The metabolic syndrome is defined by raised values of plasma cholesterol, raised plasma triglycerides and elevated waist circumference (1), among other parameters. Nevertheless, the role of apolipoprotein E (ApoE) in the on set of obesity in the metabolic syndrome remains unclear, although apolipoprotein E is a key surface component of triglyceride-rich lipoproteins, low density lipoproteins (VLDL) chylomicrons remnants and high density lipoprotein (HDL). Also, traces of it are found in the hypothalamic area of the hunger center (2). Objective: This study searches for the possible cause for obesity in metabolic syndrome due to a hypothalamic ApoE deficiency, associated with an increased level of combined ApoE in the systemic circulation, using a metabolic syndrome model in rats. Methods: Wistar rats (male, 179-240 g, n=10), on a high caloric, high fat diet (20 g/day/rat of combined fodder grain + pork lard as fat supplement 2ml/day/rat) for 60 days, had measurements of their plasma levels of triglycerides, cholesterol and glycaemia taken every 30 days. Also weight and arterial pressure were measured. A group (n=10) of male Wistar rats (148g-220 g) on a normal caloric diet (20 g/day/rat ad libidum of combined fodder grain) was used as control. After showing raised blood lipids and obesity, according to the diagnostic criteria (cholesterol level ranging from 158 – 170 mg/dl, triglycerides levels 201- 558 mg/dl) the rats were injected with 8 µl liquid ApoE (Millipore apolipoprotein E, Merck) in the hypothalamic area, following the coordinates of 2.2 mm posterior to bregma and 7.4 mm ventral to dura (3). The procedure was performed under anesthesia with a mixture of ketamine 10% and Xilazine 2%. Blood samples were taken by non traumatic tail incision and arterial pressure was measured using the tail-cuff method. Results: After the intracerebroventricular administration of apolipoprotein E the two parameters of plasma lipids have fallen to lower values (cholesterol) or even to normal values (triglycerides values ranging between 94-113 mg/dl) and a decrease in the food appetite of the rats was noticed. Daily food intake was noted to fall to 63%. Further measurements of the plasma leptin values, before and after administration of ApoE will take place. Conclusion: Preliminary data shows that apolipoprotein E has hypothalamic effects that concern metabolic disorders and raised plasma lipid values. Although further study is highly necessary we can conclude that deficient ApoE in the hypothalamic area can lead to a greater food intake and have possible consequences in raised plasma lipid values.