Abstract
Objective: The role of apolipoprotein E (ApoE) in the onset of metabolic syndrome remains unclear, ApoE being a key surface component of triglyceride-rich lipoproteins, low- and high density lipoproteins (VLDL, HDL) and also found in the hypothalamic area. This study researches the effect of ApoE on hypertension, associating increased combined ApoE at circulatory level to a hypothalamic ApoE deficiency, using a metabolic syndrome model in rats. Design and method: Wistar rats (male, 179–240 g, n = 10), on a high caloric, high fat diet (20 g/day/rat of fodder grain + pork lard as fat supplement 2 ml/day/rat) for 60 days, had measurements of their systolic arterial pressure (SAP), diastolic arterial pressure (DAP) values, weight and plasma lipid levels taken, days 0(T0), 60(T60) and 65(T65). Two groups (n = 20) of male Wistar rats (148g-220 g) on a normal caloric diet (20 g/day/rat ad libidum of combined fodder grain) and on the high caloric, high fat diet, were used as control. After showing raised SAP, DAP and lipid values (cholesterol range 158 – 170 mg/dl, triglycerides 201- 558 mg/dl, SAP 148–206 mmHg, DAP 98–150 mmHg)(T60) the rats were injected with 8 μl liquid ApoE (Millipore apolipoprotein E, Merck) in the hypothalamic area, 2.2 mm posterior to bregma and 7.4 mm ventral to dura. The procedure was performed under anesthesia (ketamine 10% + Xilazine 2%). Arterial pressure was measured using the tail-cuff method. Results: Mean value of SAP decreased from 183,62 (s = 27,22) (p < 0,007) before injection of ApoE to 181,87 (s = 23,44) (p < 0,38), while the control group injected with intracerebroventricular saline showed no decrease. Mean value of DAP decreased from 130,37 (s = 16,22) (p < 0,0004) to 121,37(s = 18,57)(p < 0,14).Conclusions: Preliminary data show the ApoE hypothalamic effects, that influence metabolic disorders and hypertension. Further study is highly necessary, yet we can conclude that deficient ApoE in the hypothalamic area can lead to raised SAP and DAP values.
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