LAUSR

Tamoxifen is widely used as an effective adjuvant treatment and prevention of estrogen receptor-positive breast cancer [1]. Tamoxifen decreases food intake, body weight and (at least in the short-term) fat mass in rodents. Despite lowering body weight in obese women, tamoxifen may increase the incidence of diabetes [2]. This potential side effect has been attributed to decreased β-cell survival and proliferation, but also hepatic steatosis in rodents [3]. We and others have recently demonstrated that tamoxifen affects glucose, lipid metabolism, transient body composition changes which may originate from tamoxifen-induced adipose tissue necrosis followed by de novo adipocyte recruitment and fat redistribution including fat accumulation in the liver in the longer term [3, 4]. Indeed, the development of fatty liver was observed as early as 3 months after initiation of tamoxifen treatment in women with breast cancer [5]. However, the precise mechanisms of potential diabetogenic effects of tamoxifen are still not entirely clear. Therefore, we aimed to systematically elucidate the development of tamoxifenrelated hyperglycemia using the hyperinsulinemic–euglycemic clamps. Methods