**Abbreviations**

DFFA, DNA fragmentation factor, alpha subunit; HF, High fat diet; HF + F, High fat diet supplemented with fucoxanthin; HS, High sucrose diet; HS + F, High sucrose diet supplemented with fucoxanthin; qRT, Quantitative real-time; RQ, Respiratory quotient. 

## **1. Introduction**

Obesity, defined as excess accumulation of adipose, is a worldwide endemic health problem. Obesity and its related disorders are associated with increased morbidity, mortality and healthcare costs [1]. Mitochondria play an important role in adipose biology [2]. Mitochondria dysfunction is linked to obesity [3] and type 2 diabetes [4,5]. Mitochondria biogenesis is thus considered a potential target for the intervention of insulin resistance in obesity and diabetes [6–8]. Mitochondrion is a dynamic organelle that is continuously remodeled by fusion and fission [9], which is important for bioenergetic adaptation to metabolic demand. Cells exposed to a nutrient-rich environment tend to maintain their mitochondria in a separated state, while cells under starvation tend to have mitochondria in a connected state [10]. Reduction in the mitochondrial network, but unaltered mitochondrial mass have been reported in skeletal muscle of obese Zucker rats [3] and type 2 diabetic patients [11]. Moreover, mRNA and the protein, Mfn2, an important protein located in the mitochondrial outer membrane and mediating mitochondrial fusion, were reduced in skeletal muscle of obese subjects compared to lean subjects [12]. 

Peroxisome proliferator-activated receptor · coactivator-1 ΅ (PGC-1 ΅) is a strong promoter of mitochondrial biogenesis and oxidative metabolism through nuclear respiratory factor, NRF1 and NRF2, ERR ΅, PPAR· and PPAR ΅ [13–15]. ERR ΅ further activated the transcriptional activity of the Mfn2 promoter, and the effects were synergic with those of PGC-1 ΅ [16]. In addition, NRF1 and NRF2 themselves are able to stimulate mitochondrial transcription factor A (TFAM), a mitochondrial matrix protein essential for the replication and transcription of mitochondria DNA [17,18]. PGC-1 ΅ mRNA expression is reduced in subcutaneous fat of morbidly obese patients [19]. Ectopic expression of PGC-1 ΅ in white adipose tissue (WAT) increased brown adipocyte specific genes, including uncoupling protein 1 (UCP1) and mitochondrial activity [20]. 

Fucoxanthin (FX) is a major carotenoid in brown algae and has an unusual allenic structure [21]. FX has a suppressive effect on adipose accumulation in genetically diabetic KK-*A*y mice [22–24], Wistar rats [25,26] and diet-induced obese C57BL/6J mice [27–29]. FX feeding significantly increased fecal triglyceride and cholesterol excretion and Ά-oxidation in liver and epididymal WAT (eWAT) and also reduced fatty acid, cholesterol synthesis-related enzyme activity, serum and hepatic lipid accumulation [28,30,31]. Previous studies also showed that FX increased UCP1 mRNA expression in abdominal WAT of mice with reduced adipose mass [25,28,31]. PGC-1΅ expression in the skeletal muscles was upregulated in KK-*A*y mice fed FX [32]. 

UCP1 is a thermogenic mitochondria protein that was thought to express exclusively in brown adipose tissue (BAT). However, its expression in WAT has been confirmed in most recent studies, and these UCP1 expressing adipocytes in WAT were named "Beige/Brite" or "recruited (in contrast to the traditional "constituted") brown adipocytes [33,34]. Increases in the recruited brown adipocytes can enhance thermogenic activity and reduce adiposity in rodents [33,34] and humans [35]. As a dominant regulator of mitochondrial biogenesis and oxidative metabolism [15], PGC-1΅ regulates thermogenic activity by inducing the expression of UCP1 and key enzymes of the mitochondrial respiratory chain in both constituted and recruited brown adipocytes [33]. Mitochondrial biogenesis and dynamics regulate mitochondrial function, respiratory capacity, apoptosis and oxidative phosphorylation and, thus, impact energy balance [3,12,36]. Whether FX increased expressions of genes in the PGC-1΅ regulated pathways in WAT and metabolic rate has not been reported. 

Here, we examined the suppressive effect of adipose accumulation of FX under a high sucrose or a high saturated fat diet using a 2 × 2 factorial design. Whole body O2 consumption and CO2 production were measured and expressions of PGC-1΅ regulated genes in WAT analyzed.
