Fig. 7: GCGR mAb treatment improved DKD.
From: Prolonged glucagon exposure rewires lipid oxidation and drives diabetic kidney disease progression
a GCGR mAb treatment protocol for DKD mice: modeled as in Fig. 1b, 5 mg/kg GCGR mAb i.p. injected for 5 week starting 4 week post-STZ, sacrificed 5 week later. b–c Renal p-Creb/total Creb by western blot. d–g UACR, 24-h urine volume, urine Kim-1/NAG/creatinine in the indicated groups of mice. h–j TG and TC levels in the kidney cortex and serum of mice in the indicated groups. k Kidney H&E/Oil Red O staining. Scale bar: black, 100 μm; yellow, 500 μm. l–n qRT‒PCR analyses of the key genes related to lipogenesis, fatty acid oxidation, and lipid transport. o Renal Masson/Sirius red/PAS staining. Scale bar: 100 μm. p Western blot and quantification of Collagen I in the kidneys. q TEM analyses of kidney glomeruli and proximal tubules in the kidney cortex. Scale bar: white, 2 μm; red, 5 μm. r-sGBM width and number of mitochondria. t–v Renal p-mTORC1/p-S6 levels. w GCGR mAb protocol for type 1 diabetic DKD rats: 6-week-old male Sprague‒Dawley rats were intraperitoneally injected with 65 mg/kg STZ, and 4 weeks after STZ injection, 5 mg/kg GCGR Ab was i.p. injected once a week for 7 weeks. x Urine protein levels in rats in the different groups. y–z Serum creatine and BUN levels in rats in the different groups. Mice were male and sampled after 5 weeks of GCGR mAb injection (b–v), and rats were male and sampled after 7 weeks of GCGR mAb injection (x–z). The error bars represent the SEMs; n = 4-10 in each group (d–j, l–n, s, x–z); n = 3 in each group (b, c, p, s–v). BUN, blood urea nitrogen.
