A study of Hs-CRP and lipid profile in overweight individuals.
Overweight is generally defined as having more body fat than is optimally healthy. The degree to which a person is overweight is generally described by body mass index (BMI). In India 12.6% of women and 9.3% of men are obese.  Being overweight increases the likelihood of developing type 2 diabetes and cardiovascular disease (CVD). Being overweight parse is not the problem rather it may be the metabolic abnormalities that often coexist with overweight and obesity.  It is now scientifically well established that inflammation plays a role in the initiation, growth and destabilization of atherosclerotic plaques that lead to clogged arteries and most heart attacks.  Lipids and lipoproteins are well known risk factors for ischemic heart disease. Elevated levels of triglyceride, cholesterol and LDL-C are documented as risk factors for atherogenesis.  There is growing recognition that coronary heart disease (CHD) has an inflammatory component. Prospective studies have shown that plasma C-reactive protein (CRP) concentration, a marker of the acute-phase reaction, can predict CHD events in subjects with or without established cardiovascular disease beyond what can be estimated by traditional risk factors.
Materials and Methods
120 healthy overweight (BMI>25) individuals were selected for the study. These overweight individuals were divided into two distinct groups: Group I (n=60) included people with high triglyceride and low HDL-C (dyslipidaemic group), whereas the Group II (n=60) included normolipemic people. Inclusion Criteria: Males and Females 20-50 yr, BMI > 25. Exclusion Criteria: Acute and chronic inflammatory diseases, Diabetes, H/o smoking, H/o alcoholism, H/o angina, myocardial infarction, H/o recent illness, H/o taking anti-inflammatory drugs or statins. Informed consent was obtained from all 120 subjects; their weight (in kg) and height (in meters) was taken. BMI was calculated by the formula BMI = Weight/[Ht.sup.2]. Participants were in the 12 hr of fasting state. 3 ml venous blood was collected in 5 mg% EDTA collection bottle for plasma (for lipid profile and glucose), 3 ml venous blood was collected in plain bottle and allowed to clot to separate serum (for CRP). Plasma and Serum were separated within one hour after sample collection. Care was taken to avoid haemolysis. The following methodology was applied to the samples to obtain the required biomarker levels; HS-CRP-Automation-Immunoturbidimetry method; Total Cholesterol-Spectrophotometer-Cholesterol Oxidase enzymatic method; HDL-C-Spectrophotometer-Cholesterol Oxidase enzymatic method; Triacylglycerol-Spectrophotometer-GPO-PAP enzymatic method; LDL-C-by Friedwalds equation; VLDL-C-TG/5; T-C/HDL-C ratio; LDL-C/HDL-C ratio; GLUCOSE-GOD-POD method. Data obtained was analyzed by SPSS statistical software (v 15.0)
Unpaired T test was used for comparison between the two groups. The results were expressed as Mean [+ or -] SD and p value. The mean BMI was higher in group I than group II. Plasma Hs-CRP levels were significantly higher in group I than the group II (p < 0.05). Group I individuals had significantly higher levels of T-C, TAG, VLDL, LDL, T-C/HDL-C ratio, LDL-C/HDL-C ratio and Glucose when compared to group II(p<0.05). The HDL-C levels were significantly lower in group I when compared to group II.
In the present study the dyslipidaemic group had significantly higher fasting levels of serum Hs-CRP than the normolipemic group. The normolipemic group had the mean Hs-CRP of 2.08, which is higher than the normal reference range (<1 mg/l). This is because as they are all overweight and adipose tissue is a source for the production and release of cytokines, which will stimulate the synthesis of CRP by the liver.  Dyslipidaemic individuals have significantly higher glucose levels than the normolipemic and are more at risk of getting diabetes. The cause might be due to insulin resistance. Similar results (high levels of Hs-CRP and Glucose) were observed by Philip barter et al.  In a recent statement issued jointly by the American Heart Association and the Centers for Disease Control, the Hs-CRP test was recommended for use in the identification of risk for CVD.  As the presence of inflammation can precede a heart attack or stroke by eight or more years , Hs-CRP testing can allow for effective preventative therapies .
In the present study out of 120 overweight individuals 60 were dyslipidaemic and 60 were normolipemic. Although overweight (BMI>25) individuals tend to be insulin resistant, hyperinsulinemic, glucose intolerant, and dyslipidaemic, not all overweight or obese individuals are insulin resistant, nor do they all have the characteristic disturbances in glucose or lipid metabolism. [9-12] Unknown genetic factors could be the cause for this difference. The dyslipidaemic group had significantly higher levels of Total Cholesterol, TAG, VLDL, LDL, T C/HDL-C, LDL-C/HDL than the normolipemic individuals. However the HDL-C levels were significantly low in dyslipidaemic individuals than the normolipemic individuals. Plasma triglyceride and high-density lipoprotein (HDL) cholesterol levels are independently associated with insulin resistance  and are independent predictors of CVD. In addition, the plasma concentration ratio of total cholesterol to HDL cholesterol is well recognized as a predictor of CVD  and is also highly correlated with insulin resistance . The cause for dyslipidaemia in overweight individuals could be primary insulin resistance which might be due to genetic factors.
Mechanisms underlying the observed association of dyslipidaemia with the other metabolic derangements are uncertain. Dyslipidaemia has been shown to be an important risk factor for CAD , since Triacylglycerol brings changes in LDL particle size, density, distribution and composition producing small dense LDL which is more atherogenic. Considerable evidence has established the presence of oxidized components of LDL in atherosclerotic lesions. Other cytokines regulated by components of oxidized LDL can activate the leukocytes within the intimal layer, provoking their production of further inflammatory mediators. Moreover, these activated leukocytes can generate reactive oxygen species that augment oxidant stress, the constant companion of inflammation in atherosclerosis.  These inflammatory mediators (TNF-[alpha], IL-6) will stimulate the synthesis of CRP by the liver.  Thus Hs-CRP levels are elevated in this study. Estimation of serum triglyceride levels is thus an indirect measurement of LDL particle size.
A growing number of studies suggest that CRP is an independent risk factor for atherosclerotic vascular disease. It has been suggested that Hs-CRP may not only be a marker of generalized inflammation but directly and actively participate in atherogenesis.  CRP binds to the LDL particle in atherosclerotic plaques leading to activation of complement and tissue factor production by macrophages , thus being pro-inflammatory and contributing to atherogenesis.
Limitations: The present study is a small scale study so large scale studies are indicated to further establish the findings.
Hs-CRP is a simple cost effective test, which can predict the cardiovascular risk. Hence it is recommended in overweight individuals.
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Source of Support: Nil
Conflict of interest: None declared
H Kishan Reddy (1), B Laxmikanth (2), P Sujatha (3), Prabhavati Modi (4)
(1) Department of Biochemistry, Prathima Institute of Medical Sciences, Karimnagar, Andhra Pradesh, India
(2) Department of Biochemistry, Shri Sathya Sai Medical College & Research Institute, Chennai, India
(3) Department of Biochemistry, Eralucknow Medical College, Lucknow, India
(4) Department of Biochemistry, Apollo Medical College, Hyderabad, India
Correspondence to: H Kishan Reddy (email@example.com)
Received Date: 27.01.2013
Accepted Date: 28.01.2013
Table-1: Comparison of Group I and Group II Parameter Group I Group II P value BMI 27.80 [+ or -] 1.05 27.08 [+ or -] 1.01 0.000 Hs-CRP 2.86 [+ or -] 1.31 2.08 [+ or -] 0.92 0.000 T-C 200.70 [+ or -] 32.80 173.91 [+ or -] 28.09 0.000 HDL-C 36.88 [+ or -] 5.09 56.60 [+ or -] 10.57 0.000 TAG 216.68 [+ or -] 50.47 88.93 [+ or -] 25.81 0.000 VLDL 43.33 [+ or -] 10.09 17.79 [+ or -] 5.19 0.000 LDL 122.28 [+ or -] 29.13 99.50 [+ or -] 29.66 0.000 T-C/HDL-C 5.54 [+ or -] 1.18 3.18 [+ or -] 0.83 < 0.0001 LDL/HDL-C 3.38 [+ or -] 0.93 1.85 [+ or -] 0.75 < 0.0001 Glucose 98.93 [+ or -] 12.89 90.26 [+ or -] 10.47 0.000 P < 0.05, significant
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|Title Annotation:||RESEARCH ARTICLE; C-reactive protein|
|Author:||Reddy, H.Kishan; Laxmikanth, B.; Sujatha, P.; Modi, Prabhavati|
|Publication:||International Journal of Medical Science and Public Health|
|Date:||Apr 1, 2013|
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