Diabetic kidney disease (DKD) is a major complication for diabetic patients.
Adiponectin is an
insulin sensitizer and anti-inflammatory
adipokine and is mainly secreted by adipocytes. Two types of
adiponectin receptors, AdipoR1 and AdipoR2, have been identified. In both type 1 and
type 2 diabetes (T2D) patients with DKD, elevated
adiponectin serum levels have been observed, and
adiponectin serum level is a prognostic factor of
end-stage renal disease.
Renal insufficiency and tubular injury possibly play a contributory role in increases in serum and urinary
adiponectin levels in
diabetic nephropathy by either increasing biodegradation or elimination of
adiponectin in the kidneys, or enhancing production of
adiponectin in adipose tissue. Increases in
adiponectin levels resulted in amelioration of
albuminuria, glomerular
hypertrophy, and reduction of inflammatory response in kidney tissue. The renoprotection of
adiponectin is associated with improvement of the endothelial dysfunction, reduction of oxidative stress, and upregulation of
endothelial nitric oxide synthase expression through activation of
adenosine 5'-monophosphate-activated
protein kinase by AdipoR1 and activation of
peroxisome proliferator-activated receptor (
PPAR)-α signaling pathway by AdipoR2. Several single nucleotide polymorphisms in the AdipoQ gene, including the promoter, are associated with increased risk of the development of T2D and DKD. Renin-angiotensin-aldosterone system blockers,
adiponectin receptor agonists, and
PPAR agonists (e.g.,
tesaglitazar,
thiazolidinediones,
fenofibrate), which increase plasma
adiponectin levels and
adiponectin receptors expression, may be potential therapeutic drugs for the treatment of DKD.