Fig 2: The effect of 120 min of hyper insulin stimulation on protein abundance of ATGL (delta value, arbitrary units) in abdominal (A) and femoral (B) adipose tissue in pre- and post-menopausal women before and after 3 months of high-intensity training. Insulin stimulation suppressed ATGL in femoral subcutaneous adipose tissue in pre- but not in post-menopausal women. Difference between groups *p = 0.05. Data are presented as mean (95% confidence limits). ATGL, Adipose triglyceride lipase.

Fig 3: Heterozygous deletion of the ß-catenin leads to the inhibition of triacylglycerols (TAG) hydrolysis in the hearts of trained and untrained WT/CKO mice. (A) Thin layer chromatography of lipids extracted from LV from WT/WT and WT/CKO mice in sedentary conditions (Control) and after the endurance training (Training). (B) Densitometry of TAG. (C) Densitometry of diacylglycerols (DAG). (D) Densitometry of free fatty acids (FFA). (E) Western blot of ATGL, ABHD5, G0S2, pHSL at Ser563, pHSL at Ser565, total HSL, and in LV lysates from WT/WT and WT/CKO mice in sedentary conditions (Control) and after the endurance training (Training). (F) Densitometry of ATGL protein normalized to GAPDH. (G) Densitometry of G0S2 protein normalized to GAPDH. (H) Densitometry of ABHD5 protein normalized to Gapdh; (I) Densitometry of HSL protein normalized to GAPDH. (J) Densitometry of pHSL at Ser563 normalized to total HSL. (K) Densitometry of pHSL at Ser565 normalized to total HSL. (L) Densitometry of CD36 protein normalized to GAPDH. The data are expressed as the mean ± SD of arbitrary fold of change relative to control levels. n = 5/group. * p < 0.05, ** p < 0.01 (Kruskal–Wallis test followed by Dunn’s multiple-comparison post hoc test).

Fig 4: siRNA-mediated knockdown of ATGL and HSL in 3T3-L1 adipocytes. a Representative immunoblots of ATGL and HSL knockdown in 3T3-L1 adipocytes. Image is representative of six independent experiments. b NEFA secretion and c TAG content in 3T3-L1 adipocytes electroporated with either non-targeting (control) or LIPE (HSL) and PNPLA2 (ATGL) siRNAs (four independent experiments performed in triplicate). d Transfer of adipocyte-derived 3H-fatty acids to MCF-7 and MDA-MB-231 cells (three independent experiments performed in duplicate). e MDA-MB-231 and f MCF-7 cell proliferation co-cultured with or without ATGL/HSL knockdown 3T3-L1 adipocytes (three independent experiments performed in quadruplicate). g, h Migration of MDA-MB-231 cells co-cultured with or without ATGL/HSL knockdown 3T3-L1 adipocytes (three independent experiments performed in quadruplicate). Data are means and SEM. b–d *P < 0.05 compared to control siRNA with Student’s t test. e–g *P = 0.05 vs. basal media, #P = 0.05 compared to ATGL and HSL KD by two-way ANOVA repeated measures followed by Tukey’s multiple comparisons test and h *P = 0.05 vs. basal media by one-way ANOVA followed by Tukey’s multiple comparisons test

Fig 5: PLIN5 relates to oxidative capacity in mouse and human skeletal muscle.Representative blots (A) and quantification of PLIN5 (B) and ATGL (C) protein content in different mouse skeletal muscles (n = 5) (EDL: extensor digitorum longus, TA: tibialis anterior, Sol: soleus). **p < 0.01, ***p < 0.001 versus EDL. (D) Quantification of PLIN5 protein content in vastus lateralis muscle of healthy lean and endurance-trained volunteers (n = 11 per group). Correlations between muscle PLIN5 protein and (E) cytochrome oxidase activity, and (F) glucose disposal rate (n = 33). *p < 0.05 versus lean.