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 Table of Contents  
ORIGINAL ARTICLE
Year : 2018  |  Volume : 16  |  Issue : 2  |  Page : 99-104

Role of insulin resistance in essential hypertensive patients in Qena Governorate, Egypt


1 Department of Internal Medicine, Faculty of Medicine, South Valley University, Qena, Egypt
2 Department of Clinical and Chemical Pathology, Faculty of Medicine, South Valley University, Qena, Egypt
3 Department of Community Medicine, Faculty of Medicine, South Valley University, Qena, Egypt
4 Department of Internal Medicine & Cardiology, Sohag Faculty of Medicine, Sohag, Egypt

Date of Submission22-Oct-2017
Date of Acceptance05-Aug-2018
Date of Web Publication27-Feb-2019

Correspondence Address:
Mohamed Alsenbsey
Department of Internal Medicine, Qena University Hospital, South Valley University (SVU), Qena, 83523
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/AZMJ.AZMJ_56_17

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  Abstract 

Introduction Essential hypertension is associated with multiple metabolic abnormalities; one of the most important is hyperinsulinemia. On the contrary, euglycemic state has been elicited in hypertensive patients.
Aim To explore the pathogenic role of hyperinsulinemia in essential hypertensive patients even with euglycemia.
Patients and methods A total of 60 euglycemic patients (30 hypertensive patients and 30 normotensive controls) were recruited in a case–control study. Blood pressure, insulin level, lipid profiles, BMI, and waist circumference (WC) were estimated for both groups. In addition, the severity of hypertension was classified according to the European hypertension guidelines.
Results Significant increases of fasting insulin level, BMI, WC, and dyslipidemia (increase total cholesterol, triglycerides, and low-density lipoprotein-cholesterol) and a significant decrease of high-density lipoprotein-cholesterol in hypertensive patients than the controls were found. Moreover, a highly significant correlation was detected between the severity of hypertension and the parameters of fasting insulin level, BMI, WC, and triglycerides level.
Conclusion The study showed a significant increase in fasting insulin level in hypertensive patients than the control group. Besides, there was a highly significant increase of fasting insulin level with hypertension severity; therefore, this supports a possible pathogenic role of hyperinsulinemia (through insulin resistance) in the onset of hypertension even when the fasting blood sugar is within the normal limits (euglycemic).

Keywords: hypertension, insulin resistance, metabolic syndrome, Qena Governorate, waist circumference


How to cite this article:
Alsenbsey M, Asham B, Aly SS, Ahmed SS, Boghdady A. Role of insulin resistance in essential hypertensive patients in Qena Governorate, Egypt. Al-Azhar Assiut Med J 2018;16:99-104

How to cite this URL:
Alsenbsey M, Asham B, Aly SS, Ahmed SS, Boghdady A. Role of insulin resistance in essential hypertensive patients in Qena Governorate, Egypt. Al-Azhar Assiut Med J [serial online] 2018 [cited 2020 Jul 6];16:99-104. Available from: http://www.azmj.eg.net/text.asp?2018/16/2/99/253093


  Introduction Top


Hypertension is a major public health problem that affects approximately one billion people worldwide [1]. In Egypt, 26.3% of adult had high blood pressure (BP) from 1991 to 1993, and it was projected to increase to reach 15 million of 80 million or more Egyptians [2]. Hypertension is a known risk factor of cardiovascular and renal diseases. Cardiovascular mortality risk doubles with every 20/10 mmHg increase in systolic blood pressure (SBP) and diastolic blood pressure (DBP) [1]. Overall, 80–90% of hypertension causes are unknown (essential hypertension), and the remaining causes (secondary hypertension) are because of other diseases [3]. Possible causes of essential hypertension include hereditary, genetic factors, environmental factors, blood vessel endothelial damage and atherosclerosis, insulin resistance (IR) [4],[5], and lifestyle factors such as obesity, stress, excess sodium, smoking, and alcohol intake. In addition, diseases that cause secondary hypertension include renal diseases, endocrine diseases, cardiovascular diseases, drugs, and eclampsia of pregnancy [6].

Fasting insulin level is a clinical index reflecting the state of glucose metabolism. Hyperinsulinemia occurs as a compensation for impaired glucose tolerance, and it is an early clinical manifestation of IR [7]. Insulin resistance (IR) or metabolic syndrome is an abnormal metabolic state during which the body cells lose sensitivity to insulin, meaning diminished their ability to respond to insulin transporting glucose from the blood stream into muscle and other cells. As a result, the pancreas produces large quantities of insulin to maintain normal levels of glucose in the blood to cope with the body’s demands. Eventually, the pancreas cannot cope with the increase of blood glucose even in the fasting state leading to the development of diabetes mellitus (DM) type 2 [8]. Insulin also contributes toward the regulation of BP through vasorelaxation induced by stimulating the production of nitric oxide in the endothelium [9] and regulation of sodium homeostasis by enhancing sodium reabsorption in the kidney [10].

IR and hyperinsulinemia are known to have profound relationship with various medical diseases, such as dyslipidemia, cardiovascular diseases, and obesity. These diseases are significantly associated with hypertension, which suggest a clinical relation between hyperinsulinemia and hypertension [11],[12]. In addition to hyperinsulinemia, other factors that possibly promote the development of hypertension through IR include visceral obesity, oxidative stress, activated renin–angiotensin system, and increased inflammatory mediators. These factors in conjunction with IR may induce sympathetic overactivity, vasoconstriction, and increased intravascular fluid leading to hypertension [13]. However, still the current data regarding the relationships between IR and hypertension remain inconclusive and contradictory; therefore, further studies are needed.


  Aim Top


The study aims to find out if the higher fasting insulin level (hyperinsulinemia as markers of IR) has a role in the pathogenesis and development of hypertension.


  Patients and methods Top


A case–control study was carried out on outpatients attending the Internal Medicine Clinic at Qena University Hospital during the period from July to December 2016.

According to estimated sample size, a total of 30 essential hypertensive patients as cases and 30 healthy age-matched and sex-matched individuals as controls were enrolled in the study.

Inclusion criteria were individuals more than 18 years old, euglycemic individuals (fasting glucose level <110 mg/dl according to WHO) [14], and essential hypertensive patients who were included if they fulfilled the following criteria: newly diagnosed, had uncomplicated hypertension, not receiving treatment, and their SBP was more than or equal to 140 mmHg or DBP was more than or equal to 90 mmHg for three visits provided that the patients were in complete physical and mental rest. BP was recorded with a mercury sphygmomanometer in lying down position on the left arm. Hypertensive patients were categorized into having mild, moderate, or severe degree of hypertension according to the European hypertension (ESH and ESC) guidelines as follow.

Mild hypertension (grade 1): considered if SBP=140–159 mmHg or DBP=90–99 mmHg.

Moderate hypertension (grade 2): considered if SBP=160–179 mmHg or DBP=100–109 mmHg.

Severe hypertension (grade 3): considered if SBP more than or equal to 180 mmHg or DBP more than or equal to 110 mmHg [15].

Exclusion criteria were patient with impaired glucose tolerance, diabetes, complicated hypertension, or receiving corticosteroids or lipid-lowering agents.

All patients and control group were subjected to detailed medical history and physical examination; anthropometric measurements, including height, weight, waist circumference (WC), and BMI calculated as weight (kg)/height (m2); and laboratory investigations, which were done after an overnight fasting for a minimum of 10 h, including fasting blood glucose level, and lipid profiles [cholesterol, high-density lipoprotein-cholesterol (HDL-C), low-density lipoprotein-cholesterol (LDL-C), and triglycerides (TGs)]; serum insulin level by enzyme-linked immunosorbent assay; and kidney function tests (blood urea nitrogen and creatinine level).

Specimen collection and analytic procedures: Overall, 5 ml of venous blood was collected in a plain red-top venipuncture tube without additives. Blood was allowed to clot. Then, the specimen was centrifuged to separate the serum from the cells. If specimen could not be assayed in time for insulin assay, the serum was frozen and stored at −30°C to be measured within 30 days (as it is not stable in serum basis). Repeated freezing and thawing was avoided.

Serum total cholesterol, TGs, HDL-C, fasting blood glucose, blood urea nitrogen, and creatinine were analyzed by Cobas c311 chemical analyzer, Roche Diagnostics Deutschland GmbH, Mannheim, Germany. LDL-C was calculated by the formula devised by Friedewald and colleagues [16],[17]. Insulin level was measured using Human Insulin Immunoassay Test Kit (Catalog No. E29-072), Immunuspec, Canoga Park, CA, USA.

Based on the clinical data in concordance with published literature, the normal adult values of insulin level are considered to be 0.7–9.0 μU/ml [18].

Before starting the study, the study protocol was approved by the Ethical Research Committee of Qena Faculty of Medicine. An informed consent was obtained from each participant after explanation of the nature and purpose of the study. Furthermore, the researchers assured the confidentiality of all information.

Statistical analysis

Statistical analysis was done using SPSS-20 statistical software package after data entry and coding. For quantitative variables, data were presented as means and SDs, whereas qualitative variables were presented by number and frequency. Unpaired Student’s t test was used to compare two independent groups regarding quantitative variables. χ2 was used to compare qualitative variables. For multiple groups comparison, analysis of variance (ANOVA) and Tukey’s test were used. Tukey’s test is used in conjunction with ANOVA to find the means that are significantly different from each other. Pearson’s bivariate correlation test was used to find the association of hyperinsulinemia (a marker of IR) and hypertension. Statistical significant is considered if P value less than 0.05 or less than 0.001.


  Results Top


The study was conducted on 30 patients diagnosed as having essential hypertensive without disturbed renal functions and 30 healthy normotensive as control group. Control group was age and sex matched with cases. Moreover, both hypertensive and control groups were euglycemic. The mean age of hypertensive patients was 49.9±7.6 years. The hypertensive group included 18 females and 12 males, and their mean fasting blood glucose was 95.9±6.1. The mean age of the control group was 49.6±7.5 years. The control group included 17 females and 13 males, and their mean fasting blood glucose was 95.8±7.9. Blood urea nitrogen for hypertensive group was 47.2±10 and for control group was 43±11.6, with no significant difference. Similarly for creatinine, no significant difference was detected between hypertensive group (0.83±0.5) and control group (0.87±0.4).

[Table 1] shows a highly significant difference in SBP, DBP, and mean BP, BMI, and WC in hypertensive patients than the control (P<0.001); moreover, there was a significant difference in hyperinsulinemia in the hypertensive group than in the control group.
Table 1 Comparison between hypertensive patients and control group in systolic blood pressure, diastolic blood pressure, mean blood pressure, fasting serum insulin, and anthropometric measurements (BMI and waist circumference)

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[Table 2] depicts a highly significantly higher hypercholesterolemia and hypertriglyceridemia and lower HDL-C in hypertensive group than the control one (P<0.001); moreover, LDL-C was significantly higher in the hypertensive patients than the control group.
Table 2 Lipid profiles in hypertensive patients and control group

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In [Table 3], by using ANOVA and Tukey’s test, a highly significant increase of BMI, WC, SBP, DBP, mean BP, TG, and fasting insulin with the increase of hypertension severity was found (P<0.001) and a significant decrease of HDL-C with the severity of hypertension (P<0.05).
Table 3 Comparing the three severity grades of hypertension among patients according to age, fasting glucose and insulin, blood pressure, anthropometric measurements, and lipid profiles

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[Table 4] illustrated that there is a positive correlation between fasting insulin level and both SBP and DBP in hypertensive patients; this means that an increase in fasting insulin (hyperinsulinemia) increases BP. Hyperinsulinemia can be used as a marker of IR, and in turn, IR is positively correlated and associated with an increase in BP.
Table 4 Correlation between fasting serum insulin level and systolic blood pressure and diastolic blood pressure in the studied sample

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  Discussion Top


IR as a component of the metabolic syndrome affects ∼25% of the world’s population and is considered as a risk factor for various diseases. IR and abdominal obesity are risk factors for developing hypertension, cardiovascular diseases, and type 2 DM [20]. IR along with type 2 DM has a risk of impaired glucose regulation, abdominal obesity, hypertension, atherogenic dyslipidemia, and cardiovascular diseases. In those with normal glucose tolerance, the presence of the metabolic syndrome predicts a high risk of developing type 2 DM [21] Hypertension usually coexists with DM. The overlap between hypertension and diabetes in etiology and disease mechanisms is thought to be caused by IR, obesity, inflammation, and oxidative stress [22]. Hypertension with DM type 2 aggravates DM complications, increases cardiovascular morbidity and mortality, and magnifies risk of end-stage renal disease [23]. Effective interventions of IR, type 2 DM, and hypertension with all of its morbid complications include weight loss; diet modification with more fruits, vegetables, whole grains, monounsaturated fats, and low-fat dairy products; physical activity and exercise; and use of pharmacological lipid-lowering agents [20].

The present study aimed to explore the hypothesis that hyperinsulinemia resulting from IR is associated with and even plays a pathogenic role in euglycemic essential hypertensive patients in Egyptian population of Qena Governorate. Significantly higher fasting insulin level (P=0.002) in hypertensive patients 8.7±5.7 than the control group 4.7±2.9 was reported in our study. These findings are in line with those who observed that fasting serum insulin levels were significantly higher in hypertensive patients compared with controls (P<0.01) [24]. These findings correlate with Xun et al. [25], who concluded that hyperinsulinemia in young adulthood was positively associated with incidence of hypertension later on in life for men and women, African American and whites, and those with normal weight and overweight. Some previous publications have stated that hypertensive patients were found to have significantly higher hyperinsulinemia and IR than normotensives (P=0.02 and 0.04) and even that IR is considered as an independent risk factor for hypertension in Koreans [26],[27]. In agreement, our current study revealed a positive correlation between insulin level − as a marker of IR − and the severity of hypertension. Besides, Roopa et al. [28] found that IR correlates with the severity of essential hypertension, as IR is seen in patients with very high BP.

Zhou et al. [29] postulated and discussed the mechanism of hyperinsulinemia in enhancement of hypertension; as IR impairs insulin stimulation of nitrous oxide and activates the mitogen-activated protein kinases pathway resulting in vasoconstriction of blood vessels, production of proinflammatory cytokines, increased sodium and water retention and elevation of BP. Moreover; animal and clinical studies suggest that hyperinsulinemia, IR, and hypertension are associated with salt sensitivity [30], as insulin has been shown to inhibit sodium excretion by increasing sodium reabsorption in the kidney. Sodium accumulation causes water retention and often high BP.

Some other contrary data suggested no association between IR and hypertension, as those who had been classified according to fasting insulin level had insignificant correlations with hypertension [19],[31].

In this study, there was a highly significant increase in BMI in hypertensive patients more than the control group (P<0.001). These findings are in line with previously published data [32], which reported that weight gain is associated with increased risk of hypertension, and even modest weight loss is associated with substantial reduction in BP in obese [32]. However, other contrary findings reported that obesity is not often related to hypertension, as no significant increase of the BP level could be detected when compared with nonobese populations [33].

Our results showed significant increase of WC in hypertensives compared with the control group. These findings agrees with former data stated that WC is the only clinical index associated with elevated BP rather than any of adiposity or weight measurement indices [34]. In addition to that, a recently published logistic regression analysis revealed that both BMI and WC are significant predictors of hypertension [35].

In our study, the lipid profiles of hypertensive patients along with hyperinsulinemia showed significant increase in total cholesterol, TG, LDL-C and lower HDL-C (P<0.001) compared with controls. This is in accordance with Avramoglu et al. [36], who found that essential hypertension patients had a cluster of cardiovascular risk factors common with hyperinsulinemia and IR syndrome, which are an increase of atherogenic blood lipid fractions of cholesterol, TGs and LDL-C and lower HDL-C [36]. On the contrary, some other published results support that total cholesterol, TG, and LDL-C of newly diagnosed hypertensives were not significantly different from the control groups [37],[38].

Our finding that the level of hypertriglyceridemia is significantly related to the hypertensive group is in accordance with many recently published data, which proved that hyperinsulinemia, IR, hypertriglyceridemia and even the increased TG/HDL ratio can predict the presence of and some prognostic factors for essential hypertension severity [39],[40].

Limitation and strengths of the study

Patients and controls may have specific features limited to them, so results cannot be generalized beyond the research setting in Qena governorate. IR by itself was not measured, as there were no available kits for its assay in the clinical laboratories, and we had relied on hyperinsulinemia as a marker of IR. Dietary assessment tools and questionnaires have not been inquired, as we found it could be subjective and instead we used BMI and WC as objective measurements. In this frame, some characteristics of the effect of dietary habits in the studied group could have been missed. The strength of this preliminary study is that it investigates the role of IR in the pathogenesis of hypertension, so it gives perspectives for further analysis regarding its role and involvement in complications of hypertension and related cardiovascular diseases.


  Conclusion Top


The study showed that increased serum insulin plays a fundamental role in pathophysiology of essential hypertension as hyperinsulinemia was associated with the severity of essential hypertension. It is highly supposed that increase in BP is related to change in insulin action, sensitivity, and resistance.

The study showed a significant increase of BMI and WC of essential hypertensive patients and more weight gain associated with severity of hypertension. Thus, the magnitude of weight gain and obesity is associated with increased risk of hypertension.

Increased polyunsaturated fatty acid intake manifested by higher level of TG could be used as a marker for severity of essential hypertension, hyperinsulinemia, and IR.

Recommendations

In view of our results, we recommend the following:
  1. Early detection of hyperinsulinemia as a marker of IR and applying therapeutic regimen for its control, and hence, counteracting its risk in developing hypertension.
  2. Lifestyles modification to reduce body weight as it is a risk factor of hypertension and a major component in its treatment.
  3. Periodic assessment of lipid profiles and treatment of hypocholesteremia and specifically hypertriglyceridemia by lipid-lowering agents, as it is a risk factor of hyperinsulinemia and hypertension.
  4. Further studies on the role of hyperinsulinemia and IR in essential hypertension with special reference to its involvement in long-term cardiovascular complications.


Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
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    Tables

  [Table 1], [Table 2], [Table 3], [Table 4]



 

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