Diabetic kidney disease (DKD) is the most common cause of severe renal disease, and few treatment options are available today that prevent the progressive loss of renal function. DKD is characterized by altered glomerular filtration and proteinuria. A common observation in DKD is the presence of renal steatosis, but the mechanisms underlying this observation and to what extent they contribute to disease progression are unknown.
Vascular endothelial growth factor B (VEGF-B) has been shown to control muscle lipid accumulation through regulation of trans-endothelial fatty acid transport (Hagberg et al., 2012). VEGF-B expression is under control of PGC1α, a regulator of mitochondrial energy metabolism and ERR-α, the estrogen-related receptor α (Mehlem et al., 2016). In experimental mouse models of DKD (db/db mice) renal VEGF-B expression correlates with the severity of disease. Inhibiting VEGF-B signalling in DKD mouse models, either by Vegfb gene deletion in db/db mice or targeting VEGF-B with an antagonist antibody in db/db, high fat diet and streptozotocin treated mice, reduces renal lipotoxicity, re-sensitizes podocytes to insulin signalling, inhibits the development of DKD-associated pathologies (glomerular mesangial expansion, glomerular sclerosis and podocyte loss), and prevents renal dysfunction (Falkevall et al., 2017). Elevated VEGF-B levels are found in the glomeruli of patients with DKD, suggesting that VEGF-B antagonism represents a novel approach to treat DKD.