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. 2022 Mar 8;7(5):e155260. doi: 10.1172/jci.insight.155260

Figure 1. PPKM2Tg mice were resistant to diabetes-induced kidney injury.

Figure 1

(A) Schema of PPKM2Tg mice generation. The complete mouse cDNA sequence of PKM2 (1.6 kb) was inserted to mouse Nphs2 promoter (1.1 kb) constructor. (B–D) Western blotting of PKM2, PKM1, podocyte marker (nephrin, podocin), and proximal tubule marker AQP1 in glomeruli, tubule, and cortex of PPKM2Tg and WT mice (n = 3 per group, *P < 0.05 versus WT). (B) Representative image. (C and D) Quantification of data. (E) PK activity in glomeruli, tubule, and cortex of PPKM2Tg and WT mice. (WT [n = 4], PPKM2Tg [n = 3]; *P < 0.05 versus WT). (F) Schema of prevention study designed using STZ-induced diabetic WT (WT 7MSTZ) or PPKM2Tg mice (Tg 7MSTZ). Mice were given 5 consecutive days of i.p. injections of 50 mg streptozotocin (STZ)/kg body weight (50 mg/kg) or vehicle at age of 8 weeks, and they were harvested after 7 months since diabetes onset. (G) Fasting blood glucose 7 months after STZ. (H) Kidney weight/body weight ratio 7 months after STZ. (I) Albumin creatinine ratio 7 months after STZ. Nondiabetic WT mice (n = 3); PPKM2Tg mice (n = 3); WT 7MSTZ mice (n = 6); Tg 7MSTZ mice (n = 6). *P < 0.05; **P < 0.01. Data are mean ± SEM, 2-way ANOVA followed by correction for multiple comparison.