Tumour necrosis factor-a (TNF-a) pl

Tumour necrosis factor-a (TNF-a) plays a pivotal role in cellular insulin resistance and can
induce insulin resistance in mouse FL83B hepatocytes. Caffeic acid and cinnamic acid were
found to improve glucose uptake in TNF-a-treated insulin-resistant mouse FL83B hepatocytes.
The mechanism of glucose metabolism by caffeic acid and cinnamic acid was further
investigated. The result from Western blot analysis revealed that caffeic acid and cinnamic
acid increased expression of glycogen synthase, whereas the expression of glycogen synthase
kinase and phosphorylation of glycogen synthase at Ser641 in insulin-resistant
mouse hepatocytes was decreased. Caffeic acid and cinnamic acid suppressed the expression
of hepatic nuclear factor-4 in TNF-a-treated mouse FL83B hepatocytes. The activity of
phosphoenolpyruvate carboxykinase was also inhibited. Thus, caffeic acid and cinnamic
acid ameliorated glucose metabolism by promoting glycogenesis and inhibiting gluconeogenesis
in TNF-a-treated insulin-resistant mouse hepatocytes

Hasil (Bahasa Indonesia) 1:

Tumor nekrosis faktor-a (TNF-a) memainkan peran penting dalam resistensi insulin selular dan dapatmenyebabkan resistensi insulin dalam hepatosit mouse FL83B. Asam caffeic dan Asam sinamatditemukan untuk meningkatkan ambilan glukosa oleh hepatosit TNF-a-diperlakukan resistensi insulin mouse FL83B.Mekanisme metabolisme glukosa dengan asam caffeic dan Asam sinamat adalah lebih lanjutdiselidiki. Hasil dari Barat blot analisis menunjukkan bahwa asam caffeic dan cinnamicmasam meningkat ekspresi sintase glikogen, sedangkan ekspresi sintase glikogenkinase dan fosforilasi glikogen sintase di Ser641 di resistensi insulinmouse hepatosit menurun. Asam caffeic dan Asam sinamat ditekan ekspresiensefalopati nuklir faktor-4 di hepatosit TNF-a-diperlakukan mouse FL83B. Aktivitasphosphoenolpyruvate carboxykinase juga dihambat. Dengan demikian, asam caffeic dan cinnamicmetabolisme asam glukosa diperbaiki dengan mempromosikan glycogenesis dan menghambat glukoneogenesisdi TNF-a-diperlakukan resistensi insulin mouse hepatosit