Adipose Tissue Fibrosis In Perilipin1Null Mice

Background:Adipose tissue has emerged as one of the most important organs regulating metabolic homeostasis. Perilipin1is an abundant adipocyte-specific protein coating on lipid droplets, and it is required for droplet formation and maturation, optimal lipid storage, and lipolysis regulation in adipocytes. Animal studies have shown that perilipin1gene knockout (Plin1-/-) mice have reduced adipose mass and increased basal lipolysis in adipocytes. This study was undertaken to determine the effect of lipodystrophy in adipose tissue on adipose tissue fibrosis in Plin1-/-mice.Methods and Results:Results. HE staining shows that Plin1-/-mice have less adipose mass, the coulor of white adipose tissue shows red and adipocytes of Plin1-/-mice unable to develop mature lipid droplets. Sirius-Red staining shows that extracellular of adipocytes were full of collagen which implying changes in extracellular matrix in adipocytes. Hydroxyproline content testing shows that Plin1-/-mice have elevated collagen content. All evidences show that Plin1-/-mice have adipose tissue fibrosis. To study the pathway of adipose tissue fibrosis,we use western blot to determine the expression of fibrosis-associate protieins TGFbetal p-Smad2/3and one of extracellular matrix component collagen VI. that shown that expression of TGFbetal and p-Smad2/3are elevated but collagen VI is decreased which promoting that TGFbetal pathway may contribute to the developmentof adipose tissue fibrosis.Conclusions:Increased basal lipolysis in adipose tissue lead to lipodystrophy and adipose tissue fibrosis in Plin1-/-mice. Complex interactions of AT metabolizes, ECM and TGF-β pathway may contribute to adipose tissue fibrosis.