Visceral adipogenesis inhibited by Pref-1 is associated with peritoneal angiogenesis.

Abstract

Studies showed an increased visceral adipose tissue and peritoneal angiogenesis in peritoneal dialysis (PD) patients. However, the relationship between the visceral adipose expands and peritoneal angiogenesis remains unclear. Pref-1 (preadipocyte factor-1) recombinant adeno-associated virus (AAV) and control AAV were constructed. Mice were divided into four groups, mice in control and PD group were injected intraperitoneally with PBS, mice in control-AAV-PD were injected intraperitoneally with plaque-forming unit (PFU) control AAV and mice in pref-1-AAV-PD group were injected with PFU recombinant AAV. Two weeks later, control group was injected intraperitoneally with normal saline while other groups were injected intraperitoneally with 4.25% peritoneal dialysis fluid (PDF). Thirty days later, viscerall adipose tissue was collected and weighed. Pref-1 protein expression was measured by Western blot, and peritoneal permeability was measured by Evans blue. Cluster of differentiation 31(CD31) immunohistochemical staining was used to detect mesenteric blood vessel number, and vascular endothelial growth factor (VEGF) in serum were measured by enzyme-linked immunosorbent assay. Pref-1 protein expression increased in pref-1-AAV-PD group. Visceral adipose expanded in PD and control-AAV-PD group while decreased in pref-1-AAV-PD group, which approves PD fluid enhance visceral adipogensis, and the process could be inhibited by Pref-1 recombinant AAV. The reduction of peritoneal vessel number and the decrease of vascular permeability as well as down-regulation of serum vascular endothelial growth factor observed in pref-1-AAV-PD group suggested peritoneal angiogenesis could be inhibited following visceral adipose tissue reduction. Visceral adipose expands is associated with peritoneal angiogenesis in PD treatment, and prevention of visceral adipogenesis may be an alternative way to protect the validity of peritoneum. Copyright © 2019 John Wiley & Sons, Ltd.