Many evidences were reported showing that apolipoprotein A1/C3/A4/A5 gene cluster is associated with premature coronary artery disease  and serum lipid levels . Recent findings indicate that APOA5 could also influence cholesterol homeostasis and probably could play a role in hypertriglyceridemia associated with diabetes and inflammation .
The APOA5 polymorphisms were also identified to be implicated in regulation of blood pressure and in the development of hypertension in Japanese population .
Our data demonstrate that the 56C > G SNP has a significant influence on blood pressure and triglyceride levels. This variant had not previously been investigated in Moroccan populations, although several different studies of other populations are available, supporting the importance of our study. The frequency of the 56G rare allele detected in Moroccan patients (22%) is higher than that of European populations. Indeed, studies carried out with North Americans and Europeans found that the 56G allele frequency is around 6% [6, 7, 13], whereas its frequency in North Americans of Hispanic ancestry is around 15% . Ruiz- Narváez registered a value of 10.2% for the 56G allele in Costa Rica, while other populations exhibited lower frequencies in the same study (Caucasians 6%, African-Americans 7%) . In addition to these studies, in 2003, Lai et al. investigated the frequency of the same polymorphism in people resident in Singapore . The Chinese, Malay and Indian populations living in this region exhibited extremely low frequencies of the 56G polymorphism (0.1%, 1% and 3%, respectively). The 56G allele frequency varies between 0.1% in a Chinese population  and 15.8% in Hispanic males .
APOA5 gene codes for an apolipoprotein involved in the regulation of LPL activity [17, 18]. ApoAV protein could facilitate the interaction between TG rich lipoproteins and proteoglycan-bound LPL. Transgenic mice models also suggested that apoAV might inhibit VLDL hepatic production but these findings were not confirmed in lipoprotein kinetic studies .
Although the association of 56C > G polymorphism with lipid profile was already shown in various healthy populations , their impact on AHT dyslipidemia remains undocumented. In another study, this polymorphism was associated with higher TG and lower HDLc in diabetic patients, but only for Indian-Asian carriers . There was no report of the impact of this polymorphism on history of dyslipidemia in AHT. Nevertheless, an increased 56G allele frequency was previously reported in non diabetic patients with severe hypertriglyceridemia [22, 23]. The association between the 56G allele and increased triglycerides has already been documented in other populations, such as the North American and Northern Irish populations [24, 25]. The results of the present study confirm the relationship between APOA5 56C > G polymorphism and plasma triglycerides, as carriers of the 56G variant were associated strongly with triglyceride levels. In addition to elevated triglyceride levels, the APOA5 56G was associated with higher systolic blood pressure relative to 56C carriers. A direct effect of APOA5 on blood pressure regulation is unlikely. In contrast, there is experimental evidence to suggest that chronic hypertriglyceridemia leads to endothelium dysfunction, which is associated with an impaired response to vasodilator stimulation  and a subsequent decrease in nitric oxide availability phenomena, which may result in increased blood pressure.
We found a significant difference between patients with AHT and controls regarding the frequency of 56C > G and -1131 T > C genotypes in the additive, dominant and recessive models.
Several studies demonstrated that the presence of polymorphisms in the A1-C3-A4 cluster and other gene loci determines the variability of the postprandial lipoprotein response [27, 28]. Recently a gene coding for APOA5 was identified in this cluster, and this is emerging as a main candidate gene for modulating TG metabolism in humans . Two polymorphisms,-1131 T > C and 56C > G, have been extensively studied and are independently associated with higher TG levels [6, 28, 29]. Previous studies have shown that plasma TG concentrations were 69% higher in CC subjects than TT subjects with the-1131 T > C polymorphism [8, 30] and 20–30% higher in CG than CC subjects with the 56C > G polymorphism [6, 31]. Moreno et al. demonstrated that carriers of the -1131C allele (-1131 T > C) displayed a higher plasma TG concentration . However, association studies using haplotypes should increase our ability to detect true associations and interactions.
The ApoA5 -1131C allele in our study population was similar to that in Chinese (29.9%) [33–35], Singaporean (29.4%) , Malays (30.0%) , slightly lower than that in Japanese (34.0%) [36, 37], but much greater than that of whites (8.0%) , Hispanic Americans (13.0%-16.0%) [6, 38] or Tunisian (13.0%) . The frequency of ApoA5 c.553G > T allele in this study is extremely low, and is in agreement with that of two previous studies in Chinese (3.97%)  and Chinese Taiwanese (4.2-7.2%) [41, 42]. The ApoA5 c.553 T allele has been reported to be absent in Caucasians . The ApoA5 c.553TT homozygous was similarly detected in our study population in agreement with a previous study .
To the best of our knowledge, this study is the first to determine that different haplotypes of APOA5 gene modulate the systolic, diastolic blood pressure and lipid levels in AHT patients. Thus, our data show markedly higher systolic and diastolic blood pressure in subjects with the APOA5 H2 and APOA5 H4 haplotypes, which may explain the higher risk of coronary heart disease associated with the 56G and -1131C alleles [31, 44].
In our study, both the APOA5 H2 and APOA5 H4 haplotypes were significantly associated with increase in systolic blood pressure. In addition the H4 haplotype was associated with higher DBP and TG levels. In contrast the H1 haplotype showed significant association with lower SBP, DBP and total plasma TG. These results suggest that each of these haplotypes may be associated with different mechanisms that enhance the plasma lipid levels and the risk of atherogenesis.
All these data suggested the importance of APOA5 in the regulation of plasma triglyceride concentrations. Furthermore, pair wise linkage disequilibrium comparison performed in this study between APOA5 -1131 T < C and APOA5 56C > G demonstrated that they are linked, suggesting cooperation mechanisms for the associations with plasma lipoproteins and related traits. Metabolic syndrome (MetS) is a cluster of disorders which includes visceral obesity, dyslipidaemia, hyperglycaemia, and hypertension . The association of APOA5 polymorphisms with increased risk of metabolic syndrome was showed in several studies . The APOA5 gene plays an important role in regulating triglyceride levels. This regulation may contribute to the association between APOA5 and hypertension showed in this paper, but we cannot exclude other mechanisms.
Our study has same limitations; waist conference wasn’t measured to assess central obesity. In addition, the APOA5 -1131 T > C and c.553G > T polymorphisms were not in Hardy-Weinberg equilibrium.
In summary, we demonstrated that common variants of APOA5 gene are associated with AHT and contribute to the variation in human plasma TG. Therefore, APOA5 variant was a significant predictor for high triglyceride risk and the APOA5 haplotypes affected dyslipidemia appreciably among the Moroccan population.