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Original Research Paper
Biochemistry
KEYWORDS : Metabolic syndrome, Anthropometric indices, Lipid profile, Malon di-aldehyde, Glutathione, Ascorbic acid
Abbreviations:- BMI-Body mass index, CVD-Cardiovascular (WC), blood pressure (BP), fasting blood glucose (FBG) and serum
diseases, FBG-Fasting blood glucose, GSH-Glutathione (reduced triglyceride (TG) and high density lipoprotein cholesterol (HDL)
form), MDA-Malon-dialdehyde, MetS-Metabolic syndrome, OS- levels [12].
Oxidative stress, HDL-HDL cholesterol, LDL-LDL cholesterol, OS-
Oxidative stress, TC-Total cholesterol, T2DM-Type 2 diabetes The prevalence of MetS increases with increasing glucose intolerance
mellitus, TG-Triglyceride, WC-Waist circumference and with the increasing worldwide prevalence of T2DM, the expected
increase in the frequency of occurrence of the MetS will expectedly be
Introduction in geometric proportions. The prevalence of the MetS in the general
Metabolic syndrome (MetS) is a widely prevalent and multi-factorial population is estimated to be between 17-25% and in people with DM,
disorder that presents in a distinct, albeit heterogeneous phenotype. It reported prevalence rates range from 59% to 61% [13]. Useful
is a cluster of disorders that occur together, increasing the risk of anthropometric markers in MetS are body mass index (BMI) and waist
cardiovascular diseases (CVD) and type 2 diabetes mellitus (T2DM) circumference (WC). Obesity is closely associated with the
[1, 2]. The disorders include elevated blood pressure, insulin components of MetS including hyperglycemia, dyslipidemia and
resistance, and excess body fat around the waist and/or dyslipidemia hypertension [13, 14]. Though (BMI) is the most common measure of
[2, 3]. The prevalence of MetS depends on age, ethnic background, obesity, it does not reflect body shape. WC is a more accurate measure
and gender. It rises linearly from 20 to 50 years and plateaus thereafter of the distribution of body fat [18, 19]. The prognostic importance of
[4, 5]. With the increasing urbanization in developing countries like high WC has been recognized within the diagnostic criteria to identify
India, the incidence of MetS is expected to increase several-fold in the individuals with features of the MetS [14, 15].
coming years [5, 6]. The current worldwide obesity epidemic also
contributes to increased prevalence of MetS. The clinical relevance of One of the defining features of MetS is atherogenic dyslipidemia,
MetS is related to visceral obesity and its role in the development of manifested by lipoprotein disturbances like elevated TG, diminished
cardiovascular disease (CVD) [6, 7]. The two potential etio- HDL and increased low-density lipoprotein cholesterol (LDL) levels
pathogenetic factors of MetS are central obesity and insulin resistance. [16, 17]. Other features of MetS dyslipidemia include elevated very
Other important factors also influence the development of MetS low density lipoproteins (VLDL), and reduced HDL-2, which are the
including genetic profile, physical inactivity, ageing and hormonal large buoyant anti-atherogenic subspecies of total HDL [17, 18]. In
deregulation [7, 8]. some individuals, apo lipoproteins B (apo B) levels may be elevated,
reflecting an increase in VLDL and LDL. All of these abnormalities
MetS is a complex web of metabolic factors that are associated with a have been implicated as being independently atherogenic [19, 20].
2-fold risk of cardiovascular disease (CVD) and a 5-fold risk of .
diabetes [9]. Individuals with MetS have a 30%–40% probability of Oxidative stress (OS) results due to disturbed equilibrium between
developing DM and/or CVD within 20 years, depending on the pro-oxidants and anti-oxidants and plays a role in pathophysiology of
number of components present. Cardiovascular mortality is markedly T2DM and CVD. Some factors of MetS, such as hyperglycemia and a
increased in subjects with the MetS [10]. In the US, the unadjusted and pro-inflammatory state may lead to increased production of reactive
age-adjusted prevalence of the MetS have been estimated to be 21.8% oxygen species (ROS) [21, 22]. Antioxidants delay or inhibit cellular
and 23.7%, respectively. The Third Report of the US National damage mainly through their free radical scavenging properties [22,
Cholesterol Education Program Adult Treatment Panel III (US NCEP 23]. Malondialdehyde (MDA) is a lipid peroxidation bye product that
ATP-III) has recommended appropriate measures to identify is used as markers in lipid per oxidation assay [23, 24]. Glutathione
individuals with the MetS [11]. In 2005, the International Diabetes (GSH) is the most abundant intracellular thiol-based anti-oxidant,
Federation (IDF) provided new modified criteria for the diagnosis of prevalent in millimolar concentrations in all living aerobic cells, and
MetS, based on the following four features: waist circumference plays an important role in the cellular defense cascade against
Wome 75.68 85.56 <0.001 77.27 90.85 <0.001 17. Deedwania P, Barter P, Carmena R, Fruchart JC, Grundy SM, Haffner S, et al. Reduction
n 2.23 3.43 2.45 6.23 of low-density lipoprotein cholesterol in patients with coronary heart disease and
metabolic syndrome: Analysis of the Treating to New Targets study. Lancet 2006;
FBG Men 85.22 ± 96.26 <0.001 89.75 ± 108.73 <0.001 368:919-928.
(mg/dl) 6.34 10.87 8.76 21.92 18. EA Enas, V Mohan, M. Deepa, S. Farooq, S. Pazhoor, H. Chennikkara. The metabolic
Wome 84.46 ± 94.74 <0.001 88.63 ± 104.02 <0.001 syndrome and dyslipidemia among Asian Indians: a population with high rates of
diabetes and premature coronary artery disease. J Cardiomet Syndr. 2007; 2: 267–275.
n 6.15 10.23 8.14 20.77 19. Juonala M, Viikari JS, Kahonen M, Solakivi T, Helenius H, Jula A, et al. Childhood
TC Men 167.38 208.76 <0.001 172.45 212.74 <0.001 levels of serum apo lipoproteins B and A-I predict carotid intima-media thickness and
brachial endothelial function in adulthood: the cardiovascular risk in young Finns study.
(mg/dl) 12.85 16.34 14.52 18.43 J Am Coll Cardiol. 2008; 52: 293-299.
Wome 165.38 201.96 <0.001 171.71 210.84 <0.001 20. Sajimon Thomas, Suresh S., Sudheesh M., T. Vijayakumar. Changes in the Atherogenic,
n 11.76 15.84 14.13 17.67 Inflammatory and Thrombotic Markers in Patients with Metabolic Syndrome. Proc Nat
Sem Adv Clin Res. 2014; 192-196.
TG Men 91.85 136.47 <0.001 101.75 148.63 <0.001 21. De Mattia G, Bravi MC, Laurenti O, Moretti A, Cipriani R, Gatti A, et al. Endothelial
(mg/dl) 10.51 15.73 13.96 17.84 dysfunction and oxidative stress in type 1 and type 2 diabetic patients without clinical
Wome 90.77 138.95 <0.001 100.93 151.65 <0.001 macrovascular complications. Diabetes Research and Clinical Practice. 2008;
79:337–342.
n 10.22 15.84 13.67 16.26 22. Marjani AJ. 2005 Plasma lipid peroxidation zinc and erythrocyte Cu-Zn superoxide
HDL-C Men 48.95 35.24 <0.001 47.75 33.72 <0.001 dismutase enzyme activity in patients with type 2 diabetes mellitus in Gorgan city. 2005;
Internat J. Endocrinol. 2: 1-11.
(mg/dl) 7.86 4.51 6.663 3.98 23. Grattagliano I, Palmieri VO, Portincasa P, Moschetta A, Palasciano G. Oxidative stress-
Wome 56.71 47.66 <0.001 55.64 46.37 <0.001 induced risk factors associated with the metabolic2 syndrome: a unifying hypothesis.
n 5.14 5.63 5.02 5.28 2008; J Nutr Biochem. 19:491-504.
24. Shaikh AK, Suryakar AN. Oxidative stress and antioxidant status before and after
LDL-C Men 106.58 158.75 <0.001 113.64 159.98 <0.001 supplementation of anti-oxidant tablets in coronary artery disease. 2009; Biomed Res.
(mg/dl) 28.79 42.33 30.55 22.30 20: 136-140.
Wome 103.91 156.62 <0.001 110.98 145.88 <0.001 25. Padayatty S, Katz A, Wang Y, Eck P, Kwon O, Lee J, et al. Vitamin C as an antioxidant:
evaluation of its role in disease prevention. 2003; J Am Coll Nutr. 22: 18-35.
n 27.54 41.17 30.06 22.31 26. Thankappan KR, Shah B, Mathur P, Sarma PS, Srinivas G, Mini GK, et al. Risk factor
VLDL-C Men 17.23 23.75 <0.001 18.87 27.27 <0.001 profile for chronic non-communicable diseases: results of a community-based study in
Kerala, India. Indian J Med Res. 2010; 131:53-63.
(mg/dl) 4.87 10.36 5.21 12.85 27. Soman CR, Kutty VR, Safraj S, Vijayakumar K, Rajamohanan K, Ajayan K. All-Cause
Wome 16.98 22.08 <0.001 18.14 25.96 <0.001 Mortality and Cardiovascular Mortality in Kerala State of India: Results from a 5-Year
n 4.23 10.11 5.02 12.04 Follow-up of 161942 Rural Community Dwelling Adults. Asia Pac J Public Health.
2011; 23:896-903.
MDA Men 0.81 1.74 <0.001 0.98 2.18 <0.001 28. Soman CR, Shahulhameed S, Ramankutty V, Vijayakumar K, Kunjukrishnapillai R,
(µmol/ml 0.47 0.51 0.53 0.62 Ajayan K, Sajikumar S. Cohort Profile: The PROLIFE study in Kerala, India. Int J
) Epidemiol. 2011; 40:10-14.
Wome 0.72 1.68 <0.001 0.92 1.97 <0.001 29. Mahajan BK. Methods in biostatistics for medical students and research workers. 7th ed.
n 0.36 0.43 0.46 0.59 New Delhi: Jaypee Brothers; 2010.p. 80–194.
Ascorbic Men 0.49 0.37 <0.001 0.45 0.35 <0.001
acid 0.07 0.11 0.07 0.13
(mg/dl) Wome 0.48 0.40 <0.001 0.45 0.37 <0.001
n 0.05 0.09 0.06 0.08
GSH Men 10.74 9.26 <0.001 9.66 8.58 <0.001
(mg/dl) 4.13 3.27 3.83 3.14
Wome 11.18 9.73 <0.001 10.09 9.11 <0.001
n 4.22 3.12 3.78 3.24
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