Non-Alcoholic Fatty Liver Disease (NAFLD) is a multifactorial disease, mainly characterized by diffuse bubble-like fatty degeneration of liver cells and accumulation of triglycerides (TGs) [1]. Oxidative stress is activated by free radicals generated from β-oxidation and inflammatory factors released by hematopoietic stem cells and Kupfer cells [2]. Furthermore, increased endoplasmic reticulum pressure can lead to further progression of NAFLD from simple steatosis to non-alcoholic steatohepatitis, fibrosis, and cirrhosis [3,4]. NAFLD affects the hepatobiliary system, and is also closely related to obesity, type 2 diabetes, hyperlipidemia, atherosclerosis, and cardiovascular diseases [5,6]. Minimizing the incidence of NAFLD is therefore important in reducing NAFLD-related diseases.

Breast cancer is one of the most common malignant tumors in females [7]. It is divided into estrogen receptor positive (ER+) breast cancer and ER negative (ER−) breast cancer. ER positive breast cancer accounts for about 70 %. Clinically, tamoxifen (TAM) is a first-line therapeutic drug for ER + breast cancer. It acts as an ER antagonist. TAM can compete with estrogen binding for estrogen receptors, block ER-mediated cell proliferation signals, and inhibit tumor growth [8]. However, recent studies domestically and abroad have reported that the risk of NAFLD of breast cancer patients increased, and the incidence of fatty liver disease of people treated with TAM was approximately 30%–40 % [9,10]. Therefore, to identify preventive strategies, it is important to understand the mechanism of TAM-inducing NAFLD.

Nuclear receptor (NR) transcription factors are especially well-suited for regulating the lipid metabolic gene programs. Liver X receptor (LXR) is a member of the nuclear receptor superfamily and is required for regulating cholesterol, lipid, and glucose metabolisms. During the development of NAFLD, LXR and sterol regulatory element binding protein (Srebp-1c) are two key genes involved in adipogenesis, and LXR can upregulate the expression of the Srebp-1c gene and increase lipid synthesis [11,12]. It is therefore important to identify the specific mechanism by which LXR plays a key role in TG synthesis. It has been shown that in the liver, LXR forms a heterodimer with the retinoxine X receptor (RXR) and binds to specific DNA sequences of the LXR response element. Identifying the mechanism of action of nuclear receptors therefore can provide the experimental basis for the clinical use of nuclear receptor-targeted therapy for NAFLD.

Vitamin D (VD), a fat-soluble vitamin, can be synthesized from food and sunlight. Food sources include marine fish, liver, fortified foods with vitamin D (such as milk and cereals), and supplements (such as cod liver oil). Most people usually obtain 90 % of vitamin D needs from the sunlight effects on metabolites. In the skin, 7-dehydrocholesterol is converted into vitamin D3 in the presence of ultraviolet radiation, which is converted into 25(OH) D in the liver and 1,25(OH)2D in the kidney for human use [13]. In addition to its physiological role in regulating calcium and phosphorus metabolisms in the skeletal system [14], levels of VD are also closely related to liver disease, multiple sclerosis, Alzheimer's disease, cancer, and other diseases [15]. Epidemiological studies have reported that the occurrence of NAFLD was associated with VD deficiency, and that serum levels of 25(OH)D were lower in patients with NAFLD than in those without NAFLD [16,17]. However, there is still a lack of evidence regarding the relationship between VD and NAFLD. Therefore, whether vitamin D has an ameliorative effect on NAFLD needs to be further determined.