## 4 Discussion  
This study used the administration of 30% sucrose from week 4 of the rats' life for 20 weeks to provide a model of MetS and 8 weeks of study treatment [24] to provide a model of MetS. We used MPJ as a natural treatment of this induced MetS. We chose to use male Wistar rats because of the evidence that males have a higher risk of cardiovascular  
Figure 6: LDL-c and HDL-c of Wistar rats with MetS after being treated with MPJ. Mean \(\pm\) SD of LDL-c and HDL-c. * = statistically significant difference versus MetS group (\(p<0.05\)). Ctrl = Control; MetS = Metabolic syndrome; MetS + MPJ1 = 30% sucrose + MPJ 600 mg/kg; MetS + MPJ2 = 30% sucrose + MPJ 1800 mg/kg; MetS + MPJ3 = 30% sucrose + MPJ 2900 mg/kg. Week 8 tests were lost. Figure 7: Triglycerides of Wistar rats with MetS after being treated with MPJ. Mean \(\pm\) SD of Triglycerides * = statistically significant difference versus MetS group (\(p<0.05\)). Ctrl = Control; MetS = Metabolic syndrome; MetS + MPJ1 = 30% sucrose + MPJ 600 mg/kg; MetS + MPJ2 = 30% sucrose + MPJ 1800 mg/kg; MetS + MPJ3 = 30% sucrose + MPJ 2900 mg/kg. disease [27]. We previously reported that MPJ consumption is safe in doses of up to 5000 mg/kg bw and does not cause subacute or subchronic toxicity [28]. While MPJ alone reduced weight gain relative to controls, the MetS + MPJ treatments did not lower weight gain (Figure 2). The MetS+ MPJ lowered systolic and diastolic blood pressures (Figure 3), glucose (except MPJ1, Figure 4), total cholesterol (Figure 5), and HDL-c (Figure 6). MPJ did not consistently affect LDL-c (Figure 6). This work confirmed that a storage form of pomeranate juice, microencapsulated pomeranate juice (MPJ), has anti-metabolic-syndrome effects. Obesity is a chronic non-communicable disease that develops from a complex combination of nutritional, genetic, and environmental factors [29]. In this study, the body mass of all rats increased because they were still growing, while 30% sucrose increased the caloric content and caused weight gain. Interestingly, no significant differences in body mass were found in either group versus the MetS group or between them. At time zero (after 20 weeks of drinking 30% sucrose), it was observed that the MetS group had even less weight than the Ctrl group, which was unexpected due to the high sucrose intake and lack of treatment but which agrees with a study in which free fatty acids, adipocyte size, and systemic blood pressure were measured in Wistar rats with MetS induced by 30% sucrose administered with glycine for 4 weeks. When measuring fluid intake, diet, and body mass during four weeks of treatment, the researchers found no significant differences among the groups [24]. In another study [30], the effect of a daily water intake with 30% sucrose on food intake and weight was evaluated in male Wistar rats. At the end of the treatment, food intake and biochemical indicators showed that sugar water reduced the balanced food intake by more than 90%; therefore, sugar water consumption could cause malnutrition in the long term, as it causes a reduction in the nutrient-rich food intake. This result agrees with a previous study in rats [31], which showed that sugar water intake with 12% sucrose decreased balanced food intake by 47.54%, suggesting a sucrose-concentration-dependent effect. Another explanation is that the elevated insulin levels in the brain cause a decrease in the intake of food [32]. Pomeranate extracts have been reported to decrease body mass in animal models fed a high-fat, high-calorie diet [33; 34; 35]. Possible mechanisms of action could be the inhibition of pancreatic lipase, thereby increasing the excretion of fats in feces [36], improving mitochondrial function [37], controlling AMP-activated protein kinase (AMPK), leading to lipolysis in adipose tissue, and stimulating fatty acid oxidation in the liver [38]. In this study, the Ctrl + MPJ group had a minor increase in body mass.