Key result
Insulin inhibited high glucose-stimulated ANG gene expression and increased MAPK phosphorylation in normal rat renal proximal tubular cells, but failed to do so in diabetic rat cells.
Population
Male adult Wistar rats (controls and streptozotocin-induced diabetic rats at 2, 4, 8 and 12 weeks post-STZ…
Comparison
Insulin (10(-7) M) in high glucose (25 mM) medium vs Normal glucose (5 mM) medium and normal rat RPTCs
Design
Preclinical
Follow-up
up to 12 weeks post-STZ administration
Authors
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Highlights insulin resistance in diabetic rat renal cells; leaves open MAPK modulation as a human nephropathy target.
Hyperglycemia induces insulin resistance on angiotensinogen gene expression in diabetic rat renal proximal tubular cells by altering the MAPK signal transduction pathway.
Sl et al. (2002) studied Diabetes. Insulin vs. Control (normal rat RPTCs) was evaluated on ANG gene expression, IR-rANG secretion, and p44/42 MAPK phosphorylation. Insulin inhibited high glucose-stimulated ANG gene expression and increased MAPK phosphorylation in normal rat renal proximal tubular cells, but failed to do so in diabetic rat cells.
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