PNPLA2 Antibody - #DF7756

Fig. 4: Decrease of Atgl and Ept1 is an important cause of lipid disorders. A Investigating genetic mechanisms affecting lipid homeostasis through a working model of lipid homeostasis pathways including glycerolipid metabolism and synthesis process. G-3-P glycerol-3-phosphate, LPA lysophosphatidic acid, PA phosphatidic acid, DG diglyceride, TG triglyceride, FFA free fatty acid, Etn ethanolamine, P-Etn phosphoethanolamine, CDP-Etn CDP-ethanolamine, PE phosphatidylethanolamine, LPE lysophosphatidylethanolamine, PC phosphatidylcholine. B Heatmap of genes related to lipid catabolism and synthesis (data obtained from GEO database with an accession number of GSE204986). C Correlation heatmap between total lipid metabolites and genes associated with TG metabolism and PE synthesis (n = 5 per group). D Pearson’s correlation between Atgl expression and TG content, and Pearson’s correlation between Ept1 expression and PE content. E Correlation heatmap between species of TG containing different lengths of fatty acids and genes associated with TG metabolism and PE synthesis. F Pearson’s correlation between Atgl expression and TG(54:7) or PE(48:1) content. G Correlation heatmap between species of PE containing different lengths of fatty acids and genes associated with TG metabolism and PE synthesis. H Pearson’s correlation between Ept1 expression and PE(36:3) or PE(40:7) content. I Correlation heatmap between mice phenotypes and genes associated with TG metabolism and PE synthesis. J Western blot analysis of LXRα, ATGL and EPT1 proteins in mice from group WT Chow, LXRα−/− Chow, WT HFD and LXRα-/− HFD (n = 3 per group). Data are presented as mean ± SD. *P 

Fig. 5. Effects ofL. plantarum Q16 on key proteins involved in hepatic lipid metabolism in HFD-fed obese mice. Data are presented as mean ± SD (n = 6). Different lowercase alphabet letters were significantly different at the level of P < 0.05.

Fig. 6. Oridonin (ORI) protects against hepatic steatosis by restoring lipid homeostasis between triglyceride (TG) and phosphatidylethanolamine (PE) via the LXRα-ATGL/EPT1 pathway. (A) Schematic showing how the ORI affects lipid homeostasis. (B) Representative T1-MRI images showing lipid accumulating contents in livers of WT and LXRα−/− mice induced a high-fat diet (HFD) with or without ORI treatment. (C) Representative in vivo imaging system images of mice after tail vein injection of cy7-labeled phosphoethanolamine. The insert shows representative images of cy7-labeled phosphoethanolamine fluorescence intensity in mice liver, kidney and intestine. Mice livers, kidneys and intestines were collected at 24 h after tail vein injection of cy7-labeled phosphoethanolamine. (D) Representative in vivo imaging system images of mice after tail vein injection of cy7-labeled cholesterol. The insert shows representative images of cy7-labeled cholesterol fluorescence intensity in mice liver. Mice livers were collected at 6 h after tail vein injection of cy7-labeled cholesterol. (E, F) Protein expression of LXRα, ATGL and EPT1 in liver tissues of WT mice after continuously treated with various doses of ORI for 7 days (n = 3). Data are presented as mean ± standard deviation (SD). ∗P < 0.05 and ∗∗P < 0.01 were compared with vehicle group. (G, H) Protein expression of LXRα, and EPT1 in the livers from WT and LXRα−/− mice in the indicated groups. #P < 0.05 and ##P < 0.01 were compared with Chow group; ∗P < 0.05 and ∗∗P < 0.01 were compared with HFD group. TG: triglyceride; DG: diglyceride; P-Etn: phosphoethanolamine; CDP-Etn: CDP-ethanolamine; PE: phosphatidylethanolamine.

Fig. 4 |Metabolic pathway enrichment analysis and lipolysis metabolismrelated protein and mRNA expression. Correlation analysis of 9 metabolites (a); metabolic pathway analysis in MICT versus SED (b);mRNA levels of PPAR-γ, HSL, ATGL, and TNF-α in adipose tissues (c);correlation analysis of 6 metabolites (d); metabolic pathway analysis in HIIT versus SED (e); and contents of PPAR-γ, HSL, ATGL, TNF-α, and P450scc protein (f).