angiotensin-i and Non-alcoholic-Fatty-Liver-Disease

Uganda was affected by two major waves of coronavirus disease 2019 (COVID-19). The first wave during late 2020 and the second wave in late April 2021. This study compared epidemiologic characteristics of hospitalized (HP) and non-hospitalized patients (NHP) with COVID-19 during the two waves of COVID-19 in Uganda.. Wave 1 was defined as November-December 2020, and Wave 2 was defined as April-June 2021. In total, 800 patients were included in this study. Medical record data were collected for HP (200 for each wave). Contact information was retrieved for NHP who had polymerase-chain-reaction-confirmed COVID-19 (200 for each wave) from laboratory records; these patients were interviewed by telephone.. Demographic and epidemiologic characteristics of HP and NHP differed between and within Waves 1 and 2 of COVID-19 in Uganda.

Topics: Angiotensin I; Angiotensin-Converting Enzyme 2; Animals; Anti-Inflammatory Agents; Antioxidants; Biomarkers; Cyprinidae; DNA Damage; Flavonoids; Fresh Water; Fructose; Gills; Insecticides; Non-alcoholic Fatty Liver Disease; Oxidative Stress; Peptide Fragments; Peptidyl-Dipeptidase A; Pyridines; Rats; Receptors, G-Protein-Coupled; Renin-Angiotensin System; Water; Water Pollutants, Chemical

Nonalcoholic fatty liver disease (NAFLD) is the most general liver disease characterized by a continuum of liver abnormalities ranging from simple fatty liver to advanced stage of nonalcoholic steatohepatitis, cirrhosis, and even hepatocellular carcinoma. The pathological drivers of NAFLD are complex and largely undefined. It is increasingly identified that the imbalance between renin-angiotensin system and ACE2/Ang-(1-7)/Mas axis, as well as mitochondrial dysfunction associated with NAFLD. However, no known empirical research has focused on exploring the effect of the regulation of mitochondrial respiration chain activity by Ang-(1-7)/Mas on the prevention of NAFLD. Here, we evaluated the interaction and relevance of hepatic Ang-(1-7)/Mas-axis challenge with glucolipid metabolism and mitochondrial condition in vivo and in vitro. In this context, we found that Mas deletion in mice contributed to the severe glucose intolerance, insulin resistance, and hepatic steatosis which accompanied by elevated levels of serum/ hepatic alanine aminotransferase, aspartate aminotransferase, and triglycerides, as well as the mitochondrial dysfunction. Whereas forced upregulation of Mas or Ang-(1-7) administration could significantly attenuate these consequences by downregulating the expression of hepatic lipogenic proteins and enzymes for gluconeogenesis. Furthermore, activation of Ang-(1-7)/Mas arm could improve the IRS-1/Akt/AMPK pathway and enhance the mitochondrial energy utilization. Considered together, it is becoming extremely hopeful to provide a new perspective for Ang-(1-7)/Mas axis for the therapeutics of NAFLD.

Topics: Angiotensin I; Angiotensin-Converting Enzyme 2; Animals; Cell Line, Tumor; Down-Regulation; Glycolipids; Hep G2 Cells; Humans; Insulin Resistance; Lipid Metabolism; Liver; Male; Mice; Mice, Inbred C57BL; Mitochondria; Non-alcoholic Fatty Liver Disease; Peptide Fragments; Proto-Oncogene Mas; Proto-Oncogene Proteins; Receptors, G-Protein-Coupled; Signal Transduction