Fig. 3.

Evidence for increasing β-oxidation upon addition of various FAs to pancreatic islets A–E) Respiration rates of pancreatic islets (averaged from N = 5) without any addition (gray) and with added 50 μM palmitic acid (30 μM BSA) alone (A); or in the presence of 2.5 μM etomoxir (B) and 10 nM SkQ1 (C). When indicated, 5 μM oligomycin was added. Time window is selected to emphasize PA-induced respiration increase. For examples of complete timing, see Fig. S4 A-C,D,E) Exemplar islet respiration (otherwise N = 3) before and after the addition of 70 μM, lauric (D) and 90 μM, hexanoic acid (E) (both with 30 μM BSA) without and with 2.5 μM etomoxir. G,H) A complete etomoxir blockage of insulin secretion (FASIS) induced with lauric and hexanoic acid, under the same conditions as for panels D and E. H) Unbiased lipidomics of INS-1E cells – a Volcano plot shows statistically significant changes 60 min after the addition of 15 μM palmitic acid (15 μM BSA; N = 6). TG – triglyceride; PC – phosphatidylcholine; PE – phosphatidyletanolamine; PG – phosphatidylglycerol; PI – phosphatidylinositol; SM – sphingomyelin. I) Existence of M + 4¹³C-butyryl-carnitine („C4carn”) and of M + 2¹³C-acetyl-carnitine („C2carn”) in INS-1E cells 60 min after U–¹³C-PA addition (50 μM, 30 μM BSA; n = 3) indicates the ongoing β-oxidation. It was inhibited by 2.5 μM etomoxir. Data multiplied by 100 (i.e. expressed in %) represent calculated ratios of M+4/(M+0 + M+4) and M+2/(M+0 + M+2), respectively.