Journal: BMC biology

Article Title: Lipid metabolites affected by deficient autophagy antagonize the occurrence of autophagy through AMPK signaling in insects.

doi: 10.1186/s12915-025-02274-z

Figure Lengend Snippet: Fig. 7 Effects of metabolites on autophagy occurrence in Drosophila fat body and B. mori BmN cells. A and B LysoTracker Red staining (A), western blots and protein quantification of BmAtg8–PE and p-AMPKα (T172) (B) of Drosophila fat body at W stage after treatment with 40 μM LPE(19:0), LPC(0:0/17:0), LPC(0:0/19:0), or LPC(20:0/0:0) for 2 h, individually. C LysoTracker Red staining from nutritious and starved BmN cells after treatment with LPE(19:0), LPC(0:0/17:0), LPC(0:0/19:0), or LPC(20:0/0:0) (40 μM) for 2 h (N, normal nutrient; S, starvation). D-G Western blots and protein quantification of BmAtg8–PE and p-AMPKα (T172) after treatment with 40 μM LPE(19:0) (D), LPC(0:0/17:0) (E), LPC(0:0/19:0) (F), or LPC(20:0/0:0) (G) for 2 h in normal-nutrition and starved BmN cells (S, starvation). The solvent PBS was used as control. Data are presented as means ± SD; P values were determined by unpaired two-tailed Student’s t-test. Significance test was performed between control and each metabolite treatment. *P < 0.05, **P < 0.01, ***P < 0.001. ns, no significant difference

Article Snippet: The primary antibodies for V5 (Cell Signaling Technology, 13202S; 1:3000), FLAG (Cell Signaling Technology, 14793S; 1:3000), HA (Santa Cruz Biotechnology, sc-7392; 1:2000), BmAtg8–PE (Abcam, ab109364; 1:4000), Phospho-AMPKα (Thr172) (Cell Signaling Technology, 50081; 1:3000), and Tubulin (Beyotime Biotechnology, AT819; 1:5000) were used for western blotting according to the standard procedure as previously described [17, 41].

Techniques: Staining, Western Blot, Solvent, Control, Two Tailed Test

Journal: Metabolism: clinical and experimental

Article Title: Serum metabolomics analysis reveals increased lipid catabolism in mildly hyperbilirubinemic Gilbert's syndrome individuals.

doi: 10.1016/j.metabol.2021.154913

Figure Lengend Snippet: Fig. 4. AMPK, PPARα, PGC1α and lipid catabolism. The figure presents the % increase of AMPK, PPARα and PGC-1α measured in PBMCs of GS vs. control individuals, as previously published by Mölzer et al. [22] and correlation coefficients (r) between UCB, AMPK; PPARα and PGC-1 α. The table shows correlations coefficients and p-values of AMPK (blue), PGC1α (orange), PPARα (green) and UCB (yellow) with their downstream lipid metabolites in the whole study population using Pearson or Spearman-Rho. Significant correlations are in bold type, t = trend.

Article Snippet: The following antibody set-up was used: rabbit anti-human monoclonal to AMPK α1 (phos-T183) and AMPKα2 (phos-T172) (ab133448, Abcam) and secondary antibody: goat anti-rabbit IgG H & L AlexaFluor 488 (ab150077, Abcam); rabbit anti-human polyclonal to PgC1α PE-labelled (orb124814, Biorbyt) and rabbit anti-human polyclonal to PPARα (phos-Ser12) FITClabelled (bs-4055R-FITC, Bioss).

Techniques: Control