The worldwide prevalence of obesity represents a major health challenge, contributing to a decline of both life quality and expectancy. Thermogenic adipose tissues (brown and beige fat) dissipate energy in the form of heat, protecting from metabolic complications, including obesity and diabetes. RNA-binding protein Lin28a inhibits Let-7 microRNA biogenesis and regulates mRNA translation in various physiological processes, whereas the function of Lin28a in brown fat remains unclear. Here we reported Lin28a is expressed in mature brown fat and associated with the brown fat thermogenic activity. When overexpressed (OE) in brown fat, Lin28a elevates the expression of thermogenic markers, including uncoupled protein 1 (Ucp1), leading to enhanced whole-body energy expenditure. At the molecular level, Lin28a binds to mRNAs related to thermogenesis and promotes their translation. Conversely, loss of Lin28a damages thermogenic program and cellular respiration, increases the level of the mitochondrial associated membrane (MAM), and induces mitochondrial calcium overload in brown adipocytes. Adipose tissue-specific Lin28a OE transgenic mice obtained more beige fat under cold and exhibited retarded body weight gain and improved glucose metabolism on high-fat diet (HFD). In addition, we also found the ectopic brown adipose tissue formation promotes energy expenditure after brown adipose progenitor cells (BAPCs) transplantation in skeletal muscle, and Lin28a overexpressing BAPCs transplantation further enhances the thermogenic activity and ameliorates streptozotocin (STZ)-induced hyperglycemia. Therefore, our studies revealed Lin28a as a therapeutic target for boosting thermogenic activity to protect from metabolic diseases.