tetano
Editor, Senior Moderator
Sci Rep
. 2020 Jul 2;10(1):10879.
doi: 10.1038/s41598-020-67879-6.
Influenza Virus Infection Affects Insulin Signaling, Fatty Acid-Metabolizing Enzyme Expressions, and the Tricarboxylic Acid Cycle in Mice
Marumi Ohno[SUP] 1 [/SUP], Toshiki Sekiya[SUP] 2 [/SUP], Naoki Nomura[SUP] 1 [/SUP], Taku Ji Daito[SUP] 1 [/SUP], Masashi Shingai[SUP] 1 [/SUP], Hiroshi Kida[SUP] 3 [/SUP]
Affiliations
Abstract
Although the severity of influenza virus infections has been associated with host energy metabolism, the related mechanisms have not yet been clarified. Here we examined the effects of influenza virus infection on host energy metabolism in mice. After infecting mice with intranasal applications of 500 plaque-forming units of A/Puerto Rico/8/34 (H1N1; PR8) virus, the serum levels of most intermediates in the tricarboxylic acid (TCA) cycle and related metabolic pathways were significantly reduced. These data suggest that substrate supply to the TCA cycle is reduced under these conditions, rather than specific metabolic reactions being inhibited. Then, we focused on glucose and fatty acid metabolism that supply substrates to the TCA cycle. Akt phosphorylation following insulin injections was attenuated in the livers of PR8 virus-infected mice. Furthermore, glucose tolerance tests revealed that the PR8 virus-infected mice showed higher blood glucose levels than the vehicle-inoculated control mice. These results suggest that influenza virus infection impairs insulin signaling, which regulates glucose uptake. However, increases in the hepatic expressions of fatty acid-metabolizing enzymes suggest that fatty acids accumulate in liver cells of infected mice. Collectively, our data indicate that influenza virus infection dysregulates host energy metabolism. This line of investigation provides novel insights into the pathogenesis of influenza.
. 2020 Jul 2;10(1):10879.
doi: 10.1038/s41598-020-67879-6.
Influenza Virus Infection Affects Insulin Signaling, Fatty Acid-Metabolizing Enzyme Expressions, and the Tricarboxylic Acid Cycle in Mice
Marumi Ohno[SUP] 1 [/SUP], Toshiki Sekiya[SUP] 2 [/SUP], Naoki Nomura[SUP] 1 [/SUP], Taku Ji Daito[SUP] 1 [/SUP], Masashi Shingai[SUP] 1 [/SUP], Hiroshi Kida[SUP] 3 [/SUP]
Affiliations
- PMID: 32616893
- DOI: 10.1038/s41598-020-67879-6
Abstract
Although the severity of influenza virus infections has been associated with host energy metabolism, the related mechanisms have not yet been clarified. Here we examined the effects of influenza virus infection on host energy metabolism in mice. After infecting mice with intranasal applications of 500 plaque-forming units of A/Puerto Rico/8/34 (H1N1; PR8) virus, the serum levels of most intermediates in the tricarboxylic acid (TCA) cycle and related metabolic pathways were significantly reduced. These data suggest that substrate supply to the TCA cycle is reduced under these conditions, rather than specific metabolic reactions being inhibited. Then, we focused on glucose and fatty acid metabolism that supply substrates to the TCA cycle. Akt phosphorylation following insulin injections was attenuated in the livers of PR8 virus-infected mice. Furthermore, glucose tolerance tests revealed that the PR8 virus-infected mice showed higher blood glucose levels than the vehicle-inoculated control mice. These results suggest that influenza virus infection impairs insulin signaling, which regulates glucose uptake. However, increases in the hepatic expressions of fatty acid-metabolizing enzymes suggest that fatty acids accumulate in liver cells of infected mice. Collectively, our data indicate that influenza virus infection dysregulates host energy metabolism. This line of investigation provides novel insights into the pathogenesis of influenza.