Does the Metabolic Syndrome Improve Identification of Individuals at Risk of Type 2 Diabetes and/or Cardiovascular Disease?

University of Texas at San Antonio, San Antonio, Texas, United States
Diabetes Care (Impact Factor: 8.42). 12/2004; 27(11):2676-81. DOI: 10.2337/diacare.27.11.2676
Source: PubMed


The metabolic syndrome has been promoted as a method for identifying high-risk individuals for type 2 diabetes and cardiovascular disease (CVD). We therefore sought to compare this syndrome, as defined by the National Cholesterol Education Program, to the Diabetes Predicting Model and the Framingham Risk Score as predictors of type 2 diabetes and CVD, respectively.
A population-based sample of 1,709 initially nondiabetic San Antonio Heart Study (SAHS) participants were followed for 7.5 years, 195 of whom developed type 2 diabetes. Over the same time interval, 156 of 2,570 SAHS participants experienced a cardiovascular event. A population-based sample of 1,353 initially nondiabetic Mexico City Diabetes Study (MCDS) participants were followed for 6.5 years, 125 of whom developed type 2 diabetes. Baseline measurements included medical history, age, sex, ethnicity, smoking status, BMI, blood pressure, fasting and 2-h plasma glucose levels, and fasting serum total and HDL cholesterol and triglycerides.
The sensitivities for predicting diabetes with the metabolic syndrome were 66.2 and 62.4% in the SAHS and the MCDS, respectively, and the false-positive rates were 27.8 and 38.7%, respectively. The sensitivity and false-positive rates for predicting CVD with the metabolic syndrome in the SAHS were 67.3 and 34.2%, respectively. At corresponding false-positive rates, the two predicting models had significantly higher sensitivities and, at corresponding sensitivities, significantly lower false-positive rates than the metabolic syndrome for both end points. Combining the metabolic syndrome with either predicting model did not improve the prediction of either end point.
The metabolic syndrome is inferior to established predicting models for either type 2 diabetes or CVD.

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    • "The observation that older, nondiabetic adults are two times more likely to have the MetS with hyperglycemia than hyperglycemia only confirms an overlap between the conditions [17]. The MetS is associated with a 5-fold increased risk for diabetes [18]. While most assume this to be driven by hyperglycemia, MetS without prediabetes carries a similar level of risk [19]. "
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    ABSTRACT: Sympathetic tone is well recognised as being implicit in cardiovascular control. It is less readily acknowledged that activation of the sympathetic nervous system is integral in energy homeostasis and can exert profound metabolic effects. Accumulating data from animal and human studies suggest that central sympathetic overactivity plays a pivotal role in the aetiology and complications of several metabolic conditions that can cluster to form the Metabolic Syndrome (MetS). Given the known augmented risk for type 2 diabetes, cardiovascular disease, and premature mortality associated with the MetS understanding the complex pathways underlying the metabolic derangements involved has become a priority. Many factors have been proposed to contribute to increased sympathetic nerve activity in metabolic abnormalities including obesity, impaired baroreflex sensitivity, hyperinsulinemia, and elevated adipokine levels. Furthermore there is mounting evidence to suggest that chronic sympathetic overactivity can potentiate two of the key metabolic alterations of the MetS, central obesity and insulin resistance. This review will discuss the regulatory role of the sympathetic nervous system in metabolic control and the proposed pathophysiology linking sympathetic overactivity to metabolic abnormalities. Pharmacological and device-based approaches that target central sympathetic drive will also be discussed as possible therapeutic options to improve metabolic control in at-risk patient cohorts.
    Full-text · Article · Jun 2015 · Journal of Diabetes Research
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    • "Approximately three-fourths of individuals with both IFG and IGT have metabolic syndrome (MetS)[4], which is characterized by dyslipidemia, disorders of glucose metabolism, hypertension and obesity. Pre-diabetes is somewhat predictive of macrovascular diseases, but most of this association seems to be mediated through MetS456. Therefore, MetS can be considered a pre-diabetic state[4,7]. "
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    ABSTRACT: Increased energy intake and reduced physical activity can lead to obesity, diabetes and metabolic syndrome. Transcriptionalmodulation ofmetabolic networks has become a focus of current drug discovery research into the prevention and treatment of metabolic disorders associated with energy surplus and obesity. Tang-Nai-Kang (TNK), a mixture of five herbal plant extracts, has been shown to improve abnormal glucose metabolism in patients with prediabetes. Here, we report the metabolic phenotype of SHR.Cg-Leprcp/NDmcr (SHR/cp) rats treated with TNK. Pre-diabetic SHR/cp rats were randomly divided into control, TNK low-dose (1.67 g/kg) and TNK high-dose (3.24 g/kg) groups. After high-dose treatment for 2 weeks, the serum triglycerides and free fatty acids in SHR/cp rats weremarkedly reduced compared to controls. After 3 weeks of administration, the high dose of TNK significantly reduced the body weight and fat mass of SHR/cp rats without affecting food consumption. Serum fasting glucose and insulin levels in the TNK-treated groups decreased after 6 weeks of treatment. Furthermore, TNK-treated rats exhibited obvious improvements in glucose intolerance and insulin resistance. The improved glucose metabolism may be caused by the substantial reduction in serum lipids and body weight observed in SHR/cp rats starting at 3 weeks of TNK treatment. ThemRNA expression of NAD+-dependent deacetylase sirtuin 1 (SIRT1) and genes related to fatty acid oxidation was markedly up-regulated in the muscle, liver and adipose tissue after TNK treatment. Furthermore, TNK promoted the deacetylation of two well-established SIRT1 targets, PPARγ coactivator 1α (PGC1α) and forkhead transcription factor 1 (FOXO1), and induced the phosphorylation of AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC) in different tissues. These observations suggested that TNK may be an alternative treatment for pre-diabetes and metabolic syndrome by inducing a gene expression switch toward fat oxidation through the activation of SIRT1 and AMPK signaling.
    Full-text · Article · Apr 2015 · PLoS ONE
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    • "Robust evidence showed that individuals diagnosed with MetS using these definitions have a greater risk of significant clinical consequences, the two most prominent of which are the development of T2DM and CVD [12] [13] [14] [15]. Individuals with MetS have a fivefold greater risk of developing T2DM [12], while a systematic review of 37 studies involving more than 170,000 patients has shown that MetS doubles the risk of cardiovascular events [15]. Irrespective of the diagnostic criteria used, epidemiological studies from various parts of the world have clearly demonstrated that MetS is an increasing global health problem , not only in the western societies, but also in the Asian populations [16] [17]. "

    Full-text · Dataset · Nov 2014
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