The essence of obesity is that

The essence of obesity is that the energy intake is larger than that consumption. When the amount of glucose used as direct energy material excesses that of daily requirement in the body, the extra glucose is transferred to the cells of liver or skeletal muscle and is transformed into liver- or muscle-glycogen to provide energy of the body during times of energy deficit. Because of the limited storage capacity of glycogen in the body, the extra part on the one hand is turned into fat by the liver cells and stored in them; on the other hand, the fat by fat mobilization or gluconeogenesis is removed. When the amount of fat storage is greater than the clearance, the fat accumulation in the liver cells occurs and fatty liver is formed. Therefore, obesity or fatty liver often accompanied by the increased free fatty acids and blood glucose [43]. Free fatty proton pump inhibitor or glucose accumulation in obesity can enter the mitochondria to undergo β-oxidation or tricarboxylic acid cycle (TCA). During the process of oxidation, ROS are generated via the mitochondrial respiratory chain, and elevated ROS also contributes to proinflammatory cytokine production, such as NO, TNF-α, and cellular apoptosis, meanwhile, increased ROS can result in increased lipid peroxidation, causing injury of liver cell membrane and organelles [44]. In our study, the activities of ALT, AST and liver index in high-fat diet rats increased significantly, relative to the normal control group, indicating that the liver of rats fed with high-fat diet appeared lesions (Fig. 4). However, after the intervention of Pu-erh tea extracts, the ALT and AST activities and liver index in low-, middle- and high-concentrations groups reduced significantly and these results showed Pu-erh tea extracts have hepatoprotective effect in the rats fed with high-fat diet. The mechanism may be that Pu-erh tea extracts can increase the SOD, GSH-PX and CAT activities in liver, reduce the MDA level and NOS activity by restraining the growth of body weight, thus enhancing the innate antioxidant defense system in the liver. By reducing oxidative stress and inhibiting liver lipid peroxidation, Pu-erh tea extracts can protect liver tissue from ROS damaging, thereby reducing the ALT and AST activities in serum. Weight loss can lead to the reduction in ALT and AST activities and MDA level, and improve oxidative stress status and restrain lipid peroxidation so as to protect liver from damaging, and this result is consistent with our the experiment. Obesity, especially abdominal obesity, have enlarged fat cells in common. The sensitivity of fat cells to insulin is greatly reduced and thereby causes insulin resistance. Obesity can lead to the increase of blood glucose level, and further stimulate the production of ROS. ROS can damage islet cells lead to impaired glucose tolerance in body, and eventually cause diabetes. In this study, the levels of body weight and abdominal fat in high fat control group were significantly higher than those of the normal control group (Table 1). And the synthesis ability of glycogen and the PK activity in the high fat control group were significantly reduced, and the glucose level significantly increased (Figs. 5 and 6). However, under the Pu-erh tea extract intervention, the rising trends of weight and fat had been under control, and the HGL and PK activity in Pu-erh tea extract treatment groups were significantly increased, and the glucose level reduced significantly. In the previous experiment, we have proved that Pu-er tea extracts can effectively improve insulin resistance in mice fed with high fat diet by reducing body weight and abdominal fat mass, keeping the glucose level at appropriate level [45]. Therefore, the mechanism of Pu-erh tea extracts on regulating glucose may be attributed to reducing the weight and visceral fat of rats, and these effects can improve insulin resistance, increase the sensitivity of insulin, and promote the synthesis and decomposition of glucose, thus regulating the glucose level and preventing the occurrence of type II diabetes and fatty liver.