Chonnam Med J.  2011 Dec;47(3):139-143. 10.4068/cmj.2011.47.3.139.

The Role of Visfatin in Diabetic Nephropathy

• Kang YS
• Cha DR

• KMID: 2172221
• DOI: http://doi.org/10.4068/cmj.2011.47.3.139

Abstract

As a result of the energy overload in obesity, insulin resistance, type 2 diabetes, dyslipidemia, hypertension, and atherosclerosis develop, which together comprise the metabolic syndrome. Although the kidney becomes a victim of hyperglycemia in diabetes mellitus, recent work has shown that the abnormalities of lipid and glucose metabolism in the kidney are similarly important to those in adipose tissue. Interestingly, obesity triggers the release of adipokines such as leptin, resistin, and visfatin, and these can then be associated with the progression of diabetic nephropathy and other vascular complications. These adipokines, which are also synthesized in the kidney, appear to have an important role in renal injury associated with insulin resistance. Our studies found that visfatin is not only a surrogate marker of systemic inflammation in type 2 diabetic patients but is also up-regulated in diabetic kidney through the uptake of glucose into renal cells, which leads to the activation of the intracellular insulin signaling pathway and pro-inflammatory mechanisms. However, we also observed a beneficial effect of visfatin administration to type 2 diabetic mice. Visfatin injection improved diabetic nephropathy in vivo, in contrast to our previous in vitro study of cultured renal mesangial cells. These results suggest the possibility of multiple cross-talk between adipose tissue and kidney in the metabolic syndrome, particularly in diabetic nephropathy. Further study should be undertaken to understand the role of adipose tissue and kidney as major organs in the metabolic syndrome.

Keyword

Nicotinamide phosphoribosyltransferase; Diabetic nephropathy

MeSH Terms

Adipokines
Adipose Tissue
Animals
Atherosclerosis
Biomarkers
Diabetes Mellitus
Diabetic Nephropathies
Dyslipidemias
Glucose
Humans
Hyperglycemia
Hypertension
Inflammation
Insulin
Insulin Resistance
Kidney
Leptin
Mesangial Cells
Mice
Nicotinamide Phosphoribosyltransferase
Obesity
Resistin
Adipokines
Glucose
Insulin
Leptin
Nicotinamide Phosphoribosyltransferase
Resistin