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Fig. 6 | Microbiome

Fig. 6

From: Commensal microbe-derived acetate suppresses NAFLD/NASH development via hepatic FFAR2 signalling in mice

Fig. 6

FFAR2 signalling play key roles in hepatic insulin signalling and NAFLD/NASH development. Impairment in the FFAR2-induced enhancement of insulin signalling exacerbates insulin resistance in the liver but not in the adipose tissue or muscle. a Oral glucose tolerance testing performed in WT and Ffar2−/− mice fed an HFC diet for 19 weeks (WT, n = 6; Ffar2−/−, n = 7). b HOMA-IR was calculated according to the following formula: HOMA-IR = {[fasting insulin (mU/ml) − fasting glucose (mg/dl)]/405} (WT, n = 6; Ffar2−/−, n = 7). c Pyruvate tolerance testing performed in WT and Ffar2/− mice fed an HFC diet for 20 weeks (WT, n = 6; Ffar2−/−, n = 7). d Insulin-stimulated Akt phosphorylation at Ser473 in the liver, muscle and epididymal fat of Ffar2−/− mice fed an HFC diet, after 6 h of fasting (n = 3 each). e Adenovirus-mediated Ffar2 knockdown in the liver increases insulin resistance and triglyceride accumulation in the liver. Male 8-week-old C57BL/6 mice were administered with a control or Ffar2 shRNA adenovirus (Control, n = 8; shFFAR2, n = 7) and were fed an HFC diet for 4 weeks. Pyruvate tolerance testing performed after 16 h of fasting. f Liver triglyceride. g Liver cholesterol. Data represent mean ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001 (unpaired Student’s t test)

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