Fig. 2: ARSA expression and secretion in humans with NAFLD/NASH and type 2 diabetes. | Nature Communications

Fig. 2: ARSA expression and secretion in humans with NAFLD/NASH and type 2 diabetes.

From: Deep proteomic profiling unveils arylsulfatase A as a non-alcoholic steatohepatitis inducible hepatokine and regulator of glycemic control

Fig. 2: ARSA expression and secretion in humans with NAFLD/NASH and type 2 diabetes.

a ARSA mRNA expression in patients grouped by no adverse pathology (i.e., No NAFLD, n = 17, white bar), NAFL (n = 66, light-blue bar) or NASH (n = 43, dark-blue bar). *P = 0.047 No NAFLD vs. NASH. bd ARSA secretion from precision-cut liver slices in patients grouped by (b) No NAFLD (n = 24, white bar), NAFL (n = 58, light-blue bar) or NASH (n = 10, dark-blue bar). *P = 0.016 No NAFLD vs. NAFL, P = 0.064 No NAFLD vs NASH. c steatosis score (0, n = 24; 1, n = 39; ≥2, n = 31), P = 0.112 score 0 vs. score 1, *P = 0.022 score 0 vs. score >2. d type 2 diabetes status (no diabetes n = 23, white bar; diabetes n = 24, blue bar), *P = 0.047 no diabetes vs. diabetes. e Plasma ARSA in insulin-sensitive chow-fed mice (white bar) and age-matched obese insulin-resistant mice fed a high-fat diet for 8 weeks (blue bar) (n = 6/group), *P = 0.0002. f ARSA secretion from mouse precision-cut liver slices, intact tendon-to-tendon extensor digitorum longus (EDL) and soleus skeletal muscles (combined conditioned media denoted as muscle), precision-cut heart slices, and epididymal and inguinal adipose tissues (n = 4/group). For all panels, data are means ± SEM. *P < 0.05 vs. No NAFLD, no diabetes, insulin-sensitive as assessed by one-way analysis of variance (ANOVA) and Bonferroni post hoc analysis (ac) or two-tailed unpaired t tests (d, e). Source data are provided as a Source Data file. Ep.WAT epididymal white adipose tissue, Ing.WAT inguinal white adipose tissue, NAFL nonalcoholic fatty liver, NAFLD nonalcoholic fatty liver disease, NASH nonalcoholic steatohepatitis.

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