New Insight on Adipose Tissue Function in Advanced Renal Failure.
In contrast, few adipokines act as anti-inflammatory agents and could be protective against the
metabolic complications. Obesity could induce kidney disease through disrupting the balance
between protective such as adiponectin and pathologic such as TNF-α adipokines. The changes of the adipokines’ levels such as leptin, adiponectin, visfatin, resistin, IL-6 and TNF-α could
result in the reduction of Glomerular Filtration Rate (GFR) and increasing albuminuria, which
are among the major pathophysiological mechanisms in CKD. Although the exact mechanism
of adipokines’ action is still unclear, they may play their role by affecting various types of cells
in kidney nephrons. Previous studies have shown that increased levels of leptin could lead to
hypertrophy in glomerular mesangial cells that could activate fibrotic and inflammatory pathways, and also thickening of the basement membrane and consequently glomerulosclerosis. Moreover, it has been demonstrated that hyperleptinemia could alter the metabolic function of proximal tubular cells and lead to tubular apoptosis.
Regardless of the roles of adipocytokine in the pathophysiology of renal diseases, the gene expression and circulating levels of these peptides change significantly along with disease progression, particularly in ESRD and dialysis therapy. Considering the multiple effects of adipocytokines, their alterations may have considerable biologic, metabolic, and clinical outcomes, which are not well studied in uremic conditions so far. Moreover, with the identification of new adipokines including Zinc alpha-2 glycoprotein (ZAG), apelin, lipocalin, adiploin, etc. investigating their probable roles in different metabolic aspects of advanced kidney insufficiencies are of major importance.
Obes Res Open J. 2015; 2(1): e5-e7.doi: 10.17140/OROJ-2-e002
