Obesity, Insulin Resistance, and Renal Function
Article first published online: 26 JAN 2010
Volume 14, Issue 4-5, pages 349–362, June-July 2007
How to Cite
Knight, S. F. and Imig, J. D. (2007), Obesity, Insulin Resistance, and Renal Function. Microcirculation, 14: 349–362. doi: 10.1080/10739680701283018
- Issue published online: 26 JAN 2010
- Article first published online: 26 JAN 2010
- Received 26 January 2007; accepted 1 February 2007.
- insulin resistance;
- renal disease;
- Type 2 diabetes
There is a growing body of evidence indicating that obesity and insulin resistance contribute to the progression of renal disease. A low-grade inflammatory response occurs in obesity and insulin resistance that causes an increase in macrophage infiltration into the adipose tissue and the kidney. The infiltration of macrophages gives rise to the production of an array of pro-inflammatory cytokines and downstream elements such as interleukin-6, NFκB, and cellular adhesion molecules. In addition, increased adiposity triggers the release of adipokines such as leptin that can cause vascular remodeling and disruption of renal function. Insulin resistance can alter the balance between endogenous vasoactive molecules such as nitric oxide and reactive oxygen species, resulting in altered renal endothelial function. Moreover, hyperinsulinemia has direct renal effects such as induced relaxation of the afferent arteriole, resulting in glomerular hyperfiltration and renal damage. High insulin levels also stimulate angiogenesis and mesangial cell proliferation, associated with the development of diabetic nephropathy. Current evidence indicates a direct link between increased adiposity and insulin resistance with renal vascular injury; however, further investigation into the renal microvascular effects of obesity and insulin resistance are required to better understand this disease process.