High-Fat Diets and LXRs Expression in Rat Liver and Hypothalamus
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ORIGINAL RESEARCH
High‑Fat Diets and LXRs Expression in Rat Liver and Hypothalamus Mariana Rey1 · María Sol Kruse1 · Rocío Nahimé Magrini‑Huamán1,2,3 · Héctor Coirini1,3,4 Received: 26 February 2019 / Accepted: 25 May 2019 © Springer Science+Business Media, LLC, part of Springer Nature 2019
Abstract Disturbances on lipid metabolism are associated with health disorders. High-fat diets (HFDs) consumption promotes cardiovascular and neurodegenerative diseases where cholesterol plays an important role. Among regulators of this steroid homeostasis, the liver X receptors (LXRs) induce genes that protect cells from cholesterol overload. We previously described how both hypothalamic LXRα and LXRβ are sensitive to a high-fructose diet, suggesting that these receptors trigger responses related to control of energy and food intake. The present work’s main objective was to study the effect of different HFDs on LXRs expression (in hypothalamus and liver), and lipid profile. Male rats received control diet (CD), H FD1 (CD + bovine fat (BF)), H FD2 (CD + BF + cholic acid (CA)), HFD3 (CD + BF + cholesterol), or HFD4 (CD + BF + CA + cholesterol) for different time periods. Hypothalamic LXRβ, both hepatic LXRs subtypes, and total cholesterol (TC) raised after 2 weeks of HFDs. Four and 8 weeks of H FD3 and H FD4 increased the LXRs subtypes in both tissues and TC levels. Only H FD4 reduced triglycerides (TG) levels after 2 and 8 weeks. The TC and TG values correlated significantly with LXRs expression only in rats fed with HFD4. These data add relevant information about how diet composition can produce different scales of hypercholesterolemia states accompanied with central and peripheral changes in the LXRs expression. Keywords High-fat diets · Oxysterols · Cholic acid · Cholesterol · Triglycerides
Introduction Cholesterol homeostasis disturbances are associated with serious health disorders. In fact, it is well known that regular high-fat diets (HFDs) consumption constitutes a risk factor for metabolic, cardiovascular, and neurodegenerative
* Héctor Coirini [email protected] 1
Laboratorio de Neurobiologia, Instituto de Biologia y Medicina Experimental (IBYMECONICET), Vuelta de Obligado 2490, C1428ADN Ciudad Autonoma de Buenos Aires, Buenos Aires, Argentina
2
Facultad de Ingenieria, Instituto de Biotecnologia, Universidad Nacional de San Juan, Av. Libertador Gral. San Martín 1109, J5400ARL San Juan, Argentina
3
Facultad de Ciencias Medicas, Universidad Catolica de Cuyo, Av. José Ignacio de la Roza 1516, Rivadavia, J5400 San Juan, Argentina
4
Departamento de Bioquimica Humana, Facultad de Medicina, Universidad de Buenos Aires, Paraguay 2155, 5to Piso, C1121ABG Ciudad Autonoma de Buenos Aires, Buenos Aires, Argentina
diseases (Cullen 2000; Ghibaudi et al. 2002; Riccioni and Sblendorio 2012; Shanmugasundaram et al. 1986; Sparks et al. 1993). One of the major sites of endogenous cholesterol synthesis is the liver. After a HFDs intake, this organ activates mechanisms to handle the elevated
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