Key result
Streptozotocin-induced diabetes significantly reduced renal tissue levels of active kallikrein compared to controls (25.6 vs 54.7 ng/mg protein, p<0.001), which was reversed by insulin treatment.
Why the study?
Does insulin treatment normalize renal kallikrein synthesis and activation in STZ-induced diabetic rats?
Population
Male Sprague-Dawley rats weighing 185-220 g, including streptozotocin-induced diabetic rats and nondiabetic…
Comparison
Insulin treatment. vs Untreated STZ-diabetic rats and vehicle-injected…
Design
Preclinical
Follow-up
up to 14 days
Authors
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Insulin may modulate renal kallikrein in diabetic models; leaves open translation to human nephropathy.
Does insulin treatment normalize renal kallikrein synthesis and activation in STZ-induced diabetic rats?
Absolute Event Rate: 25.6% vs 54.7%
p-value: p=<0.001
Insulin modulates renal kallikrein production and activation, reversing the impairment of renal kallikrein synthesis seen in experimental STZ-induced diabetes.
Jaffa et al. (1987) studied Experimental diabetes. Insulin vs. Untreated diabetic rats or vehicle-treated control rats was evaluated on Renal tissue levels of active kallikrein (ng/mg protein) (p=<0.001). Streptozotocin-induced diabetes significantly reduced renal tissue levels of active kallikrein compared to controls (25.6 vs 54.7 ng/mg protein, p<0.001), which was reversed by insulin treatment.