Abstract
The aim of this study was to investigate whether overexpression of STAMP2 improves insulin resistance by regulating angiogenesis in adipose tissues. The characteristics of diabetic mice were measured by serial metabolite and pathology tests. Samples were obtained from epididymal, subcutaneous and brown adipose tissues. Histological and morphological analysis demonstrated that STAMP2 gene overexpression reduced adipocyte size, angiogenesis in epididymal and brown adipose tissues. On aortic ring assay, microvessels sprouting from aortas were significantly inhibited after STAMP2 gene overexpression. The cellular effect of STAMP2 on angiogenesis was explored in human umbilical vein endothelial cells (HUVECs) model. Correlation of STAMP2 and angiogenesis was validated by Ad‐STAMP2 transfection and STAMP2 siRNA inhibition. In vitro, overexpression of STAMP2 significantly inhibited endothelial cell migration, tube formation. The effects of Ad‐STAMP2 transfection on HUVECs were abolished by treatment with PPARγ antagonist GW9662 (2.5 μM), and the roles of STAMP2 siRNA on HUVECs were also reversed by treatment with PPARγ agonist rosiglitazone (RSG) (0.1 mM). RT‐PCR indicated that STAMP2 could regulate levels of adhesion molecules, vascular endothelial growth factor A and CD36. The expression of PPARγ and CD36 was decreased when STAMP2 was inhibited by siRNA, while PPARγ and CD36 were highly expressed after overexpression of STAMP2. Our results suggested that STAMP2 gene overexpression may improve insulin resistance via attenuating angiogenesis in epididymal and brown adipose tissues through the PPARγ/CD36 signalling pathway.
Highlights
Adipose tissue is considered to be one of the main driving forces for the development of insulin resistance (IR) [1]
Consistent with our previous publication [28], diabetes mellitus (DM) induced by high fat and sugar diet combined with a small dose of STZ in male ApoEÀ/À/LDLrÀ/À mice could resemble human diabetes mellitus and Six transmembrane protein of prostate 2 (STAMP2) overexpression decreased risk factor of insulin resistance in diabetic ApoEÀ/ÀLDLRÀ/À mice (Fig. S1, Table S1)
We found that overexpression of STAMP2 could effectively attenuate angiogenesis in the epididymal white adipose tissue (EWAT) and brown adipose tissues (BAT) of diabetic ApoEÀ/À/LDLRÀ/À mice
Summary
Adipose tissue is considered to be one of the main driving forces for the development of insulin resistance (IR) [1]. The vasculature as a key anatomical structure to furnish nutrition to adipose tissues plays a vital role in the pathogenesis of IR. It has been demonstrated that angiogenesis could promote or improve IR via regulating the adipogenesis and energy balance [2, 3]. Adipose tissues consist of white and brown adipose tissues (WAT and BAT). Adipose tissue angiogenesis is closely related to IR [3, 7, 8]. In the metabolically active BAT, angiogenesis can increase energy consumption and improve IR [11]
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