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BACKGROUND While eggs are a low‐cost source of protein, rich in macro‐ and micronutrients, the association of egg intake and cardiovascular disease (CVD) remains controversial. This study investigated the effect of egg consumption on CVD parameters. Eggs were boiled, separated into four fractions (whole egg, 50% yolk‐reduced whole egg, egg yolk and egg white) and then freeze‐dried. The different egg fractions or distilled water (control) were orally gavaged to adult male Wistar rats at 1 g kg−1 rat body weight, each day for 8 weeks, following which basal blood pressure, heart rate, complete blood cell count, blood biochemistry, body fat and liver cell lipid accumulation were determined. The vascular functions of isolated thoracic aorta were studied using classical pharmacological techniques. RESULTS In comparison to the control group, none of the egg fractions affected body weight, food intake, plasma glucose or lipid profile. The yolk group experienced increased plasma alkaline phosphatase and creatinine levels, while egg white caused decreased plasma cholesterol and blood urea nitrogen. Whole egg and egg yolk increased blood pressure and mean hemoglobin concentration and the yolk increased liver lipid accumulation. Egg white decreased the white blood cell count and body fat lipids. No changes were found in basal heart rate or vascular functions in any of the groups. CONCLUSIONS Consumption of whole egg or egg yolk at the dosage given caused hypertension, with impairment of liver and kidney functions following the intake of yolk alone. However, egg white is beneficial for the cardiovascular system as it decreased plasma cholesterol and body fat accumulation. © 2020 Society of Chemical Industry

Background: Coconut milk consumption in middle-aged male rats can cause increased blood vessel endothelial nitric oxide synthase (eNOS) and cystathionine-γ-lyase (CSE) protein expression, and decreased fasting blood glucose.Objective: The present study aimed to investigate whether coconut milk oil (CO), the major constituents of the coconut milk, was responsible for those effects.Methods: CO was isolated from dried fresh coconut milk and gavaged (1 and 3 ml/kg) to middle-aged male rats for 6 weeks. Blood biochemistry, lipid profile and vascular functions were investigated.Results: In comparison to a distilled water control group, no differences were observed in any of the parameters studied in the group fed 1 ml/kg of CO except for an increase in retroperitoneal fat accumulation. Feeding 3 ml/kg of CO caused decreased fasting blood glucose, plasma alkaline phosphatase and blood urea nitrogen and liver cell lipid accumulation, but increased retroperitoneal fat tissue. It also caused decreased maximal contractile response of endothelium-intact thoracic aortic rings to phenylephrine although the effect disappeared in the presence of N-nitro-L-arginine (L-NA) or removal of the endothelium. DL-propargylglycine together with L-NA caused a higher contraction to phenylephrine in the CO-treated groups than in the control group. It also caused an increase in vasodilatation to acetylcholine, but not to glyceryl trinitrate, of the phenylephrine pre-contracted aortic rings. CO treatment caused increased vascular wall eNOS and CSE protein expression.Conclusion: CO at a dose of 3 ml/kg causes some decrease in cardiovascular risk factors in middle-aged male rats, although the amount of CO consumption should be limited as it caused an increase in retroperitoneal fat.

We investigated whether coconut milk protein (CMP) contributes to the beneficial effects of coconut milk consumption on cardiovascular health markers previously found in middle-aged rats. CMP was isolated and precipitated from dried fresh coconut milk, then gavaged (1 g/kg) to middle-aged male rats for six weeks; control rats received distilled water. Compared to controls, CMP caused decreased body fat and lipid accumulation in liver cells and the platelet count. CMP did not affect basal blood pressure or heart rate in anesthetized rats. Vascular responsiveness to phenylephrine, DL-propargylglycine (PAG), acetylcholine or sodium nitroprusside was unaffected, but vasorelaxation to glyceryl trinitrate (GTN) increased. Effects of ODQ on vasorelaxation to GTN were similar in both groups. Expression of blood vessel eNOS, CSE and sGC was normal. The cyclic guanosine monophosphate (cGMP) level of CMP-treated rats was normal but addition of GTN increased cGMP and NO concentration more in CMP-treated rats than in controls, an effect unaltered by addition of diadzin. Taken together, CMP appears partially responsible for the improvement in cardiovascular health markers caused by coconut milk in middle-aged male rats.

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