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. 2023 Feb 16;42(6):e112202. doi: 10.15252/embj.2022112202

Figure 4. Adipocyte‐specific loss of Atgl was dispensable for regulation of intestinal inflammation.

Figure 4

  1. Schematic of experimental design. DSS‐induced colitis was induced in sex‐matched and age‐matched littermates.
  2. Representative quantification of knockout efficiency measured on Atgl transcript level by qRT‐PCR in purified primary visceral adipocyte (n = 3–8/group).
  3. Ex vivo lipolysis assays on Atg7‐deficient adipose tissue explants simulated with isoproterenol (10 μM) for 1–2 h (n = 5–6/group).
  4. Body weight development upon DSS treatment (n = 8/group).
  5. Tissue weights of mWAT and visWAT on day 7 after start of DSS (n = 3–8/group).
  6. Colon length after DSS on day 7 (n = 3–8/group).
  7. Quantification of histological score at steady state (n = 3/group) and DSS colitis (n = 6–7/group).
  8. Expression of pro‐inflammatory cytokines in colon tissues on 7 days post‐DSS induction (n = 8/group). Dotted line represents noninflamed controls.
  9. Absolute number CD45+ immune cells from colons on 7 days post‐DSS induction (n = 3–8/group).
  10. Frequency of myeloid cell population in colon on day 7 post‐DSS induction (n = 8/group).
  11. Absolute number of Ly6C+ monocytes discriminated by the absence or presence of MHCII for infiltrating and inflammatory monocytes, respectively (n = 8/group).

Data are represented as mean ± s.e.m. (B, E–I, K) Unpaired Student's t‐test. (D) Two‐Way repeated measures ANOVA. (C, J) Two‐Way ANOVA. ****P < 0.0001.

Source data are available online for this figure.