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Bioactive peptides control receptor for advanced glycated end product-induced elevation of kidney insulin receptor substrate 2 and reduce albuminuria in diabetic mice. | LitMetric

AI Article Synopsis

Article Abstract

Background/aims: Sixteen-week-old db/db mice exhibit significantly elevated blood glucose and albuminuria. Kidney mesangial cell matrix expansion and collagen IV synthesis correlate with disease progression, but the underlying mechanism is unclear.

Methods: Adaptive biochemical datasets were generated in cultured 293 kidney cells and in db/db mice.

Results: In animals receiving daily subcutaneous bolus injections (weeks 8-13) of 20 microg/day humanin or 40 microg/day protein kinase C (NPKC) (a PKC-beta2 inhibitor peptide), there was a significant reduction in albuminuria, insulin receptor substrate 2 (IRS-2) and phospho-Akt (Ser473) levels in kidney tissue extracts (p < 0.05 in all cases). Elevated IRS-2 (not IRS-1), altered Akt1 and selective phosphorylation of p-Akt/Ser473 and p-IRS-1/Ser307 (but not p-Akt/Thr308 or p-IRS-2/Ser731) are correlates of the receptor for advanced glycated end product activation and are linked to albuminuria in vivo, whereas in P38 peptide-treated animals, collagen IV synthesis can be uncoupled from albuminuria altogether.

Conclusion: Taken together, our results suggest that elevated IRS-2 and altered Akt phosphorylation may be more closely tied to the cause of diabetic kidney disease in db/db mice than mesangial matrix expansion per se, though both may originate from elevated circulatory glucose, and mesangial matrix expansion may independently exacerbate kidney dysfunction.

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http://dx.doi.org/10.1159/000141042DOI Listing

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