Fig. 4: Glucagon led to lipid accumulation in the kidney under DKD conditions.
From: Prolonged glucagon exposure rewires lipid oxidation and drives diabetic kidney disease progression
a–d Renal triglyceride (TG, a)/total cholesterol (TC, b) and serum TG (c)/TC (d) levels in Glucagon-injected mouse groups. Renal TG (e)/TC (f) and serum TG (g)/TC (h)/low-density lipoprotein cholesterol (LDL-C, i) levels following renal Gcgr knockdown. j AFADESI-MSI-based spatially resolved lipidomic analysis of kidney tissues from the control, Ctrl shRNA and Gcgr shRNA groups. k The top 10 (ranked by padj) Gene Ontology terms upregulated in the kidneys of mice in the Gcgr shRNA group compared to the Ctrl shRNA group. l Gene set enrichment shows lipid synthesis pathway enrichment and fatty acid oxidation deficiency in Ctrl shRNA vs. Gcgr shRNA kidneys. m-o Renal mRNA expression of lipid biosynthesis/esterification/transport genes (m–n) and fatty acid oxidation genes (o) in different groups. p Immunofluorescence co-localization of LTL (green) with Srebp1/Scd1/Srebp2 (red) in kidney sections. Scale bar: 50 μm. Mice were male and sampled after 2 weeks of glucagon injections (a–d), mice were male and sampled after 8 weeks of STZ injections (e–i, m–o), and mice were male and sampled after 4 weeks of shRNA injections (j–l, p). The error bars represent the SEMs; n = 5–12 in each group (a–i) and 4-9 in each group (m-o). TG, triglyceride; TC, total cholesterol; padj, adjusted p value.
