Key result
Akt1 deficiency prevented hyperhexosemia-induced upregulation of extracellular matrix proteins and activation of NF-kappaB and AP-1 in the retina, heart, and kidney of galactose-fed mice.
Why the study?
Does Akt1 deficiency prevent hyperhexosemia-induced extracellular matrix protein synthesis and deposition in organs affected by chronic diabetic complications?
Population
Akt1/PKBalpha knockout mice and wild-type control littermates
Comparison
30% galactose feeding to induce hyperhexosemia… vs Wild-type control littermates subjected to the…
Design
Preclinical
Follow-up
8 weeks
Authors
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Akt1 inhibition may merit exploration in diabetic complications; leaves open human translation and requires prospective validation.
Does Akt1 deficiency prevent hyperhexosemia-induced extracellular matrix protein synthesis and deposition in organs affected by chronic diabetic complications?
Akt1 activation is a key mechanism mediating hyperhexosemia-induced extracellular matrix protein synthesis and deposition in organs affected by diabetic complications.
Xin et al. (2007) studied Hyperhexosemia and chronic diabetic complications. Akt1/PKBalpha knockout vs. Wild-type control littermates was evaluated on Extracellular matrix protein production and NF-kappaB/AP-1 activation. Akt1 deficiency prevented hyperhexosemia-induced upregulation of extracellular matrix proteins and activation of NF-kappaB and AP-1 in the retina, heart, and kidney of galactose-fed mice.
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