is urgently required to increase the energy expenditure in key metabolic organs, such as brown adipose tissue (BAT) [8]. In rodents, increasing BAT activity can effectively enhance metabolic rate and protect the animal from obesity [9]. BAT plays an essential role in non-shivering thermogenesis in mammals. Its cells are rich in mitochondria, the inner membranes of which are, in turn, rich in uncoupling protein 1 (Ucp1). BAT can specifically overexpress Ucp1, thus uncoupling transmembrane electron transfer and oxidative phosphorylation in the mitochondrial respiratory chain, thereby releasing a large amount of energy in the form of heat [10]. The known anti-obesity effect of functional BAT has drawn research and attention to the activation and regulation mechanism of brown fat functioning, and the specific expression of Ucp1 by BAT has become a hot topic for scientists. The expression of the _Ucp1_ gene is regulated by a variety of transcription factors, such as peroxisome proliferatorator-activated receptors (PPARs), PR domain containing 16 (Prdm16), peroxisome proliferatorator-activated receptor \(\gamma\) coactivator-1(PGC-1), and mitochondrial transcription factor A(TFAM). PPAR\(\alpha\) participates in the regulation of fatty acid oxidation mainly by inducing the expression of genes related to fatty acid oxidation [11]. Prdm16 is a zinc finger structure transcription factor containing PR domain, which is highly expressed in mouse BAT. It is also a key factor in determining whether adipose precursor cells develop into skeletal muscle cells or brown adipose cells. The Prdm16 protein is greatly enriched in BAT and causes increased expression of mitochondrial genes and greater density of mitochondria [12]. The loss of Prdm16 can hinder the differentiation of brown adipocytes, while overexpression can significantly increase their numbers. Animals lacking Prdm16 in BAT have a dramatically reduced capacity to produce heat [13]. Prdm16 regulates the thermogenic function of brown fat, mainly by binding to PPAR\(\gamma\) and coactivating its transcriptional function [14]. The anti-obesity and anti-diabetic effects of anthocyanins are well-accepted experimentally [15; 16]. Anthocyanins C3G and C3R have been reported to increase the mitochondrial copy number in vitro and to promote the metabolism of carbohydrates and fat [17]. C3G can enhance whole-body metabolism by upregulating the mitochondrial function of BATT and beige formation in subcutaneous WAT [4]. However, its molecular targets have yet to be elucidated. Here, via quantitative real-time PCR, to quantify the expression of BAT-related genes _Ucp1_ and _Prdm16_ following the treatment of C\({}_{3}\)H\({}_{10}\)T\({}_{1/2}\) cells with C3G during brown adipogenesis, we speculate that _Prdm16_ may be a novel transcriptional activator of _Ucp1_. The results of a luciferase assay and yeast one-hybrid screening ascertained that C3G activates the thermogenic gene _Ucp1_ by regulating the expressions of _Prdm16_. Thus, Prdm16 can bind directly to the _Ucp1_ promoter region, from \(-500\) to \(-150\) bp to active transcription. Our results, thus, suggest that Prdm16 is indeed a novel transcriptional activator of Ucp1 and that C3G can increase energy metabolism through a previously unrecognized molecular mechanism. Consequently, these findings may support an innovative approach to the treatment of obesity and its related diseases.