• Users Online: 315
  • Home
  • Print this page
  • Email this page
Home Current issue Ahead of print Search About us Editorial board Archives Submit article Author Guidelines Subscribe Contacts Login 

 Table of Contents  
Year : 2014  |  Volume : 1  |  Issue : 3  |  Page : 59-65

The metabolic syndrome: Time for addressal

Centre for Medical Biotechnology, Maharshi Dayanand University, Rohtak, Haryana, India

Date of Web Publication24-Mar-2015

Correspondence Address:
Amita Suneja Dang
Centre for Medical Biotechnology, Maharshi Dayanand University, Rohtak - 124 001, Haryana
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2394-2010.153879

Rights and Permissions

The metabolic syndrome (Met S) is an escalating clinical and public-health challenge worldwide with increasing prevalence figures ranging from 10% to as high as 84%. Urbanization, calorie dense diet, sedentary life habits and increasing obesity are significantly associated with its increased prevalence. It is defined by a constellation of an interconnected physiological, clinical, metabolic and biochemical factors that directly increase the risk of diseases like cardiovascular disease (CVD), Type 2 diabetes mellitus (T2DM), stoke, dyslipidemia and endothelial dysfunction. The knowledge about Met S and its consequences in society is in infancy stage. Existing criteria's for defining it are ambiguous and rationale for thresholds are ill defined. This makes Met S difficult to understand, diagnose and conclude. Therefore, current national and worldwide epidemiology of Met S also remains controversial. The proliferation of various definitions demands a single unifying definition. It is important to identify and evaluate the population with Met S as early interventions can simply avoid the complications associated. Increasing the awareness of Met S itself may account for huge decline as early interventions help to abort the associated complications. Simple lifestyle changes and routine health checkups can help keep metabolic syndrome at bay. The prevalence of Met S is high as well as unrecognized among the general population. If the situation persists Met S may prove a massive killer in the years to come. This calls for prompt and incessant updating of medical community as well as public sector.

Keywords: Lifestyle, metabolic syndrome, obesity, type 2 diabetes mellitus

How to cite this article:
Dang AS, Deswal R. The metabolic syndrome: Time for addressal. J Health Res Rev 2014;1:59-65

How to cite this URL:
Dang AS, Deswal R. The metabolic syndrome: Time for addressal. J Health Res Rev [serial online] 2014 [cited 2021 Sep 23];1:59-65. Available from: https://www.jhrr.org/text.asp?2014/1/3/59/153879

  Introduction Top

Met S is present if three of the following five criterion are met: Blood pressure ≥130/85 mmHg, waist circumference ≥35 inches (women) or ≥40 inches (men), fasting high-density lipoprotein level <50 mg/dl (women) or <40 mg/dl (men), fasting triglyceride (TG) level >150 mg/dl and fasting blood sugar >100 mg/dl according to The National Cholesterol Education Program's Adult Treatment Panel III report(NCEP-ATP). [1] Studies of regional variations and temporal trends in the prevalence of the Met S is difficult because of reiterate changes made in its definition over time. [2] Met S remained ignored for most of the 20 th century. Though in the last few decades the medical science has achieved unprecedented heights in revealing multifactorial diseases, yet a mechanism which can fully explain development of Met S has not been elucidate. Met S has not been well defined and characterized, it still remains a topic of contention. However, it is now clear that metabolic syndrome often present with life threatening decompensation/complications which were once considered livable. Consumption of fat and calories rich diet, traditional to modern lifestyle transformation, combined with approbation of a sedentary life style and disturbed biological clock has led to the increased in prevalence of Met S all over the world in the last few decades. The prevention is based on availability of current scientific knowledge and education of public and medical community. Metabolic syndrome should not be missed as it presents very adverse impact on physical and psychological state of subject. An intricate web of economic, social and cultural changes are the major causes of Met S and its associated risk factors like Diabetes, Obesity, Hypertension, Dyslipedemia, Coronary heart disease, Endothelial dysfunction etc. The diagnosis is ambiguous. Practitioners should not wait to address problems until the patient is having all the five symptoms of the syndrome. Standardized methodology for diagnosis is needed.

  Background Top

The recognition of the metabolic syndrome can be dated back to 1920s when Kylin identified a triad of hypertension, and hyperglycemia and gout in his patients. Since then, studies have correlated complications like obesity, hypertension hyperinsulinemia and hypertriglyceridemia with Met S. Reaven's lecture, in 1998, defined Syndrome X as metabolic complications of IR among obese and non-obese patients. Significant cardiovascular (CV) risk factors were frequently observed in patients with type 2 diabetes mellitus. Reaven proposed that insulin resistance with the resultant compensatory hyperinsulinemia is the major pathophysiological abnormality explaining most of this clustering phenomenon and possibly the underlying cause of Cardio Vascular risk factors. Background history of Met S is shown in [Table 1].
Table 1: Background history of Met S

Click here to view

  Prevalence of Met S Top

Metabolic syndrome is a burgeoning universal problem. One in approximately every 4 or 5 adults has developed Met S depending on the daily lifestyle habits and the environmental conditions of the country of residence. Met S becomes more prevalent with increasing age paralleled by an increase in age-associated diseases and disabilities. [12] Due to global increase in obesity and sedentary lifestyles, the prevalence of the Met S is increasing throughout the world. From 1999 to 2010 National Health and Nutrition Examination Survey (NHANES) for prevalence reported the rates as high as 59%. [13] Prevalence of the Met S is also dependent on the definition used, sex, race and ethnicity. The estimation of prevalence between men and women have been somewhat different across cohorts. This grouping of abnormalities is usually viewed and attributed to people's dietary habits. However, the underlying pathophysiological processes leading to its development are unclear and there is confusion over its conceptual definitions and criteria, allowing the medical controversy over Met S to continue. [14] Approximately one third of the European population is estimated to have Met S, with a comparable prevalence in Latin America. [15] It is also considered an emerging epidemic in developing East Asian countries, including China, Japan, and Korea. Met S prevalence in East Asia may range from 2-18% in women and from 9-13% in men, depending on the population and definitions used. [16],[17],[18] Worldwide prevalence of Met S is shown in [Table 2].
Table 2: Prevalence of Met S across the world

Click here to view


The exact cause of Met S is unknown. Its pathophysiology is intensely complicated and has been only partially interpreted. Most patients of Met S are often obese, sedentary and have a degree of Insulin resistance. The most important contributory factors that have been identified are (i) aging, (ii) genetic makeup, and (iii) daily lifestyle and habits (e.g. inadequate physical activity and excess caloric intake). [34] Met S is thought to be caused by insulin resistance and adipose tissue dysfunction. Deteriorated adipose tissue also plays an significant role in the pathogenesis of obesity-related insulin resistance. Both infiltration of macro-phages and adipose tissue enlargement result in the release of proinflammatory cytokines and insulin resistance advancement. IR appears to be the primary mediator of Met S. These abnormalities may result from obesity with associated increase in the levels of free fatty acid and changes in the distribution patterns of Insulin. Adipose tissue distribution also affect development of metabolic syndrome. Fat that is visceral or intra-abdominal correlates with inflammation, whereas subcutaneous fat does not. There are a number of possible descriptions expaining this, including experimental investigations that omental fat is more resistant to action of insulin and may result in accumulation of toxic free fatty acids (FFA) in the portal circulation. [35] Visceral adipocity is known to eventually produce harmful levels of cytokines such as adiponectin, leptin, resistin, tumor necrosis factor and plasminogen activator inhibitor. [36] Psychological characteristics, including anger, depression, and hostility, may be linked to increased risk for metabolic syndrome. [37] However, psychological disorders especially anxiety, may represent comorbidity or a complication of metabolic syndrome. [38] Clearly, further study is warranted.

  Pathophysiology of Met S Top

Metabolic Syndrome is the outcome of complicated interplay between environmental and genetic factors and hence the term Met S has become a burning topic of discussion in medical literature. Insulin resistance, atherogenic dyslipidemia, endothelial dysfunction, visceral adiposity, elevated blood pressure, chronic stress, hypercoagulable state and genetic susceptibility are several factors which comprises the syndrome. Insulin Resistance and abdominal obesity are viewed as the core defects in the pathophysiology of Met S. The two risk factors are highly interrelated and therefore it is difficult to ascertain which one plays the dominant role in pathogenesis and progression of Met S. [39],[40],[41],[42] The insight into the pathophysiology provides a practical tool to identify patients with increased risk of diabetes mellitus type II and cardiovascular disease (CVD). In addition, pathophysiology of Met S is complicated by certain contributing factors such as genetics, race/ethnicity, age, hormone imbalances, diet, physical inactivity, drugs, dysregulation of adipose tissue-derived cytokines and inflammation. Met S is caused by combination of numerous risk factors, primarily driven by insulin resistance and obesity which gives rise to the development of clustering of metabolic health risk factors. [43] Therefore, it is unrealistic to assume that Met S is caused by a single underlying defect.

  Clinical features Top

Insulin resistance

Insulin Resistance (IR) is defined as a pathophysiological condition in which a normal concentration of insulin does not necessarily produce a normal response in the peripheral target tissues such as liver, adipose tissue and muscles. Under this condition, β cells of pancreas secretes more insulin (i.e., hyperinsulinemia) to overcome the hyperglycemic condition in insulin-resistant individuals. The most accepted hypothesis to describe the pathophysiology of Met S is IR. Characteristics of the insulin sensitive phenotype include a normal body weight without abdominal obesity, consuming a diet low in saturated fats and being moderately active. [9],[44],[45],[46] Alternatively, insulin-resistant individuals demonstrate an impaired glucose tolerance by an abnormal response to a glucose challenge, reduction in insulin action after intravenous administration of insulin (euglycemic clamp technique) with decreased insulin-mediated glucose clearance, an elevated fasting glucose levels and reduction in the suppression of endogenous glucose production. The above insulin action results in the clinical manifestations of Met S. [47] This inability of pancreatic beta cells to produce adequate insulin to overcome the worsening IR leads to hyperglycemia and overt T2DM. [48] lnsulin signaling occurs by the binding of insulin to the insulin receptor (ligand-activated tyrosine kinase) followed by Tyrosine phosphorylation of downstream substrates with activation of two parallel pathways: The mitogen activated protein (MAP) kinase pathway and the phosphoinositide 3-kinase (PI3K) pathway. In Insulin resistance, the MAP kinase pathway functions normally while the PI3K-Akt pathway is affected leading to disequilibrium between these two parallel pathways. The PI3K-Akt pathway is inhibited leading to reduced endothelial NO production, which results in endothelial dysfunction and reduced GLUT4 translocation, leading to a decreased fat and skeletal muscle glucose uptake. [49] By contrast, the MAP kinase pathway remains unaffected, so there is a continued expression of vascular cell adhesion molecules with continued endothelin-1 (ET-1) production. [50] IR predisposes to vascular abnormalities that further leads to atherosclerosis. Insulin-resistant individuals usually have an abnormal distribution of upper body fat.

Central obesity

Central obesity accompanied by IR is a key factor in the development Met S and the associated future complications. The "obesity epidemic" is primarily driven by an increased intake of calorie rich food and decreased physical activity. Adipose tissue is defined as a heterogeneous mixture of stromal preadipocytes, adipocytes, endothelium and immune cells and it can respond dynamically and rapidly to changes in nutrient excess through adipocytes hyperplasia and hypertrophy. [51] Obesity may results in progressive adipocytes enlargement with limited blood supply to adipocytes with consequent hypoxia. [52] Hypoxia results in necrosis and macrophage infiltration into adipose tissue, leading to an overproduction of adipocytokines known as biologically active metabolites which includes free fatty acids (FFA), glycerol, proinflammatory mediators tumor necrosis factor alpha (TNF), interleukin-6 (IL-6), plasminogen activator inhibitor-1 (PAI-1) and C-reactive protein. [53] This results in localized inflammation of adipose tissue and an overall systemic inflammation associated with the obesity related comorbidities development. [48] Adipocytokines integrates the autocrine, paracrine and endocrine signals to mediate multiple processes like energy metabolism, insulin sensitivity, oxidant stress, blood coagulation, and inflammatory responses. Adiponectin, the most abundant peptide secreted by adipocytes, plays a key role in the interrelationship between adiposity, inflammation and IR. It may possibly affect insulin sensitivity and endothelial function which makes this peptide a potential multilayered therapeutic target for Met S. [54]

Atherogenic dyslipidemia

The central features of atherogenic dyslipidemia are low High Density Lipoprotein (HDL) cholesterol levels, high plasma Triglycerides (TG) levels and high Low Density Lipoprotein (LDL) levels. Visceral obesity and IR are associated with atherogenic dyslipidemia. [55] IR leads to atherogenic dyslipidemia in various ways. First, insulin normally suppresses adipocytes lipolysis, so any impairment in insulin signaling results in increased lipolysis, which further results in increased level of free fatty acids. In the liver, FFAs serve as a substrate for Triglycerides synthesis. FFAs also stabilize the production of a lipoprotein of very-low-density lipoprotein (VLDL) particles, known as apoB resulting in increased VLDL production. Second, insulin through PI3K-dependent pathway, normally degrades apoB, so IR directly increases production of VLDL. Third, insulin regulates the function of lipoprotein lipase, the major mediator of VLDL clearance. Thus, hypertriglyceridemic condition in IR is the result of both an an increase in VLDL production and decrease in VLDL clearance. VLDL is metabolized to small dense LDL and remnant lipoproteins, which can promote atheroma formation.

Endothelial dysfunction

Endothelial dysfunction is the final common pathway in development of many cardiovascular risk factors and atherosclerosis. [56],[57],[58],[59] The lining of inner surface of blood vessels is made up of endothelial cells which serves important biological as well as mechanical functions. The endothelium produces various vasoactive substances, including NO, prostacyclin and endothelins senses in respond to various physiological and pathological stimuli. Endothelial expression of different cell adhesion molecules governs interactions with circulating platelets, affecting homeostasis and thrombosis and with circulating monocytes and leukocytes, affecting inflammation. The endothelium also modulates the response of the vascular smooth muscle layer, which may contribute to intimal formation during the development of atherosclerotic plaques. Endothelial dysfunction occurs when it fails to serve its normal protective and physiological mechanisms. It may occur when the normal responses of the endothelium are affected by hyperglycemia, oxidative stress, advanced glycation products, FFAs, inflammatory cytokines or adipokines. Endothelial dysfunction plays a central role in the development of atherosclerotic lesion. A common feature of endothelial dysfunction is reduced NO bio-availability in the vasculature.

Impedements in the way of metabolic syndrome

Variability of metabolic syndrome's definition

Number of definitions for Met S have been proposed by various organizations till date. A single unified definition, although with gender- and ethnicity-specific cutoff points, is highly required for use in the at-risk population. [60] Blood pressure, lipid levels and anthropometric parametres vary with age and pubertal development. Puberty impacts distribution of fats and decreases insulin sensitivity. [61],[62] Therefore, to define abnormalities in children, single cutoff points cannot be used. Moreover, an universal agreement has not been there as to which level should be included in the criteria for the Met S.

Thresholds and dichotomizing variables

National High Blood Pressure Education Program recommends B.P cutoff points of 90 th or 95 th percentile adjusted for height, gender and age to identify prehypertension or hypertension in children and adolescents. [63] American Diabetes Association recommends cutoff points for impaired fasting glucose {100-125 mg/dL (5.6-6.9 mmol/L)} [45] and the NCEP/ATP III recommends [110 mg/dL (6.1 mmol/L)], values as cut off point for the same. [64] Criteria for defining lipids and triglycerides (TGs) imbalances are less consistent in adolescents with recommendations by NCEP/ATP III (age specific), NHANES III (age and gender specific) and the National Growth and Health Study (age, gender and ethnic specific), employing either absolute values or percentile cutoff points.

Number of criteria required to fulfill the diagnosis

The NCEP ATP III definition is easy to use and each component is justified by its prevalence in the U.S. population, however, this definition does not exclude diabetics and is criticized for the same reasons as the WHO definition. [65] Also, it fails to consider treated hypertension or dyslipidemia when defining its criteria. With respect to treatment of Metabolic Syndrome, the current WHO and ATP III definitions include those with active disease, including diabetes, hypertension and diagnosed cardiovascular disease as well as those that have normal values or milder conditions that meet the criteria for Metabolic Syndrome, but do not require specific treatment. Further research is needed to determine the value of treating particular combinations of defining criteria. Several studies have brought into question the ability of the ATP III criteria to identify insulin resistant individuals. ATP III criteria for Metabolic Syndrome have a low sensitivity for predicting insulin resistance. Disparities were also found in the prevalence of the syndrome depending on the definition used.

Different criterias for Met S are shown in [Table 3]. [66],[67],[68],[69]
Table 3: Different criterion for defining Met S

Click here to view

  Management Top

Effective management of metabolic syndrome depends in part on addressing several risk factors together. Reduction of risk of developing Met S involves lifestyle modifications, drug treatment and effective management of risk factors. First-line therapy is directed toward the major risk factors including elevated LDL cholesterol levels, hypertension, and diabetes. Although numerous persons may be genetically susceptible to Met S, in the absence of physical inactivity and obesity, it rarely manifests clinically. [70] Therefore, the prime emphasis in management of the Met S is to mitigate modifiable risk factors (e.g. diet, physical inactivity, obesity, smoking etc) through lifestyle changes. [71] Consideration can be given to incorporating drug therapy into the regimen, if the absolute risk is high enough. Met S is a lifelong disorder. If it is diagnosed once, there is no as such direct treatment. However, it can be managed indirectly by controlling certain risk factors following best possible ways listed below.

Weight reduction

Weight reduction should be the first priority in persons with metabolic syndrome. Achieving the recommended reduction in weight will lower the severity of most of the metabolic risk factors. Four therapies can be recommended for weight reduction: Calorie restriction (e.g. 500 kcal/d deficit), increased physical activity, behavioral modification and FDA-approved weight-reducing drugs. [72]

Physical activity

Increasing physical activity assists in weight reduction, has beneficial effects on metabolic risk factors, and reduces overall CVD risk. Current physical activity guidelines recommend practical, regular, and moderate regimens for exercise. The standard exercise recommendation is a daily moderate-intensity physical activity minimum of 30 minutes. The regular physical activities includes (household-work, walking breaks at work, gardening etc) using simple exercise equipment, jogging, swimming and sports eluding regular sedentary activities like computer games and television watching, in a leisure time is also advised. [73]

Lifestyle modification

Inappropriate life-style includes poor diet, poor sleep, lack of exercise, excess alcohol, smoking and stress due to extensive workload. The burden of lifestyle diseases is escalating due to certain factors which includes decreasing physical activity, increased consumption of unhealthy food, increasing tobacco consumption, rising income and longer average life span. [74] Lifestyle modification treatment should incorporate a multidisciplinary approach with a team composed of physicians and non physician health professionals, dietitian or behavioral psychologists. Although, the effect produced by lifestyle therapy is not as strong as drugs, but its advantage is that it produces a moderate reduction in most of the complications associated with the Met S.


Diet should be low in saturated fats, transfats, cholesterol, sodium, and simple sugars. In addition, there should be ample intake of fruits, vegetables, whole grains and fish. The effective, productive and healthful approaches for the long term weight loss are low calorie-diets, consisting of a moderate (500-1000) calories/day reduction. Sustained changes in dietary regime may necessitate a referral dietician to assist implementation of the recommended suggestions and ensure an adequate intake of micronutrient (e.g. iron, calcium and folate) while reducing calories. [75]

Behavior therapy

One of the most effective and important strategy to manage the MetS is behavioural therapy. The therapy provides set of approaches to modify eating and activity habits. The behavioural change techniques should include an improvement in eating habits, a regular exercise planing, the benefit of social support and stress management. e.g. Proper planningof meals, reading labels, reducing portion sizes, self-monitoring and averting eating binges. [76],[77]

Pharmacological approach

The NIH guidelines recommends consideration of pharmaceutical therapy for weight loss for the individuals with BMI greater than 27 kg/m 2 . Pharmacological approaches for weight reduction includes two main classes: Appetite inhibitors and appetite suppressants of nutrient absorption. Treatment with these drug improves lipid levels and decreases visceral fat, glycosylated haemoglobin and uric acid concentrations. [78],[79]

  Conclusion Top

Met S-a cluster of metabolic and cardiovascular risk factors-has been difficult to address. The increasing prevalence of abdominal obesity and diabetes, particularly among adults, highlights the urgency of addressing the syndrome as a health care priority. Clinicians should significantly consider screening all people regardless of age for various abnormalities reported. It is not enough to say "just treat the established risk factors." More importantly, an effort must be made to strike at the underlying causes of the syndrome. Met S still represent a great challenge to medical field. There are certain questions which need to be explored. Whether early growth patterns and low birth weight predicts future metabolic syndrome? The increasing prevalence of syndrome, calls for action to prevent and treat all its components. It is essential that the community is mindful of important risk factors to help improve on adherence to lifestyle changes and medication among those with established disease. The involvement of exercise and physical activity shows a clinically substantial aspect in the management of Met S and its complications. While the benefit of exercise and active lifestyles is well documented for prevention and risk reduction of cardiovascular and stroke outcomes, the detailed regiment and recommendations are less clear. The primary health care system needs to be strengthened and integrate the care of Met S and management of its risk factors. Additional research is necessary to establish the true burden of the syndrome across the world.

  References Top

Nakagami T, Qiao Q, Carstensen B, Nhr-Hansen C, Hu G, Tuomilehto J, et al.; DECODE-DECODA Study Group. Age, body mass index and Type 2 diabetes-associations modified by ethnicity. Diabetologia 2003;46:1063-70.  Back to cited text no. 1
Cameron AJ, Shaw JE, Zimmet PZ. The metabolic syndrome: Prevalence in worldwide populations. Endocrinol Metab Clin North Am 2004;33:351-75, table of contents.  Back to cited text no. 2
Kylin E. Studien ueber das Hypertonie-Hyperglyca "mie-Hyperurika" miesyndrom. Zentralblatt Fuer Innere Medizin 1923;44:105-27.  Back to cited text no. 3
Vague J. Sexual differentiation, a factor affecting the forms of obesity. Presse Med 1947;30:339-40.  Back to cited text no. 4
Avogaro P, Crepaldi G. Essential hyperlipidemia, obesity and diabetes. Diabetologia 1965;1:137.  Back to cited text no. 5
Haller H. Epidemiology and associated risk factors of hyperlipoproteinemia. Z Gesamte Inn Med 1977;32:124-8.  Back to cited text no. 6
Singer P. Diagnosis of primary hyperlipoproteinemias. Z Gesamte Inn Med 1977;32:129-33 concl.  Back to cited text no. 7
Leslie BR. Metabolic syndrome: Historical perspectives. Am J Med Sci 2005;330:264-8.  Back to cited text no. 8
Reaven GM. Banting lecture 1988. Role of insulin resistance in human disease. Diabetes 1988;37:1595-607.  Back to cited text no. 9
Kaplan NM. The deadly quartet. Upper-body obesity, glucose intolerance, hypertriglyceridemia, and hypertension. Arch Intern Med 1989;149:1514-20.  Back to cited text no. 10
Fletcher B, Lamendola C. Insulin resistance syndrome. J Cardiovasc Nurs 2004;19:339-45.  Back to cited text no. 11
Misra A, Singhal N, Sivakumar B, Bhagat N, Jaiswal A, Khurana L. Nutrition transition in India: Secular trends in dietary intake and their relationship to diet-related non-communicable diseases. J Diabetes 2011;3:278-92.  Back to cited text no. 12
Cook S, Weitzman M, Auinger P, Nguyen M, Dietz WH. Prevalence of a metabolic syndrome phenotype in adolescents: Findings from the third National Health and Nutrition Examination Survey, 1988-1994. Arch Pediatr Adolesc Med 2003;157:821-7.  Back to cited text no. 13
Alberti KG, Zimmet P, Shaw J; IDF Epidemiology Task Force Consensus Group. The metabolic syndrome--a new worldwide definition. Lancet 2005;366:1059-62.  Back to cited text no. 14
Tull ES, Thurland A, LaPorte RE. Metabolic syndrome among Caribbean-born persons living in the U.S. Virgin Islands. Rev Panam Salud Publica 2005;18:418-26.  Back to cited text no. 15
Ko GT, Cockram CS, Chow CC, Yeung V, Chan WB, So WY, et al. High prevalence of metabolic syndrome in Hong Kong Chinese--comparison of three diagnostic criteria. Diabetes Res Clin Pract 2005;69:160-8.  Back to cited text no. 16
Arai H, Yamamoto A, Matsuzawa Y, Saito Y, Yamada N, Oikawa S, et al. Prevalence of metabolic syndrome in the general Japanese population in 2000. J Atheroscler Thromb 2006;13:202-8.  Back to cited text no. 17
Heng D, Ma S, Lee JJ, Tai BC, Mak KH, Hughes K, et al. Modification of the NCEP ATP III definitions of the metabolic syndrome for use in Asians identifies individuals at risk of ischemic heart disease. Atherosclerosis 2006;186:367-73.  Back to cited text no. 18
Lawlor DA, Smith GD, Ebrahim S. Does the new International Diabetes Federation definition of the metabolic syndrome predict CHD any more strongly than older definitions? Findings from the British Women′s Heart and Health Study. Diabetologia 2006;49:41-8.  Back to cited text no. 19
Gorter PM, Olijhoek JK, van der Graaf Y, Algra A, Rabelink TJ, Visseren FL; SMART Study Group. Prevalence of the metabolic syndrome in patients with coronary heart disease, cerebrovascular disease, peripheral arterial disease or abdominal aortic aneurysm. Atherosclerosis 2004;173:363-9.  Back to cited text no. 20
Skoumas J, Papadimitriou L, Pitsavos C, Masoura C, Giotsas N, Chrysohoou C, et al. Metabolic syndrome prevalence and characteristics in Greek adults with familial combined hyperlipidemia. Metabolism 2007;56:135-41.  Back to cited text no. 21
Florez H, Silva E, Fernández V, Ryder E, Sulbarán T, Campos G, et al. Prevalence and risk factors associated with the metabolic syndrome and dyslipidemia in White, Black, Amerindian and Mixed Hispanics in Zulia State, Venezuela. Diabetes Res Clin Pract 2005;69:63-77.  Back to cited text no. 22
Kolciæ I, Vorko-Joviæ A, Salzer B, Smoljanoviæ M, Kern J, Vuletiæ S. Metabolic syndrome in a metapopulation of Croatian island isolates. Croat Med J 2006;47:585-92.  Back to cited text no. 23
Pousada JM, Britto MM, Cruz T, Lima Mde L, Lessa I, Lemaire DC, et al. The metabolic syndrome in Spanish migrants to Brazil: Unexpected results. Diabetes Res Clin Pract 2006;72:75-80.  Back to cited text no. 24
Aguilar-Salinas CA, Rojas R, Gómez-Pérez FJ, Mehta R, Franco A, Olaiz G, et al. The metabolic syndrome: A concept hard to define. Arch Med Res 2005;36:223-31.  Back to cited text no. 25
Lao XQ, Thomas GN, Jiang CQ, Zhang WS, Yin P, Adab P, et al. Association of the metabolic syndrome with vascular disease in an older Chinese population: Guangzhou Biobank Cohort Study. J Endocrinol Invest 2006;29:989-96.  Back to cited text no. 26
Deepa M, Farooq S, Datta M, Deepa R, Mohan V. Prevalence of metabolic syndrome using WHO, ATPIII and IDF definitions in Asian Indians: The Chennai Urban Rural Epidemiology Study (CURES-34). Diabetes Metab Res Rev 2007; 23:127-34.  Back to cited text no. 27
Santos AC, Barros H. Prevalence and determinants of obesity in an urban sample of Portuguese adults. Public Health 2003;117:430-7.  Back to cited text no. 28
Bo S, Gentile L, Ciccone G, Baldi C, Benini L, Dusio F, et al. The metabolic syndrome and high C-reactive protein: Prevalence and differences by sex in a southern-European population-based cohort. Diabetes Metab Res Rev 2005;21:515-24.  Back to cited text no. 29
Tull ES, Thurland A, LaPorte RE. Metabolic syndrome among Caribbean-born persons living in the U.S. Virgin Islands. Rev Panam Salud Publica 2005;18:418-26.  Back to cited text no. 30
Boonyavarakul A, Choosaeng C, Supasyndh O, Panichkul S. Prevalence of the metabolic syndrome, and its association factors between percentage body fat and body mass index in rural Thai population aged 35 years and older. J Med Assoc Thai 2005;88(Suppl 3):S121-30.  Back to cited text no. 31
Jericó C, Knobel H, Montero M, Sorli ML, Guelar A, Gimeno JL, et al. Hypertens in HIV-infected patients: Prevalence and related factors. Am J Hypertens 2005;18:1396-401.  Back to cited text no. 32
Aizawa Y, Kamimura N, Watanabe H, Aizawa Y, Makiyama Y, Usuda Y, et al. Cardiovascular risk factors are really linked in the metabolic syndrome: This phenomenon suggests clustering rather than coincidence. Int J Cardiol 2006;109:213-8.  Back to cited text no. 33
Pappachan MJ. Increasing prevalence of lifestyle diseases: High time for action. Indian J Med Res 2011;134:143-5.  Back to cited text no. 34
[PUBMED]  Medknow Journal  
Jensen MD, Haymond MW, Rizza RA, Cryer PE, Miles JM. Influence of body fat distribution on free fatty acid metabolism in obesity. J Clin Invest 1989; 83:1168-73.  Back to cited text no. 35
Xydakis AM, Case CC, Jones PH, Hoogeveen RC, Liu MY, Smith EO, et al. Adiponectin, inflammation, and the expression of the metabolic syndrome in obese individuals: The impact of rapid weight lose through caloric restriction. J Clin Endocrinol Metab 2004;89:2697-703.  Back to cited text no. 36
Chandola T, Brunner E, Marmot M. Chronic stress at work and the metabolic syndrome: Prospective study. BMJ 2006;332:521-5.  Back to cited text no. 37
Hjemdahl P. Stress and metabolic syndrome: An interesting but enigmatic association. Circulation 2002;106:2634-6.  Back to cited text no. 38
Lee CM, Huxley RR, Woodward M, Zimmet P, Shaw J, Cho NH, et al.; DETECT-2 Collaboration. The metabolic syndrome identifies a heterogeneous group of metabolic component combinations in the Asia-Pacific region. Diabetes Res Clin Pract 2008;81:377-80.  Back to cited text no. 39
Abate N. Obesity and cardiovascular disease: Pathogenetic role of the metabolic syndrome and therapeutic implications. J Diabetes Complications 2000;14:154-74.  Back to cited text no. 40
Dandona P, Aljada A, Chaudhuri A, Mohanty P, Garg R. Metabolic syndrome: A comprehensive perspective based on interactions between obesity, diabetes, and inflammation. Circulation 2005;111:1448-54.  Back to cited text no. 41
Godsland IF, Crook D, Proudler AJ, Stevenson JC. Hemostatic risk factors and insulin sensitivity, regional body fat distribution, and the metabolic syndrome. J Clin Endocrinol Metab 2005;90:190-7.  Back to cited text no. 42
Bamba V, Rader DJ. Obesity and atherogenic dyslipidemia. Gastroenterology 2007;132:2181-90.  Back to cited text no. 43
Bravata DM, Wells CK, Concato J, Kernan WN, Brass LM, Gulanski BI. Two measures of insulin sensitivity provided similar information in a U.S. population. J Clin Epidemiol 2004;57:1214-7.  Back to cited text no. 44
Vessby B, Uusitupa M, Hermansen K, Riccardi G, Rivellese AA, Tapsell LC, et al.; KANWU Study. Substituting dietary saturated for monounsaturated fat impairs insulin sensitivity in healthy men and women: The KANWU Study. Diabetologia 2001;44:312-9.  Back to cited text no. 45
Xu XJ, Pories WJ, Dohm LG, Ruderman NB. What distinguishes adipose tissue of severely obese humans who are insulin sensitive and resistant? Curr Opin Lipidol 2013;24:49-56.  Back to cited text no. 46
Himsworth HP. Diabetes mellitus: Its differentiation into insulin-sensitive and insulin-insensitive types. Diabet Med 2011;28:1440-4.  Back to cited text no. 47
Kim JA, Montagnani M, Koh KK, Quon MJ. Reciprocal relationships between insulin resistance and endothelial dysfunction: Molecular and pathophysiological mechanisms. Circulation 2006;113:1888-904.  Back to cited text no. 48
Jonk AM, Houben AJ, de Jongh RT, Serné EH, Schaper NC, Stehouwer CD. Microvascular dysfunction in obesity: A potential mechanism in the pathogenesis of obesity-associated insulin resistance and hypertension. Physiology (Bethesda) 2007;22:252-60.  Back to cited text no. 49
Kershaw EE, Flier JS. Adipose tissue as an endocrine organ. J Clin Endocrinol Metab 2004;89:2548-56.  Back to cited text no. 50
Halberg N, Wernstedt-Asterholm I, Scherer PE. The adipocyte as an endocrine cell. Endocrinol Metab Clin North Am 2008;37:753-68, x-xi.  Back to cited text no. 51
Lau DC, Dhillon B, Yan H, Szmitko PE, Verma S. Adipokines: Molecular links between obesity and atheroslcerosis. Am J Physiol Heart Circ Physiol 2005;288:H2031-41.  Back to cited text no. 52
Trayhurn P, Wood IS. Adipokines: Inflammation and the pleiotropic role of white adipose tissue. Br J Nutr 2004;92:347-55.  Back to cited text no. 53
Semenkovich CF. Insulin resistance and atherosclerosis. J Clin Invest 2006;116:1813-22.  Back to cited text no. 54
Gimbrone MA Jr, Topper JN, Nagel T, Anderson KR, Garcia-Cardeña G. Endothelial dysfunction, hemodynamic forces, and atherogenesis. Ann NY Acad Sci 2004;902:230-40.  Back to cited text no. 55
Yudkin JS, Kumari M, Humphries SE, Mohamed-Ali V. Inflammation, obesity, stress and coronary heart disease: Is interleukin-6 the link? Atherosclerosis 2000;148:209-14.  Back to cited text no. 56
Dimmeler S, Fleming I, Fisslthaler B, Hermann C, Busse R, Zeiher AM. Activation of nitric oxide synthase in endothelial cells by Akt-dependent phosphorylation. Nature 1999;399:601-5.  Back to cited text no. 57
Yudkin JS, Stehouwer CD, Emeis JJ, Coppack SW. C-reactive protein in healthy subjects: Associations with obesity, insulin resistance, and endothelial dysfunction: A potential role for cytokines originating from adipose tissue? Arterioscler Thromb Vasc Biol 1999;19:972-8.  Back to cited text no. 58
Alberti KG, Zimmet P, Shaw J. Metabolic syndrome-a new world-wide definition. A Consensus Statement from the International Diabetes Federation. Diabet Med 2006;23:469-80.  Back to cited text no. 59
Bloch CA, Clemons P, Sperling MA. Puberty decreases insulin sensitivity. J Pediatr 1987;110:481-7.  Back to cited text no. 60
Reinehr T, Roth C, Menke T, Andler W. Adiponectin before and after weight loss in obese children. J Clin Endocrinol Metab 2004;89:3790-4.  Back to cited text no. 61
Update on the 1987 Task Force Report on High Blood Pressure in Children and Adolescents: A working group report from the National High Blood Pressure Education Program. National High Blood Pressure Education Program Working Group on Hypertension Control in Children and Adolescents. Pediatrics 1996;98:649-58.  Back to cited text no. 62
Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. Diabetes Care 1997;20:1183-97.  Back to cited text no. 63
Grundy SM, Cleeman JI, Daneils SR, Donato KA, Eckel RH, Franklin BA, et al.; American Heart Association; National Heart, Lung, and Blood Institute. Diagnosis and management of the metabolic syndrome: An American Heart Association/National Heart, Lung, and Blood Institute scientific statement. Circulation 2005;112:2735-52.  Back to cited text no. 64
Alberti KG, Zimmet PZ. Definition, diagnosis and classification of diabetes mellitus and its complications. Part 1: Diagnosis and classification of diabetes mellitus provisional report of a WHO consultation. Diabet Med 1998;15:539-53.  Back to cited text no. 65
Balkau B, Charles MA. Comment on the provisional report from the WHO consultation: European Group for the Study of Insulin Resistance (EGIR). Diabet Med 1999;16:442-3.  Back to cited text no. 66
Moy FM, Bulgiba A. The modified NCEP ATP III criteria maybe better than the IDF criteria in diagnosing metabolic syndrome among Malays in Kuala Lumpur. BMC Public Health 2010;10:678.  Back to cited text no. 67
National Cholesterol Education Program (NCEP) Expert Panel on Detection, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) final report. Circulation 2002;106:3143-421.  Back to cited text no. 68
Grundy SM, Hansen B, Smith SC Jr, Cleeman JI, Kahn RA; American Heart Association; National Heart, Lung, and Blood Institute; American Diabetes Association. Clinical management of metabolic syndrome: Report of the American Heart Association/National Heart, Lung, and Blood Institute/American Diabetes Association conference on scientific issues related to management. Arterioscler Thromb Vasc Biol 2004;24:e19-24.  Back to cited text no. 69
Ford ES, Kohl HW 3 rd , Mokdad AH, Ajani UA. Sedentary behavior, physical activity, and the metabolic syndrome among U.S. adults. Obes Res 2005;13:608-14.  Back to cited text no. 70
Wing RR, Koeske R, Epstein LH, Nowalk MP, Gooding W, Becker D. Long-term effects of modest weight loss in type II diabetic patients. Arch Intern Med 1987;147:1749-53.  Back to cited text no. 71
Thompson PD, Buchner D, Pina IL, Balady GJ, Williams MA, Marcus BH, et al.; American Heart Association Council on Clinical Cardiology Subcommittee on Exercise, Rehabilitation, and Prevention; American Heart Association Council on Nutrition, Physical Activity, and Metabolism Subcommittee on Physical Activity. Exercise and physical activity in the prevention and treatment of atherosclerotic cardiovascular disease: A statement from the Council on Clinical Cardiology (Subcommittee on Exercise, Rehabilitation, and Prevention) and the Council on Nutrition, Physical Activity, and Metabolism (Subcommittee on Physical Activity). Circulation 2003;107:3109-16.  Back to cited text no. 72
Panagiotakos DB, Pitsavos C, Chrysohoou C, Skoumas J, Tousoulis D, Toutouza M, et al. Impact of lifestyle habits on the prevalence of the metabolic syndrome among Greek adults from the ATTICA study. Am Heart J 2004;147:106-12.  Back to cited text no. 73
Wadden TA, Butryn ML, Wilson C. Lifestyle modif ication for the management of obesity. Gastroenterology 2007;132:2226-38.  Back to cited text no. 74
Anderssen SA, Carroll S, Urdal P, Holme I. Combined diet and exercise intervention reverses the metabolic syndrome in middle-aged males: Results from the Oslo Diet and Exercise Study. Scand J Med Sci Sports 2007;17:687-95.  Back to cited text no. 75
Bellentani S, Dalle Grave R, Suppini A, Marchesini G; Fatty Liver Italian Network. Behavior therapy for nonalcoholic fatty liver disease: The need for a multidisciplinary approach. Hepatology 2008;47:746-54.  Back to cited text no. 76
Executive summary of the clinical guidelines on the identification, evaluation, and treatment of overweight and obesity in adults. Arch Intern Med 1998;158:1855-67.  Back to cited text no. 77
Wing RR. Behavioral Weight Control. In: Wadden TA, Stunkard AJ, editors. Handbook of Obesity Treatment. New York: The Guildford Press; 2002. p. 301-16.  Back to cited text no. 78
Krejs GJ. Metabolic benefits associated with sibutramine therapy. Int J Obes Relat Metab Disord 2002;26(Suppl 4):S34-7.  Back to cited text no. 79


  [Table 1], [Table 2], [Table 3]


Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

  In this article
Clinical features
Pathophysiology ...
Prevalence of Met S
Article Tables

 Article Access Statistics
    PDF Downloaded3938    
    Comments [Add]    

Recommend this journal