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Lipid Metabolic Disorders and Liver Steatosis in DOCA-Salt Hypertensive Mice | OMICS International| Abstract

Journal of Diabetes & Clinical Practice
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  • Perspective   
  • JDCE,
  • DOI: 10.4172/jdce.1000169

Lipid Metabolic Disorders and Liver Steatosis in DOCA-Salt Hypertensive Mice

Yan Wang*
Department of Internal Medicine, University of Utah and Salt Lake Veterans Affairs Medical Center, US
*Corresponding Author : Yan Wang, Department of Internal Medicine, University of Utah and Salt Lake Veterans Affairs Medical Center, US, Email: Yanwang90@gmail.com

Received Date: Nov 01, 2022 / Accepted Date: Nov 30, 2022 / Published Date: Nov 30, 2022

Abstract

Endogenous ligands for peroxisome proliferator-activated receptors include nitrooleic acid. The goal of the current investigation was to examine the therapeutic effects of OA-NO2 on lipid metabolism and hepatic steatosis in a mouse model of hypertension caused by deoxycorticosterone acetate salt. Male C57BL/6 mice were separated into two groups: one group got neither DOCA-salt nor OA-NO2, and the other received neither DOCA-salt nor OA-NO2 (control group). The hypertension was detected after a 3-week course of therapy with DOCA-salt + 1% sodium chloride in drinking water; however, OA-NO2 had no impact on the hypertension. Plasma triglyceride and total cholesterol levels in DOCA-salt-treated animals were considerably higher than those in control mice, but these parameters were markedly decreased after pretreatment with OA-NO2. Additionally, the histology of the liver showed increased lipid distribution along with more severe micro- and following DOCA-salt therapy, there was macro vesicular steatosis, which was consistent with the level of triglycerides and non-esterified fatty acids in the liver tissue.

Citation: Wang Y (2022) Lipid Metabolic Disorders and Liver Steatosis in DOCASalt Hypertensive Mice. J Diabetes Clin Prac 5: 169. Doi: 10.4172/jdce.1000169

Copyright: © 2022 Wang Y. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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