Fig. 1: Glucagon and Gcgr were elevated in DKD mice.
From: Prolonged glucagon exposure rewires lipid oxidation and drives diabetic kidney disease progression
a Serum glucagon levels in 15-week-old male db/db mice at different time points. b Schematic of UniX-HFD/STZ-induced DKD mouse model: 6-week-old male C57BL6/J mice received HFD for 4 weeks, followed by uninephrectomy, then STZ injection to induce diabetes after 2-week recovery. c Serum glucagon levels in control and DKD mice (16 weeks post-STZ injection). d, e Gcgr protein levels in liver, muscle, eWAT, and kidney of 8-week-old male mice on normal chow. f, g Western blot analysis of renal Gcgr in DKD mice (8 weeks post-STZ). h Co-immunofluorescence of Gcgr with renal cell markers (AQP1 for proximal tubule, LTL for proximal tubules, calbindin-D28K for distal tubules, α-SMA for mesangial cell and podocin for podocytes) in the normal chow-fed C57BL6/J mice (male, 8-week-old). Scale bar: 50 μm. i Schematic of glucagon injection protocol: 300 nmol/kg glucagon i.p. twice daily for 2 weeks starting 1 week after STZ. j–n Serum glucagon, UACR, urine Kim-1 (normalized to creatinine), 24-h urine volume, and kidney weight/body weight ratio. Samples were collected after 2 weeks of glucagon injections. The error bars represent the SEMs; n = 3–6 in each group (a, c–g) and 5-12 in each group (j–n). UniX, uninephrectomized; HFD, high-fat diet; STZ, streptozotocin; UACR, urinary albumin-to-creatinine ratio; Kim-1, kidney injury molecule-1.
