6 weeks consumption of pure fresh coconut milk caused up-regulation of eNOS and CSE protein expression in middle-aged male rats

Abstract

Coconut milk (CCM) has been an important cooking ingredient in the Asia-Pacific region since ancient time. Due to its high content of saturated fatty acids, it has been considered atherogenic. We have tested if chronic consumption of fresh coconut milk by middle-aged male rat affects vascular function, plasma glucose and lipid profiles. Compared to control, CCM caused lower maximal contraction to phenylephrine of thoracic aortic rings and increased relaxation to acetylcholine that was abolished by N G -nitro-L-arginine (L-NA) or disruption of the endothelium. DL-propargylglycine caused slight increase in baseline tension of L-NA treated aortic rings of CCM-treated rats and produced higher contractile response of the aortic rings to low concentrations of phenylephrine. The aortic eNOS-and cystathionine-γ-lyase(CSE) proteins expression of the CCM-treated rats were also higher than in controls. Except for lower fasting plasma glucose there were no changes in blood chemistry for the CCM treated rats. CCM consumption caused up-regulation of eNOS and CSE protein expression which resulted in increased production of NO and H 2 S from the blood vessels with attenuation of vasocontraction to phenylephrine and increased relaxation to acetylcholine. These novel benefits may be expected to reduce the development of cardiovascular risk factors in the aging rat.

Effects of six weeks consumption of coconut milk oil on vascular functions and fasting blood glucose and lipid profile in middle-aged male rats

“…The main component of the fatty acid composition of the CO was similar to that previously reported [11] : lauric acid (40%) followed by myristic acid (17%), palmitic acid (8%), linoleic acid (ω-6-unsaturated fatty acid, 5%), capric acid (4%), stearic acid (3%) and caprelic acid and linoleic acid (ω-3-unsaturated fatty acid, 1%). The cholesterol and α-tocopherol content were 0 (not detectable) and 0.09 mg/100 g, respectively (Table 1).…”

“…It has been previously demonstrated that coconut milk consumption at a dosage of 3 mg/kg but not 1 mg/kg produced some beneficial effects on the cardiovascular system in middle-aged male rats [11]. The present study thus investigated whether it is coconut oil which is responsible for such effects.…”

“…In our previous publication, it was also found that coconut milk consumption caused increased blood vessel H2S production [11]. Thus, the present study investigated whether CO consumption would affect H2S production by studying the C-R curve to phenylephrine in the presence of PAG after the aortic ring had been incubated with L-NA, in order to prevent any disturbance by the NO.…”

“…For coconut milk consumption, our group recently demonstrated that the consumption of pure dried fresh coconut milk for 6 weeks by middle-aged male rats caused an up-regulation of blood vessel endothelial nitric oxide synthase (eNOS) and cystathionine-γ-lyase (CSE) enzyme protein expression. This resulted in an attenuated contractile response to phenylephrine and potentiated relaxation to acetylcholine on the rats' thoracic aortic rings, with a decreased fasting plasma glucose level [11]. The present study aimed to investigate whether the oil from the coconut milk is responsible for those effects.…”

Decreased body-fat accumulation and increased vasorelaxation to glyceryl trinitrate in middle-aged male rats following six-weeks consumption of coconut milk protein

“…Coconut milk is a common culinary ingredient of Southeast Asian, Indian, Sri Lankan cuisines, as well as in Brazilian, Caribbean and Polynesian food (D'Amato, Fasoli, Righetti, 2012). The main constituents of coconut milk are lipids (coconut oil, 41.5 %) with a small amount of proteins (4.5 %) and carbohydrates (5.2 %) (Pehowich, Gomes, Barnes, 2000), or about 80 %, 19 % and 5 %, respectively in dried fresh coconut milk (Jansakul et al, 2018).…”