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• W2561492009 abstract "Background and Aims . Angiotensin converting enzyme 2 (ACE2) is an important component of the renin-angiotensin system. Since angiotensin peptides have been shown to be involved in hepatic steatosis, we aimed to evaluate the hepatic lipid profile in ACE2-deficient (ACE<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M1><mml:mrow><mml:msup><mml:mrow><mml:mn mathvariant=normal>2</mml:mn></mml:mrow><mml:mrow><mml:mo>-</mml:mo><mml:mo>/</mml:mo><mml:mi mathvariant=normal>y</mml:mi></mml:mrow></mml:msup></mml:mrow></mml:math>) mice. Methods . Male C57BL/6 and ACE<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M2><mml:mrow><mml:msup><mml:mrow><mml:mn mathvariant=normal>2</mml:mn></mml:mrow><mml:mrow><mml:mo>-</mml:mo><mml:mo>/</mml:mo><mml:mi mathvariant=normal>y</mml:mi></mml:mrow></mml:msup></mml:mrow></mml:math>mice were analyzed at the age of 3 and 6 months for alterations in the lipid profiles of plasma, faeces, and liver and for hepatic steatosis. Results . ACE<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M3><mml:mrow><mml:msup><mml:mrow><mml:mn mathvariant=normal>2</mml:mn></mml:mrow><mml:mrow><mml:mo>-</mml:mo><mml:mo>/</mml:mo><mml:mi mathvariant=normal>y</mml:mi></mml:mrow></mml:msup></mml:mrow></mml:math>mice showed lower body weight and white adipose tissue at all ages investigated. Moreover, these mice had lower levels of cholesterol, triglycerides, and nonesterified fatty acids in plasma. Strikingly, ACE<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M4><mml:mrow><mml:msup><mml:mrow><mml:mn mathvariant=normal>2</mml:mn></mml:mrow><mml:mrow><mml:mo>-</mml:mo><mml:mo>/</mml:mo><mml:mi mathvariant=normal>y</mml:mi></mml:mrow></mml:msup></mml:mrow></mml:math>mice showed high deposition of lipids in the liver. Expression of CD36, a protein involved in the uptake of triglycerides in liver, was increased in ACE<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M5><mml:mrow><mml:msup><mml:mrow><mml:mn mathvariant=normal>2</mml:mn></mml:mrow><mml:mrow><mml:mo>-</mml:mo><mml:mo>/</mml:mo><mml:mi mathvariant=normal>y</mml:mi></mml:mrow></mml:msup></mml:mrow></mml:math>mice. Concurrently, these mice exhibited an increase in hepatic oxidative stress, evidenced by increased lipid peroxidation and expression of uncoupling protein 2, and downregulation of sirtuin 1. ACE<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M6><mml:mrow><mml:msup><mml:mrow><mml:mn mathvariant=normal>2</mml:mn></mml:mrow><mml:mrow><mml:mo>-</mml:mo><mml:mo>/</mml:mo><mml:mi mathvariant=normal>y</mml:mi></mml:mrow></mml:msup></mml:mrow></mml:math>mice also showed impairments in glucose metabolism and insulin signaling in the liver. Conclusions . Deletion of ACE2 causes CD36/sirtuin 1 axis impairment and thereby interferes with lipid homeostasis, leading to lipodystrophy and steatosis." @default.
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• W2561492009 date "2016-01-01" @default.
• W2561492009 modified "2023-10-17" @default.
• W2561492009 title "CD36/Sirtuin 1 Axis Impairment Contributes to Hepatic Steatosis in ACE2-Deficient Mice" @default.
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• W2561492009 doi "https://doi.org/10.1155/2016/6487509" @default.
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