http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Anna Han,Natalie Bennett,Amber Macdonald,Megan Johnstone,Bettaieb Ahmed,Jay Whelan,Dallas R. Donohoe 한국식품영양과학회 2021 한국식품영양과학회 학술대회발표집 Vol.2021 No.10
Butyrate comes from the bacterial fermentation of dietary fiber in the colon. Butyrate is the primary energy source of the colonocytes and plays an epigenetic role in the colonocytes as a histone deacetylase inhibitor (HDACi). We aimed to understand butyrate oxidation and regulatory mechanisms, influencing butyrate oxidation in cancerous colonocytes. Butyrate oxidation was measured as oxygen consumption rate by Seahorse Analyzer. Normal colonocytes showed a significantly higher butyrate oxidation ability compared to cancerous colonocytes (HCT116). Decreased butyrate oxidation of cancerous colonocytes resulted from pyruvate dehydrogenase (PDH) complex inactivation. PDH kinase inhibitor (dichloroacetate, DCA) significantly increased butyrate oxidation in HCT116 compared to those without DCA. DCA also markedly increased OCNT2 and CPT1A expressions that are necessary to carnitine-dependent butyrate oxidation. Additionally, butyrate decreased its own oxidation in HCT116 by suppressing short chain acyl-CoA dehydrogenase (SCAD) expression as an HDACi. These observations offer insight into butyrate’s selective effect against colorectal cancer cells.