alexa The Relationship between Serum Apelin Concentration and Selected Anthropometric Parameters, Serum Lipids and Carotid Intima-Media Thickness in Young Subjects with Primary Arterial Hypertension | Open Access Journals
ISSN: 2167-0943
Journal of Metabolic Syndrome
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The Relationship between Serum Apelin Concentration and Selected Anthropometric Parameters, Serum Lipids and Carotid Intima-Media Thickness in Young Subjects with Primary Arterial Hypertension

Agata Strażyńska, Karolina Hoffmann*, Wieslaw Bryl, Iwona Zaporowska-Stachowiak, Magdalena Kostrzewska, Jolanta Małyszko and Andrzej Minczykowski
Department of Internal Diseases, Metabolic Disorders and Arterial Hypertension, Poznan University of Medical Sciences, Poznan, Poland
*Corresponding Author : Karolina Hoffmann
Department of Internal Diseases, Metabolic Disorders and Arterial Hypertension
Poznan University of Medical Sciences, Ul. Szamarzewskiego 84
60-569 Poznań, Poland
Tel: +4861-8549-377
Fax: +4861-8478-529
E-mail: karhof@tlen.pl
Received: September 22, 2015; Accepted: October 15, 2015; Published: October 21, 2015
Citation: Strażyńska A, Hoffmann K, Bryl W, Zaporowska-Stachowiak I, Kostrzewska M, et al. (2015) The Relationship between Serum Apelin Concentration and Selected Anthropometric Parameters, Serum Lipids and Carotid Intima-Media Thickness in Young Subjects with Primary Arterial Hypertension. J Metabolic Synd 4:185. doi:10.4172/2167-0943.1000185
Copyright: © 2015 Strażyńska A, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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Abstract

Objective: Apelin and its specific receptor, APJ system, seems to be involved in the development of arterial hypertension (HTN). The aim was to estimate plasma apelin concentration in young patients (pts) with primary HTN and to assess the relationship between apelin and selected anthropometric parameters, serum lipids and carotid intima-media thickness (right and left cIMT).

Methods: 70 pts (48 males, 22 females) aged 18-33 with newly diagnosed, untreated primary HTN were recruited. There were 15 age- and gender-matched healthy people in the control group. Anthropometric and BP measurements were done. Fasting serum apelin and lipids were evaluated. The cIMT was estimated using ultrasonography.

Results: Serum apelin was higher in whole group (but not statistically significant, 98.04 ± 51.82 vs. 79.19 ± 39.51 pg/ml, p >0.05) and in males with HTN (compared to healthy males, 105.86 ± 53.21 vs. 61.42 ± 24.04 pg/ ml, p= 0.04). We observed a statistically significant negative correlation between apelin concentration and left cIMT in normal-weight women (R = -0.74), a negative correlation between triglyceride levels and apelin concentration in overweight subjects (R = -0.49), a negative correlation between apelin concentration and right cIMT (R = -0.99) and a positive correlation between apelin concentration and WHR (R = 0.99) in obese women.

Conclusion: In whole examined group with HTN there were no statistically significant differences in serum apelin and no relationships between its concentration and anthropometric parameters, serum lipids or cIMT. However, higher serum apelin concentration in young males with HTN and some statistically significant correlations between serum apelin and analyzed parameters in groups divided by sex and BMI may suggest a possible role of apelin in the development of HTN. Further studies are required to clarify the relationship between apelin, metabolic parameters and the early markers of atherosclerosis in pts with HTN.

Keywords
Apelin; Adipocytokines; Carotid intima-media thickness; Primary arterial hypertension; Metabolic syndrome; Obesity; Overweight; Atherosclerosis
Introduction
Arterial hypertension (HTN) is one of the risk factors of cardiovascular events, such as myocardial infarction (MI) and stroke. Due to its great prevalence, HTN is a public health problem [1]. It occurs relatively rarely as an isolated disease, while being usually associated with excessive body mass and metabolic disorders.
The results of studies conducted over the past two decades highlight the role of adipose tissue and its hormones called adipocytokines in the pathogenesis of diabetes and cardiovascular diseases, including HTN and coronary heart disease (CAD) [2]. It is considered that in subjects with excessive body mass adipocytokines play an important role in the development of lipid and carbohydrate disorders, as well as in the progression of inflammation and atherosclerosis [2]. Apelin is a newly discovered adipocytokine, which is active in many biological systems, with having a well-documented role in the cardiovascular one. It influences cardiomyocytes contractility and left ventricle function [3,4]. Apelin plays role in endothelium-dependent vasodilation, as well as in the regulation of blood flow and blood pressure (BP) [5-7]. This peptide affects the progression of atherosclerosis and the development of CAD [2,8-12]. Małyszko et al. showed significant correlations between apelin and the markers of endothelial cell injury and inflammation in patients (pts) with chronic kidney disease (CKD) as well as the relationship between apelin and CAD among kidney allograft recipients [10,11]. Meanwhile, the authors of the Kozani study reported an inverse correlation between apelin concentration and the presence of CAD. What is more, they showed that apelin was reduced in pts with unstable angina (UA), compared to asymptomatic pts [2].
Apelin acts on target cells via a specific receptor, APJ. Both apelin and the APJ receptor, due to their peptide structure and tissue distribution, resemble the elements of the renin-angiotensinaldosterone system (RAAS). Many studies indicate that the apelin and APJ pathways play an opposing physiological role to RAAS [8,13]. Apelin, due to its opposing action to angiotensin-II (Ang-II) is compared to angiotensin-1-7 (Ang-(1-7). Sampaio et al. suggested that both apelin and Ang-(1-7) cause endothelium-dependent vasodilation by stimulating eNOS activation and NO production [14,15].
The impact of apelin on HTN was observed mainly in experimental animal models [5-7,16]. Studies conducted on rats revealed that apelin infusion caused a decrease in BP resulting from an increase in the concentration of nitric oxide (NO) [17,18]. Zhong et al. underlined the role of apelin in achieving a dynamic balance between Ang-II activity and NO production in diabetic mice. The authors proved there is a relationship between a diminished expression of APJ protein and enhanced contractile responses to Ang-II and Ang-IV. They showed significant increases in the phosphorylation of endothelial nitric oxide synthase (eNOS) and in NO generation in renal arteries pretreated with apelin [13].
In rats, the central control of pituitary hormones release is also involved in exerting the apelin hypotensive effect. It was observed that apelin inhibits the release of vasopressin (AVP) from the supraoptic nuclei. Thus, apelin is responsible for lowering the reabsorption of sodium and water in the distal part of renal tubules, and for the increase of natriuresis [16].
In few studies conducted on a population with primary HTN, the authors noted a negative correlation between apelin concentration and BP [3,19-21]. Decreased apelin concentration was observed in pregnant women with coexisting HTN, and the concentration correlated negatively with BP values and the presence of pre-eclampsia [22].
Aim and objective
The aim of the study is to estimate plasma apelin concentration in young pts with primary HTN prior to any treatment, as well as to assess the relationship between the concentration of apelin and: 1) selected anthropometric parameters, including body mass, body mass index (BMI), waist-to-hip ratio (WHR); 2) serum lipids, including total cholesterol (TC), LDL-cholesterol (LDL-C), HDL-cholesterol (HDL-C), triglycerides (TG); 3) intima-media thickness in right and left common carotid arteries (right and left cIMT).
Materials and Methods
The study protocol was reviewed and approved by an independent ethics committee (Bioethics Commission at Poznan University of Medical Sciences, approval no. 1117/08, date of issue: November 13, 2008). An informed written consent was obtained from each patient prior to their participation in the study.
The study was conducted between 2008-2010 in the population of 70 patients aged 18-33 years, including 48 males (68.6%) and 22 females (31.4%), with newly diagnosed, untreated primary HTN, and without comorbidities. All study participants were recruited in the Department of Internal Diseases, Metabolic Disorders and Arterial Hypertension, Poznan University of Medical Sciences, Poland. Secondary causes of HTN were excluded. Patients underwent a basic physical examination including the measurements of BP and such anthropometric parameters as: body mass, height, waist circumference (WC) and hip circumference (HC). BMI and WHR were calculated. BP was measured by means of a mercury sphygmomanometer, according to the current guidelines [23]. We used the mean values of SBP and DBP in the final analysis. We recruited 15 age-matched healthy people (10 males, 66.6%) to the control group.
Fasting serum apelin and lipids’ concentrations were determined. Apelin concentration was estimated via the radioimmunoassay (RIA) method (Phoenix Pharmaceuticals Inc., USA), while TC, LDL-C, HDL-C and TG were measured with the commercially available assay kits (Dimension®, Siemens, Germany). In order to avoid noisy data in the serum lipids’ assessment, blood was not collected from the participants immediately after public holidays, weekends and from women during menstruation.
The ultrasonographic examination of cIMT was performed by means of the color-flow B-mode doppler ultrasound. We used the GE Voluson 730 Pro ultrasound device with the linear-array imaging probe of 6-12 MHz (General Electric Company, United States of America). The measurement of cIMT was performed on the common carotid artery (CCA), approximately 15 mm proximal to the flow divider. First, the longitudinal image of the distal CCA was acquired and then cIMT was measured at the thickest point, on the near and far walls, with a specially designed computer program. The thickness of a CCA wall was described as the mean of the maximum wall thicknesses of the near and far walls, and was measured on both left and right side.
The statistical analysis was performed with the STATISTICA 8.0 software (Stat Soft, USA) in 3 groups divided by the value of BMI: 20 subjects with obesity (BMI ≥ 30 kg/m2), 19 overweight participants (BMI 25.0-29.9 kg/m2) and 31 normal-weight subjects (BMI 18.5-24.9 kg/m2). In the examined group all results were expressed as mean ± standard deviation, minimum value, maximum value and normality of data distribution was verified by the Kolmogorov-Smirnov test (the size of group was more than 30 patients). When not confirmed compatibility with the normal distribution, the results were described with the use of median, minimum and maximum value. Similarly in the control group, the results were expressed as mean ± standard deviation, minimum value, maximum value and normality of data distribution was verified by the Shapiro-Wilk test (the size of group was less than 30 patients). When not confirmed compatibility with the normal distribution, the results were described with the use of median, minimum and maximum value. For normally distributed variables, the analysis of variances (ANOVA) was used to assess the differences between the examined group and the control one. Statistical hypotheses were verified at significance level less than 0.05 (p < 0.05). To analyze the relationship between selected parameters, following methods were used: one-way analysis of variance (one-way ANOVA) or ANOVA for multiple factors with LSD (Least Significant Differences) post hoc test.
Results
We found statistically significant differences in the mean SBP, mean DBP, WC, HC, body mass and BMI between the examined and control group. The characteristics of BP, anthropometric parameters and cIMT are presented in Table 1. The examined group was characterized by a higher mean apelin concentration, but the inter-group difference did not reach statistical significance (98.04 ± 51.82 vs. 79.19 ± 39.51 pg/ ml, p>0.05). However there was a statistically significant difference in the apelin concentrations between male subjects with HTN and healthy males (105.86 ± 53.21 vs. 61.42 ± 24.04 pg/ml, p=0.04). Serum apelin and lipids in both groups are presented in Table 2.
We found statistically significant correlations between the serum apelin concentration and selected parameters in the groups divided by sex and BMI, as presented in Figures 1-3. In normal-weight males, there was a negative correlation between apelin concentration and age (R = - 0.56, Figure 1). In normal-weight women, we found a negative correlation between apelin concentration and left cIMT (R = -0.74, Figure 2). In overweight subjects, a statistically significant negative correlation between serum triglycerides and apelin was observed (R = -0.49, Figure 3).
What is more, a negative correlation between apelin concentration and right cIMT (R = -0.99) and a positive correlation between apelin concentration and WHR (R = 0.99) was demonstrated in obese women.
We did not find any statistically significant relationships between serum apelin concentration and anthropometric parameters, serum lipids or cIMT in the whole examined group (data are not presented).
Discussion
As for cardiovascular diseases, endogenous apelin was evaluated mainly in CAD and heart failure (HF) [3,24-26]. However, studies conducted on pts with essential HTN, especially on young populations, are scarce. Sonmez et al. investigated a group of newly diagnosed and untreated young hypertensive males and reported them to have significantly lower apelin concentrations in comparison to healthy controls. The authors also showed a negative correlation between serum apelin concentration and SBP [20]. In our study, young hypertensives were characterized by higher apelin concentrations, while the inter-group difference was not statistically significant. This may be associated with higher values of anthropometric parameters in the examined group. Przewłocka-Kosmala et al. reported lower apelin concentration in hypertensive subjects, who were significantly older than our patients. The authors mentioned recruiting subjects at the mean age of 56 ± 9 years, who could not be compared to our group due to different age, disease duration and previous antihypertensive therapy [19]. The effects of angiotensin-converting enzyme inhibitors (ACE-inhibitors) or Ang-II receptor antagonists (sartans) on the concentration of apelin may be significant, which was proved in the study conducted by Hung et al. [27].
cIMT is a well-documented marker of the severity of atherosclerosis [28,29]. In our study, we observed a negative correlation between serum apelin concentration and left cIMT in normal-weight women, which may indicate a possible role of apelin in the pathophysiology of atherosclerosis. Some authors mentioned that differences between parameters from right and left cIMT may be associated with anatomical conditions that lead to increased blood pressure values in left CCA. Repeated endothelial micro injuries due to the strong bloodstream may be responsible for more often detection early symptoms of atherosclerosis in left CCA [28,30]. In examined females with obesity, which is an additional cardiovascular risk factor and promotes atherosclerosis, we showed a negative correlation between apelin concentration and IMT also in right CCA. However, a strong negative correlation between apelin and left cIMT was not proved in this group, what could be explained only by a small number of study population.
It must be emphasized that numerous factors affect cIMT, including BP values, the presence of excessive body mass, and the disorders of lipid and carbohydrate metabolism. Thus, the relationship between cIMT and endogenous apelin requires further investigation [31,32].
It is hard to confront our results with other data because of the small number of published studies which investigated the problem presented in an identical or at least similar way. Publications that are available discuss some of the relationships we described, but in different populations, for instance: in pts with type 2 diabetes or prediabetes [33-36].
Assessing the relationship between serum apelin and triglycerides, we found a negative correlation between these two parameters in hypertensive, overweight pts. Tasci et al., in turn, showed that plasma apelin was decreased in non-obese, non-diabetic and normotensive subjects with elevated LDL-C. They concluded that low apelin concentration in hypercholesterolemia may be associated with insulin resistance [37]. Contrary to that, a positive correlation between fasting serum apelin and triglycerides was described by Li et al. in a population with impaired glucose tolerance or type 2 diabetes [36]. Elevated TG in pts with HTN are considered to be responsible for endothelial damage. In studies cited above, it was clarified that vasoconstriction caused by apelin is related to endothelial injury. This process may lead to the progression of organ damage in pts with HTN, irrespective of glycaemia and the severity of glucose metabolism disturbances [38-40]. Tasci et al. assessed the impact of lipid-lowering actions, such as diet or the use of statins, on serum apelin and reported that the reduction of LDL-C was related to an increase in plasma concentrations of adiponectin and apelin [41].
Similarly, Miazgowski et al. reported that abdominal obesity in premenopausal women was associated with higher DBP and higher total, abdominal (android), and hip (gynoid) fat, as well as android/body fat ratio (all p<0.01). However, the authors did not investigate apelin levels in their population [42]. In pts with hypertrophic cardiomyopathy adiponectin, resistin, and leptin levels, echocardiographic variables or LV dimensions, septum thickness was not associated with those three adipokines [43].
Strengths and limitations
In our study data was obtained from a non-randomized sample. The major drawback of the study is that it is based on relatively small number of subjects. However, authors made efforts to select very young patients with HTN, in whom secondary causes of the disease were excluded and who were not pharmacologically treated. Published studies concerning possible links between apelin and HTN in young patients are scarce as for now.
Conclusion
To conclude, further studies are required to clarify the relationship between apelin, metabolic parameters and the early markers of atherosclerosis in pts with essential HTN. So far, on the ground of the role of apelin level in HTN, it may be postulated that apelin/APJ system would be a promising therapeutic target for HTN and other cardiovascular diseases in the future [44]. On the base of this study, conducted on young hypertensives, we may only assume there is a relationship between endogenous apelin and selected markers of metabolic disorders. However, it is too speculative to conclude on the base of our study that apelin may participate in the pathogenesis of early atherosclerosis lesions.
According to our findings there were no statistically significant differences in serum apelin and no relationships between serum apelin concentration and anthropometric parameters, serum lipids or cIMT in the whole examined group with HTN. Young males with primary HTN, in comparison to healthy males, have significantly higher plasma apelin concentrations. There is a negative correlation between apelin concentration and cIMT in young women, both the normal-weight and overweight ones, with newly diagnosed primary HTN. A positive correlation between apelin concentration and WHR was found in the population of young obese women with newly diagnosed primary HTN. The lower plasma apelin concentration, the higher was fasting TG in young overweight hypertensives.
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