Non-alcoholic fatty liver disease (NAFLD) is the most common hepatic disorder, characterized by the fat accumulation in hepatocytes without significant alcohol assumption. In lipogenesis in hepatocytes, the tricarboxylic acid cycle citrate plays a crucial role as a carbon source. Citrate is transported into hepatocytes via Na⁺-coupled citrate transporter, NaCT. It has been demonstrated that knockdown of NaCT expression ameliorates diet-induced NAFLD in mice. In addition, NaCT expression in the liver has been reported to be induced in type 2 diabetic mice. Based on these findings, NaCT is considered to be involved in the high prevalence of NAFLD in patients with type 2 diabetes. On the other hand, it is still unclear for the expression level of NaCT under type 1 diabetic condition and its relationship to hepatic lipid accumulation. In this study, we investigated the gene and functional expression level of NaCT in streptozotocin (STZ)-induced type 1 diabetic mice. The mRNA and protein expression levels of NaCT in STZ-treated mice were gradually decreased after STZ treatment. On the other hand, the Na⁺-dependent citrate uptake activity in hepatocytes isolated from STZ-treated mice was not different from that isolated from non-treated mice. Nevertheless, the plasma triglyceride, cholesterol, and nonesterified fatty acid levels were much higher in STZ-treated mice. These results suggest that NaCT expression level is not closely related to the citrate uptake in hepatocytes under type 1 diabetic condition. In conclusion, unlike type 2 diabetes, NaCT may not be responsible for the pathogenesis of NAFLD in type 1 diabetes.