Endotrophin (Mus musculus)

Endotrophin (Mus musculus) (200 mg/kg; ad libitum; 8 weeks)​ administration in high-fat diet-fed mice induces local adipose tissue overexpression that promotes adipogenesis, suppresses lipolysis via reduced HSL phosphorylation, enhances lipid accumulation in adipose tissue, and shifts macrophage polarization toward a pro-inflammatory M1 phenotype^[1].
Neutralizing antibody against Endotrophin (Mus musculus) neutralizes endotrophin activity in high-fat diet-induced obese mice and significantly improves insulin sensitivity^[2].
Overexpression of Endotrophin (Mus musculus) in MMTV-PyMT transgenic mice significantly increases primary tumor volume, promotes the growth of lung metastatic lesions, and restores tumor growth in collagen VI-deficient MMTV-PyMT mice^[2].
Induction of Endotrophin (Mus musculus) confers cisplatin resistance in breast tumor-bearing mice, while neutralizing Endotrophin activity or reducing its levels using TZDs restores cisplatin sensitivity^[2].
Endotrophin (Mus musculus) induces adipose tissue fibrosis and inflammation in mice, and causes systemic dyslipidemia, hepatic steatosis and insulin resistance; blocking endogenous Endotrophin with neutralizing antibodies effectively reverses these manifestations^[3].