脂肪组织功能失调是肥胖诱发众多代谢疾病的重要因素，调控脂肪细胞形成是维持脂肪组织正常功能的关键。我们新近研究表明BAMBI在离体脂肪细胞形成中发挥显著的负调控作用，但在体内脂肪细胞形成中的生理学作用及机理尚未可知。本项目拟在前期研究基础上，以BAMBI-/-小鼠为研究对象，在正常与高脂日粮饲喂下，综合利用行为学、细胞生物学和分子生物学等研究手段，分析BAMBI-/-小鼠在摄食与体重、脂肪细胞形态、脂肪组织炎症反应方面的变化，研究相关代谢参数（血清中insulin、glucose和lipids含量，机体内insulin和glucose耐受性等）的表达水平，探讨脂肪组织中BAMBI、β-catenin、Wnt3a、TGF-β1、BMP-4和脂肪细胞分化标志因子的表达量，揭示BAMBI在体内脂肪细胞形成中的生理学作用及其机理，为进一步研究脂肪细胞形成机理奠定基础，为治疗肥胖及相关疾病提供新思路。

Adipose tissue dysfunction underpins the association of obesity with the development of metabolic disease. Modulating adipogenesis has emerged as a potential protective mechanism that reduces adipose tissue dysfunction. Our recent work has identified BMP and Activin Membrane-Bound Inhibitor (BAMBI) as a potent negative regulator of adipogenesis in vitro. The present investigation aims to extend these findings and determine the physiological significance of BAMBI with respect to adipogenesis in vivo. Using methods of ethology, cell biology and molecular biology, we will perform detailed characterizations of adipose tissue (adipocyte size and number and inflammation) in BAMBI knockout mice maintained on a standard chow diet or a high fat diet (HFD). This approach will also provide information involving in food intake, body weight, blood chemistry (insulin, glucose and lipids) as well as insulin and glucose tolerance in the body. In order to investigate the potential mechanism, BAMBI, β-catenin, Wnt3a, TGF-β1 BMP-4 and adipocyte markers (PPARγ, C/EBPα, aP2, adiponectin, G3PDH, GLUT4 etc.) mRNA/protein levels in adipose tissue will also be determined. The results and conclusions will increase the understanding of the mechanisms regulating adipogenesis and provide new insights into the pathophysiology of obesity-related diseases, which occur as a result of adipocyte hypertrophy resulting in systemic, chronic inflammation. This knowledge also provides a framework for future investigations into the role of BAMBI in cell fate determination and may ultimately help to identify novel therapeutic strategies aimed at ameliorating the metabolic sequelae of obesity such as cardiovascular disease and type 2 diabetes.