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. 2019 Jun;189(6):1226–1240. doi: 10.1016/j.ajpath.2019.02.015

Figure 3.

Figure 3

Renal injury induced by the lipolytic product of glyceryl trilinoleate [GTL; ie, linoleic acid (LA)]. A–D:In vivo renal injury induced by linoleic acid. A and B: TUNEL staining in renal tubules of control (CON) mice (A) and those given LA (B). Glomeruli (dashed ovals) were not TUNEL positive. C and D: Quantification of TUNEL-positive cells (C) and serum blood urea nitrogen (BUN) at the time of necropsy (D). E–G: Effect of lipolysis of GTL (600 μmol/L) by pancreatic lysate on injury to the HEK 293 renal cell line. Lipase activity (E), glycerol (F), and lactate dehydrogenase (LDH) leakage (G), measured after the addition of pancreatic lysates (lysate) alone or in the presence of the triglyceride GTL (600 μmol/L). When used, the lipase inhibitor orlistat (ORLI; 50 μmol/L) was added immediately before addition of GTL. All these phenomena, induced in the presence of lysates and GTL, are significantly reduced by orlistat. Lipolysis of GTL is essential to induce injury. Data are expressed as means ± SEM (C–G). n = 6 to 8 mice per group (A–D). ∗P < 0.05, ∗∗∗P < 0.001 versus control; †P < 0.05 versus without orlistat. Scale bars: 100 μm (A and B).