-02
LK http://hdl.handle.net/10668/12031
UL http://hdl.handle.net/10668/12031
LA en
DS RISalud
RD Apr 19, 2025