Fig. 5: ECHA acetylation decreases fatty acid β-oxidation.

a Acetylation levels of endogenous ECHA in rat islets treated with 3.3 mM (LG) and 16.7 mM glucose (HG). b Oxidation consumption rate (OCR) of palmitate was measured after rat islets were treated with 3.3 or 16.7 mM glucose for 6 h. c Acetylation levels of endogenous ECHA in rat islets treated with or without deacetylase inhibitors TSA plus NAM. d Detection of acetylation levels of ectopically expressed ECHA in HEK293T cells treated with or without NAM. e Flag-tagged wild type, K644K505Q (2 K/Q), and K644K505R (2 K/R) ECHA were overexpressed in HEK293T cells and acetylation levels were detected. f OCR of palmitate was measured after wild type, 2 K/Q, and 2 K/R ECHA were overexpressed in HEK293T cells. g Wild type and 2 K/Q ECHA were ectopically expressed in HEK293T cells and OCR was measured in the presence of palmitate–BSA or BSA control. Arrows indicate the time of addition for oligomycin, FCCP and rotenone/antimycin A. h Determination of basal and maximal respiration due to the utilization of exogenous palmitate in g. Data are expressed as mean ± SEM of at least three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001 vs. control (CON or WT)