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The protective roles of GLP-1R signaling in diabetic nephropathy: possible mechanism and therapeutic potential.
TLDR
GLP-1 has a crucial role in protection against increased renal oxidative stress under chronic hyperglycemia, by inhibition of NAD(P)H oxidase, a major source of superoxide, and by cAMP-PKA pathway activation.
Reduction of renal superoxide dismutase in progressive diabetic nephropathy.
TLDR
Down-regulation of renal SOD1 and SOD3 may play a key role in the pathogenesis of DN, as observed in the kidneys of diabetic mouse models that exhibit comparable levels of hyperglycemia but different susceptibility to DN.
Urinary adiponectin excretion is increased in patients with overt diabetic nephropathy.
Effects of antidiabetic treatment with metformin and insulin on serum and adipose tissue adiponectin levels in db/db mice.
TLDR
The results suggest that adiponectin synthesis in adipose tissue may be suppressed under hyperinsulinemic state sustained by insulin treatment, even though hyperglycemia is markedly reduced.
Modulation of renal superoxide dismutase by telmisartan therapy in C57BL/6-Ins2Akita diabetic mice
TLDR
It is suggested that NAD(P)H oxidase negatively regulates renal SOD, possibly by downregulation of Nrf2, and that telmisartan could upregulate renal S OD by the suppression of NAD(H) oxidase and subsequent up regulation of NRF2, leading to the amelioration of renal oxidative stress and diabetic renal changes.
Increased Urinary Excretion of Monocyte Chemoattractant Protein-1 in Proteinuric Renal Diseases
TLDR
It is suggested that heavy proteinuria, itself, probably aggravates renal tubular damage and accelerates the disease progression in diabetic nephropathy by increasing the MCP-1 expression in renal tubuli, irrespective of the types of renal disease.
Effect of metformin on adipose tissue resistin expression in db/db mice.
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