Effects of six-week consumption of lard or palm oil on blood pressure and blood vessel H2S in middle-aged male rats
Background: Cardiovascular disease is the leading cause of death. The etiology of this disease is multifactorial, with unhealthy nutrition being one of the main risk factors. Diets high in animal fats and saturated fatty acid have been associated with an increased risk for cardiovascular diseases. However, the results of investigations on the effects of lard (LO)- and palm oil (PO) on cardiovascular risk are still controversial due to the dosages used and the age of the animals investigated.
Objective: We investigated whether LO or PO consumption led to different effects on blood pressure, vascular functions, and lipid profiles within middle-aged rats.
Methods: The study was performed in middle-aged male rats, n = 6 for each group. LO, PO, or distilled water (control) 1 or 3 ml/kg were orally gavaged once a day for 6 weeks. Basal blood pressure and heart rate were measured in anesthetized rats. Fasting serum lipids were measured by enzymatic methods. The vascular functions of isolated thoracic aorta were studied using pharmacological techniques in the absence or presence of N-nitro-L-arginine, a nitric oxide synthase (eNOS) inhibitor and or DL-propargylglycine (PAG), a cystothionine-γ-lyase (CSE) inhibitor. Additionally, the aortic wall eNOS and CSE protein expression were measured by Western blotting.
Results: In comparison to the control group (distilled water, DW), no differences were observed in any of the parameters studied after the rats took 1 ml/kg of LO or PO. However, PO caused an increase in neutrophil/lymphocyte ratio and body fat. At 3 ml/kg dosage, LO caused increased basal blood pressure (LO, 153.4 ± 3.2; DW, 131.4 ± 3.2 mm Hg for systolic blood pressure and LO, 130.9 ± 2.5; DW, 107.9 ± 5.8 mmHg for diastolic blood pressure) body and liver cell lipid accumulation, while PO led to increased body fat and fasting serum triglyceride (PO, 131.5 ± 13.2; DW, 91.8 ± 4.8 mg %). Neither LO nor PO treatment had any effect on vascular contraction to phenylephrine, except in the presence of PAG which led to an increased contractile response to phenylephrine. PO but not LO treatment caused increased vascular wall CSE protein expression.
Conclusion: The results document how both LO and PO at a dose of 3 ml/kg (corresponding to three servings of Thai fast food) cause increased cardiovascular risk factors. However, the blood vessel H2S production increased while the lower dose had a minimal effect.
Keywords: Lard oil; Palm oil; blood vessel; liver lipid; NO; H2S
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