Assessment of lixisenatide-induced nephropathy in chick embryos: Implications for prevention of diabetic kidney disease

TL;DR

This study shows that lixisenatide protects kidneys in a chick embryo model of diabetes, even without improving overall metabolism.

Contribution

The paper demonstrates lixisenatide's direct nephroprotective effects independent of systemic metabolic control.

Findings

Hyperglycemia caused kidney damage in chick embryos, including oxidative stress and inflammation.

Lixisenatide reduced kidney injury markers like MDA, TNF-α, and caspase-3 activity at high doses.

The drug normalized kidney-to-body ratios and preserved renal structure in hyperglycemic embryos.

Abstract

Diabetic kidney disease (DKD) is a major cause of end-stage renal disease and the direct renal effects of GLP-1 receptor agonists
remain underexplored. Using a hyperglycemic chick embryo model (n=120), we evaluated dose-dependent nephroprotective effects of
lixisenatide. Hyperglycemia induced renal hypertrophy, histological injury, oxidative stress, inflammation and apoptosis. Lixisenatide,
particularly at high doses, significantly ameliorated these changes, normalizing kidney-to-body ratios and reducing MDA, TNF-α and
caspase-3 activity. Thus, we show that lixisenatide directly preserves renal structure and function independent of systemic metabolic
control.