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Oral Intake of Inosine 5'-Monophosphate (IMP) in Mice Promotes the Absorption of Exogenous Fatty Acids and Their Conversion into Triglycerides though Enhancing the Phosphorylation of AMPK in Liver, leading To Lipohyperplasia
Zhang, B.; Xu, Y.; Liu, J.; Wu, C.; Zhao, X.; Zhou, L.; Xie, Y. Oral Intake of Inosine 5′-Monophosphate in Mice Promotes the Absorption of Exogenous Fatty Acids and Their Conversion into Triglycerides though Enhancing the Phosphorylation of Adenosine 5′-Monophosphate-Activated Protein Kinase in the Liver, Leading to Lipohyperplasia. Int. J. Mol. Sci.2023, 24, 14588.
Zhang, B.; Xu, Y.; Liu, J.; Wu, C.; Zhao, X.; Zhou, L.; Xie, Y. Oral Intake of Inosine 5′-Monophosphate in Mice Promotes the Absorption of Exogenous Fatty Acids and Their Conversion into Triglycerides though Enhancing the Phosphorylation of Adenosine 5′-Monophosphate-Activated Protein Kinase in the Liver, Leading to Lipohyperplasia. Int. J. Mol. Sci. 2023, 24, 14588.
Zhang, B.; Xu, Y.; Liu, J.; Wu, C.; Zhao, X.; Zhou, L.; Xie, Y. Oral Intake of Inosine 5′-Monophosphate in Mice Promotes the Absorption of Exogenous Fatty Acids and Their Conversion into Triglycerides though Enhancing the Phosphorylation of Adenosine 5′-Monophosphate-Activated Protein Kinase in the Liver, Leading to Lipohyperplasia. Int. J. Mol. Sci.2023, 24, 14588.
Zhang, B.; Xu, Y.; Liu, J.; Wu, C.; Zhao, X.; Zhou, L.; Xie, Y. Oral Intake of Inosine 5′-Monophosphate in Mice Promotes the Absorption of Exogenous Fatty Acids and Their Conversion into Triglycerides though Enhancing the Phosphorylation of Adenosine 5′-Monophosphate-Activated Protein Kinase in the Liver, Leading to Lipohyperplasia. Int. J. Mol. Sci. 2023, 24, 14588.
Abstract
Inosine 5'-monophoaphate (IMP) allows animals to sense umami. Intake of IMP in C57/KsJ-db/db (db/db) mice induced lipohyperplasia causing the liver cirrhosis, however, how to that of in normal mammals injure health is still unclear. Thus, we had investigated that intake of IMP in C57BL/6J mice effected its metabolic functions. We found that intake of 255 M/d IMP in C57BL/6J mice for 4 months induced hyperlipidemia and body fat rate raised. In mechanism, the expressions of ACC1 and phosphorylated ACC2 in hepatocytes were increased though IMP promoting phosphorylation of AMPK. The increased ACC1 promoted the conversion of acetyl-CoA into TG. These TG were transported out of hepatocytes to avoid NAFLD, causing a deficiency of acetyl-CoA in liver, and then the increased phosphorylated ACC2 promoted cytoplasm fatty acids into mitochondria to convert into acetyl-CoA though the fatty acids β-oxidation pathway, causing a deficiency of fatty acids. Therefore, liver enhanced the absorption of exogenous fatty acids, which were converted into TG caused lipohyperplasia. Moreover, intake of IMP in normal mice induced complement system weaken in liver causing mild inflammation. Our data not only alerted that humans avoid excessive intake of IMP, but also provided novel insights into the adipose of metabolic dysfunctions.
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