Liver Steatosis is a Component of the Hepatocardiorenal Syndrome Provoked by a High-Lipid Diet and Activation of Ang II Pathways in Rats

Thuany Crisóstomo; Marco A. E. Pardal; Simone A. Herdy; Humberto Muzi-Filho; Debora B. Mello; Rafael Luzes; Adalberto Vieyra

doi:10.20944/preprints202112.0193.v1

How to cite: Crisóstomo, T.; Pardal, M.A.E.; Herdy, S.A.; Muzi-Filho, H.; Mello, D.B.; Luzes, R.; Vieyra, A. Liver Steatosis is a Component of the Hepatocardiorenal Syndrome Provoked by a High-Lipid Diet and Activation of Ang II Pathways in Rats. Preprints 2021, 2021120193. https://doi.org/10.20944/preprints202112.0193.v1 Crisóstomo, T.; Pardal, M.A.E.; Herdy, S.A.; Muzi-Filho, H.; Mello, D.B.; Luzes, R.; Vieyra, A. Liver Steatosis is a Component of the Hepatocardiorenal Syndrome Provoked by a High-Lipid Diet and Activation of Ang II Pathways in Rats. Preprints 2021, 2021120193. https://doi.org/10.20944/preprints202112.0193.v1

Abstract

Overweight/obesity is a growing pandemic nowadays that affects many organs and tissues. We have investigated whether a high-lipid diet provokes an imbalance between type 1 and type 2 angiotensin II (Ang II) receptors signaling, leading to liver alterations associated with previously described cardiovascular and kidney disturbances. Chronic administration of a high-lipid diet can provoke an hepatocardiorenal syndrome as the result of activation of the Ang II→type 1 receptor axis, which is completely counteracted by Ang-(3–4) the allosteric enhancer of the Ang II→type 2 receptor pathway.

Keywords

hyperlipidic diet; overweight rats; non-alcoholic liver steatosis; arterial hypertension; increased renal sodium reabsorption; hepatocardiorenal syndrome

Subject

Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Liver Steatosis is a Component of the Hepatocardiorenal Syndrome Provoked by a High-Lipid Diet and Activation of Ang II Pathways in Rats

Abstract

Keywords

Subject

Comments (0)