Key result
IGF-1 treatment significantly reduced serum TNF-α levels from 290.00 ng/L to 207.50 ng/L and attenuated myocardial apoptosis, interstitial fibrosis, and oxidative stress in diabetic rats.
Why the study?
Does insulin-like growth factor-1 (IGF-1) improve diabetic cardiomyopathy in a streptozotocin-induced rat model?
Population
24 male Wistar rats injected with streptozotocin to mimic diabetes mellitus
Comparison
Insulin-like growth factor-1 (IGF-1) vs Untreated diabetic rats
Design
Preclinical
Authors
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Should not change clinical practice; hypothesis-generating for IGF-1 in diabetic cardiomyopathy from animal data only.
Does insulin-like growth factor-1 (IGF-1) improve diabetic cardiomyopathy in a streptozotocin-induced rat model?
Absolute Event Rate: 207.5% vs 290%
p-value: p=<0.05
IGF-1 ameliorates the pathophysiological progression of diabetic cardiomyopathy in a rat model by reducing oxidative stress, inflammation, and apoptosis, potentially via the Akt/GSK-3β signaling pathway.
Wang et al. (2016) studied Diabetic cardiomyopathy (n=24). Insulin-like growth factor-1 (IGF-1) vs. Citrate buffer (vehicle) was evaluated on Serum TNF-α levels (p=<0.05). IGF-1 treatment significantly reduced serum TNF-α levels from 290.00 ng/L to 207.50 ng/L and attenuated myocardial apoptosis, interstitial fibrosis, and oxidative stress in diabetic rats.
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