This study was conducted to investigate the pharmacological activity of cocoa polyphenols (CPs) on visceral obesity markers and the possible mechanisms. In this study, Sprague-Dawley(SD) rats were fed either a low-fat diet (LFD) or a high-fat diet (HFD). After 12 wk of diet intervention, only one group of HFD rats (n = 10/group) were treated at a dose of 600mg/kg bw/day CPs (HFD+CPs) for 4 wk. The gene and protein expression levels of phosphorylation of AMPK-activated protein kinase alpha/beta(AMPK alpha/beta) were measured using realtime-PCR and Western blotting. The mRNA expression of lipogenic key enzymes(Acaca, Fasn, Mcat, and Scd-1), and beta-oxidation key enzymes (CPT1, Prkaa1, Acox1) were investigated. In addition, the upstream transcription factors (PPAR alpha, PPAR gamma, C/EBP alpha, and SREBP-1c) were also examined. In accordance with these findings, CPs treatment improved visceral adiposity, adipocytes hypertrophy, and liver steatosis. AMP-activated protein kinase alpha/beta (AMPK alpha/beta) phosphorylation in liver and adipose tissue of HFD+CPs-treated rats was activated compared with HFD-fed rats. The expression of lipogensis related-genes was decreased, while expression levels of beta-oxidation-related genes were increased compared with HFD-fed rats. Together, these data partially unravel the ameliorative effects of CPs treatment on visceral obesity markers by inhibiting lipogenesis and promoting beta-oxidation related-genes through activation of the AMPK pathway. Practical applications: There is a metabolic logic linking the expended visceral or abdominal fat depot to dyslipidemia. The conceivability of using a natural dietary supplement to regulate lipid metabolism homeostasis is appealing as this by product of the defatted cocoa juice industry is non-toxic, cheap, and has shown hypolipidemic properties. This is essentially significant in the context of the rising costs of obesity and its related diseases care. The ability of polyphenolics to suppress SREBP-1c, the target of statins, while activating PPAR alpha, the target of fibrates, suggest it can naturally find its role in the treatment of hyperlipidemia.