Fig. 3: Mat1a antisense oligonucleotides protect from high-fat diet (HFD)-induced hepatosteatosis.

Two-month-old C57BL/6 J mice were fed a chow diet (CD) or a high-fat diet (HFD) for 10 weeks. During the last 4 weeks mice were treated with Mat1a antisense oligonucleotide (ASO) or with control ASO (25 mg/kg/week) until sacrifice. a Representative microphotographs of liver sections stained with Hematoxylin/Eosin (H&E), Sudan III, Sirius Red and F4/80, and liver triglyceride (TG) content, and quantification of Sirius red and F4/80 in CD- (n = 6) and HFD-fed control (n = 7) and Mat1a (n = 8) ASO-treated mice. b Liver fatty acid β-oxidation was determined measuring the amount of [¹⁴C]-acid-soluble metabolites (ASM) (incomplete oxidation of palmitate), [¹⁴C]-CO₂ (complete oxidation of palmitate) and serum ketone bodies levels in HFD-fed control (n = 7 for ketone bodies and n = 7 for β-oxidation) and Mat1a (n = 5 for ketone bodies and n = 8 for β-oxidation) ASO-treated mice. c Liver TG de novo lipogenesis determined by incorporation of [³H]-acetate into TG in HFD-fed control (n = 7) and Mat1a (n = 8) ASO-treated mice liver pieces. d Representative blots and densitometries of acetyl-coenzyme A carboxylase (ACC), fatty acid synthase (FAS) and transferrin, as representative loading control, in liver of HFD-fed control (n = 7) and Mat1a (n = 8) ASO-treated mice. Values are presented as means ± SD. Statistically significant differences between groups are indicated by *p < 0.05, **p < 0.01, and ***p < 0.001 (two-tailed Student’s test). Source data are provided as a Source data file.