Associations of fibroblast growth factor 21 gene 3' untranslated region single-nucleotide polymorphisms with metabolic syndrome, obesity, and diabetes in a Han Chinese population

Fibroblast growth factor 21 (FGF-21) is a novel regulator for metabolic syndrome (MetS), diabetes, and obesity. However, no study has been performed on the association of these diseases with FGF-21 gene polymorphism. The aim of the study was to investigate the association of 3' untranslated region (UTR) single-nucleotide polymorphisms (SNPs) in the FGF-21 gene with MetS, obesity, and diabetes in the Han Chinese population. A total of 291 subjects were recruited from the Han Chinese population in Sichuan province. The genotypes of FGF-21 were determined by polymerase chain reaction-restriction fragment length polymorphism. The genotypes were confirmed by sequencing. No polymorphisms were found in rs11665841 (1 of 291) and rs3745706 (2 of 291). We did not find an association between genotype frequencies of SNP rs11665896 and lipid concentration, glucose concentration, or blood pressure. The TG/GG genotype relative to the TT genotype had an age- and sex-adjusted odds ratio of 1.41 for MetS (p=0.149), 1.84 (p=0.016) for obesity (body mass index ≥25?kg/m(2)), and 1.19 (p=0.492) for diabetes. Genetic variation of the 3' UTR of the FGF-21 gene was associated with obesity, however, not with MetS or diabetes.     

Resistance to high-fat diet in the female progeny of obese mice fed a control diet during the periconceptual, gestation, and lactation periods

With the worldwide epidemic of metabolic syndrome (MetS), the proportion of women that are overweight/obese and overfed during pregnancy has increased. The resulting abnormal uterine environment may have deleterious effects on fetal metabolic programming and lead to MetS in adulthood. A balanced/restricted diet and/or physical exercise often improve metabolic abnormalities in individuals with obesity and type 2 diabetes mellitus (T2D). We investigated whether reducing fat intake during the periconceptual/gestation/lactation period in mothers with high-fat diet (HFD)-induced obesity could be used to modify fetal/neonatal MetS programming positively, thereby preventing MetS. First generation (F1) C57BL/6J female mice with HFD-induced obesity and T2D were crossed with F1 males on control diet (CD). These F1 females were switched to a CD during the periconceptual/gestation/lactation period. At weaning, both male and female second generation (F2) mice were fed a HFD. Weight, caloric intake, lipid parameters, glucose, and insulin sensitivity were assessed. Sensitivity/resistance to the HFD differed significantly between generations and sexes. A similar proportion of the F1 and F2 males (80%) developed hyperphagia, obesity, and T2D. In contrast, a significantly higher proportion of the F2 females (43%) than of the previous F1 generation (17%) were resistant (P<0.01). Despite having free access to the HFD, these female mice were no longer hyperphagic and remained lean, with normal insulin sensitivity and glycemia but mild hypercholesterolemia and glucose intolerance, thus displaying a "satiety phenotype." This suggests that an appropriate dietary fatty acid profile and intake during the periconceptual/gestation/lactation period helps the female offspring to cope with deleterious intrauterine conditions.     

Génétique du syndrome métabolique

Metabolic syndrome (MetS) is a common phenotype, affecting about 24 % of the US population. It is associated with an increased risk for type 2 diabetes and cardiovascular disease. Although there is no universally accepted definition for MetS, affected individuals commonly have a cluster of features, including abdominal obesity, hypertension, dyslipidemia, and dysglycemia. Recently, there has been extensive interest in potential genetic contributions to MetS. At present, no single gene or cluster of genes has been consistently replicated for MetS among different populations, likely due to the complex interplay between gene and environment necessary for expression of this phenotype. We review recent studies regarding the genetic contributions to MetS.     

Maternal micronutrient disturbance as risks of offspring metabolic syndrome

Metabolic syndrome (MetS) is defined as a constellation of individual metabolic disturbances, including central obesity, hypertension, dyslipidemia, and insulin resistance. The established pathogenesis of MetS varies extensively with gender, age, ethnic background, and nutritional status. In terms of nutritional status, micronutrients are more likely to be discounted as essential components of required nutrition than macronutrients due to the small amount required. Numerous observational studies have shown that pregnant women frequently experience malnutrition, especially in developing and low-income countries, resulting in chronic MetS in the offspring due to the urgent and increasing demands for micronutrients during gestation and lactation. Over the past few decades, scientific developments have revolutionized our understanding of the association between balanced maternal micronutrients and MetS in the offspring. Examples of successful individual, dual, or multiple maternal micronutrient interventions on the offspring include iron for hypertension, selenium for type 2 diabetes, and a combination of folate and vitamin D for adiposity. In this review, we aim to elucidate the effects of maternal micronutrient intake on offspring metabolic homeostasis and discuss potential perspectives and challenges in the field of maternal micronutrient interventions.     

Different associations of apoE gene polymorphism with metabolic syndrome in the Vojvodina Province (Serbia)

The metabolic syndrome (MetS) is a polygenic multifactorial metabolic disorder with strong socioeconomic influence. MetS has became a worldwide epidemic, that directly increases the risk of cardiovascular diseases and type 2 diabetes mellitus. The human apoE gene, coding Apolipoprotein E, has three common polymorphisms in human population: e2, e3 and e4, which are proved to be associated with impaired lipid metabolism. The contribution of apoE polymorphism to MetS disorders has not been investigated previously in Vojvodina Province, region with the highest number of obese people in Serbia. The aim of this study was to evaluate apoE gene polymorphism in relation to MetS disorders. The healthy control group of 30 individuals and 63 MetS patients were examined for apoE variants in relation to biochemical and anthropometric parameters. The genotypes were determined by PCR–RFLP. Regarding all parameters, significantly higher values were detected in MetS group compared to control. The MetS group of patients had significantly higher frequency of e4 allele. In addition, positive relation was revealed between e4 allele presence and all measured parameters. It was found that the e4 allele was related with a significantly increased OR of MetS disorders according to the International Diabetes Federation definition. These results suggested that e4 allele may act as a one of determinants for development of metabolic syndrome.     

Type 2 diabetes mellitus in children and adolescents: a review from a European perspective

Changes in food consumption and exercise are fueling a worldwide increase in obesity in children and adolescents. As a consequence of this dramatic development, an increasing rate of type 2 diabetes mellitus has been recorded in children and adolescents in the USA and, more recently, in many countries around the world. Both genetic and environmental factors contribute to the pathogenesis of type 2 diabetes. Lower susceptibility in white Caucasians and higher susceptibility in Asians, Hispanics and blacks have been noted. There is a high hidden prevalence and a lack of exact data on the epidemiology of the disease in Europe: in Germany only 70 patients below the age of 15 years were identified in the systematic, nationwide DPV (Diabetessoftware für prospektive Verlaufsdokumentation) diabetes survey, but our calculations suggest that more than 5000 young people in Germany at present would meet the diagnostic criteria of type 2 diabetes. In Australasia, the prevalence of type 2 diabetes is reportedly high in some ethnic groups and again is linked very closely to the obesity epidemic. No uniform and evidence-based treatment strategy is available: many groups use metformin, exercise programmes and nutritional education as a comprehensive approach to treat type 2 diabetes in childhood and adolescence. The lack of clear epidemiological data and a strong need for accepted treatment strategies point to the key role of preventive programmes. Prevention of obesity will help to counteract the emerging worldwide epidemic of type 2 diabetes in youth. Preventive programmes should focus on exercise training and reducing sedentary behaviour such as television viewing, encouraging healthy nutrition and supporting general education programmes since shorter school education is clearly associated with higher rates of obesity and hence the susceptibility of an individual to acquire type 2 diabetes.     

Comparison of the prevalence of the metabolic syndrome by WHO, AHA/NHLBI, and IDF definitions in a German population with type 2 diabetes: the Diabetes in Germany (DIG) Study.

This study investigated the prevalence of the metabolic syndrome (MetS) in a German population with type 2 diabetes (T2DM) using the three definitions for MetS according to WHO 1999, AHA/NHLBI 2005, and IDF 2005 criteria. Four-thousand and twenty participants as a cross section of daily practice of diabetes care in Germany (238 unselected sites) were included in the Diabetes in Germany (DIG) study. Inclusion criteria: T2DM and age between 35-80 years. Exclusion criteria: major cardiovascular event < 3 months before entry, NYHA-IV, macroproteinuria, and cancer < 5 years before entry. The components of MetS were measured following a standard protocol for anthropometric and laboratory control. The average diabetes duration was 8.4 years and HbA (1C) 7.0%. The prevalence of MetS by WHO criteria was 26.1%, by AHA/NHLBI 79.3%, and by IDF 82.6%. The degree of agreement (kappa statistic) was kappa = 0.69 between AHA/NHLBI and IDF definitions, but only 0.12 for WHO VS. IDF, and 0.17 for WHO vs. AHA/NHLBI. The frequency of central obesity by WHO was 50.9%, by AHA/NHLBI 72.9%, and by IDF 92.0% and for hypertension 29.3%, 92.6%, and 92.6%, respectively. However, the frequencies of lipid components by the three definitions were in the same range (57.8%, 59.5%, 59.5%). In this representative German sample of patients with type 2 diabetes, the prevalence of MetS was very highly independent of using the IDF or AHA/NHLBI definition. Females were significantly more affected than males. The distinctly lower prevalence delineated from WHO criteria is due to low frequency of central obesity and hypertension as consequence of higher cutoff limits for these components used in the WHO definition.     

Metabolic syndrome,Mediterranean diet,and polyphenols: Evidence and perspectives

Metabolic syndrome (MetS) is defined as the co-occurrence of metabolic risk factors that includes insulin resistance, hyperinsulinemia, impaired glucose tolerance, type 2 diabetes mellitus, dyslipidemia, and visceral obesity. The clinical significance of MetS consists of identifying a subgroup of patients sharing a common physiopathological state predisposing to chronic diseases. Clinical and scientific studies pinpoint lifestyle modification as an effective strategy aiming to reduce several features accountable for the risk of MetS onset. Among the healthy dietary patterns, the Mediterranean diet (MedDiet) emerges in terms of beneficial properties associated with longevity. Current evidence highlights the protective effect exerted by MedDiet on the different components of MetS. Interestingly, the effect exerted by polyphenols contained within the representative MedDiet components (i.e., olive oil, red wine, and nuts) seems to be accountable for the beneficial properties associated to this dietary pattern. In this review, we aim to summarize the principal evidence regarding the effectiveness of MedDiet–polyphenols in preventing or delaying the physiopathological components accountable for MetS onset. These findings may provide useful insights concerning the health properties of MedDiet–polyphenols as well as the novel targets destined to a tailored approach to MetS.     

Insulin Resistance is the Best Predictor of the Metabolic Syndrome in Subjects With a First‐Degree Relative With Type 2 Diabetes

Although obesity is associated with insulin resistance and the metabolic syndrome (MetS), some obese individuals are metabolically healthy. Conversely, some lean individuals are insulin resistant (IR) and at increased cardiometabolic risk. To determine the relative importance of insulin sensitivity, BMI and waist circumference (WC) in predicting MetS, we studied these two extreme groups in a high‐risk population. One thousand seven hundred and sixty six subjects with a first‐degree relative with type 2 diabetes were stratified by BMI and homeostasis model assessment of insulin resistance (HOMA_IR) into groups. IR groups had higher triglycerides, fasting glucose, and more diabetes than their BMI‐group insulin sensitive (IS) counterparts. Within both IS and IR groups, obesity was associated with higher HOMA_IR and diastolic blood pressure (BP), but no difference in other metabolic variables. MetS (Adult Treatment Panel III (ATPIII)) prevalence was higher in IR groups (P < 0.001) and more subjects met each MetS criterion (P < 0.001). Within each BMI category, HOMA_IR independently predicted MetS (P < 0.001) whereas WC did not. Within IS and IR groups, age and WC, but not BMI, were independent determinants of MetS (P < 0.001). WC was a less meaningful predictor of MetS at higher values of HOMA_IR. HOMA_IR was a better predictor of MetS than WC or BMI (receiver operating characteristic (ROC) area under the curve 0.76 vs. 0.65 vs. 0.59, P < 0.001). In conclusion, insulin sensitivity rather than obesity is the major predictor of MetS and is better than WC at identifying obese individuals with a healthier metabolic profile. Further, as many lean individuals with a first‐degree relative with type 2 diabetes are IR and metabolically unhealthy, they may all benefit from metabolic testing.     

Geographic Variation in the Prevalence of Obesity,Diabetes, and Obesity‐Related Behaviors**

Objective: To examine the variation in the prevalences of obesity and type 2 diabetes in weight loss counseling by health providers and in other potential obesity‐related determinants in 100 metropolitan statistical areas in the United States. Research Methods and Procedures: We performed a cross‐sectional study using data from the 2000 Behavioral Risk Factor Surveillance System, the largest telephone survey of health behaviors in the United States, of age‐adjusted prevalence of obesity, type 2 diabetes, intake of ≥five servings of fruits and vegetables per day, participation in 150 minutes of leisure‐time physical activity per week, receipt of weight management advice, and reports of trying to lose or maintain weight among men and women more than 18 years old. Results: The age‐adjusted prevalence of obesity ranged from 13.1% to 30.0% and that of type 2 diabetes from 3.3% to 9.2%. Among participants who had visited a physician for a routine checkup in the previous 12 months, 13.1% to 27.1% of all participants recalled receiving advice from a health professional about their weight, and 11.7% to 34.6% of overweight or obese participants recalled receiving advice to maintain or lose weight. Discussion: Significant differences in the prevalence of obesity and self‐reported type 2 diabetes and in medical practice patterns regarding weight management advice exist among metropolitan statistical areas. These results suggest important opportunities to investigate reasons for these variations that could potentially be used to mitigate the current epidemic of obesity and to identify areas where obesity and diabetes prevention efforts may need to be targeted.     

Increased Serum Hepcidin Levels in Subjects with the Metabolic Syndrome: A Population Study

The recent discovery of hepcidin, the key iron regulatory hormone, has changed our view of iron metabolism, which in turn is long known to be linked with insulin resistant states, including type 2 diabetes mellitus and the Metabolic Syndrome (MetS). Serum ferritin levels are often elevated in MetS (Dysmetabolic hyperferritinemia - DHF), and are sometimes associated with a true mild-to-moderate hepatic iron overload (dysmetabolic iron overload syndrome - DIOS). However, the pathophysiological link between iron and MetS remains unclear. This study was aimed to investigate, for the first time, the relationship between MetS and hepcidin at population level. We measured serum hepcidin levels by Mass Spectrometry in 1,391 subjects from the Val Borbera population, and evaluated their relationship with classical MetS features. Hepcidin levels increased significantly and linearly with increasing number of MetS features, paralleling the trend of serum ferritin. In multivariate models adjusted for relevant variables including age, C-Reactive Protein, and the HFE C282Y mutation, ferritin was the only significant independent predictor of hepcidin in males, while in females MetS was also independently associated with hepcidin. Overall, these data indicate that the fundamental iron regulatory feedback is preserved in MetS, i.e. that hepcidin tends to progressively increase in response to the increase of iron stores. Due to recently discovered pleiotropic effects of hepcidin, this may worsen insulin resistance and contribute to the cardiovascular complications of MetS.     

Metabolic syndrome in relation to Barrett⿿s esophagus and esophageal adenocarcinoma: Results from a large population-based case-control study in the Clinical Practice Research Datalink

Gastroesophageal reflux disease (GERD) causes local chronic inflammation that increases risks of Barrett⿿s esophagus (BE) and esophageal adenocarcinoma (EA), yet symptomatic GERD is absent in approximately half of all such patients. Obesity exacerbates GERD and is also a component of metabolic syndrome (MetS). We evaluated the hypothesis that MetS is a GERD-independent mechanism by which obesity is associated with increased risks of BE and EA using data from the UK Clinical Practice Research Datalink. BE cases (n = 10,215) and EA cases (n = 592) were each individually matched to five population controls based on age, sex, and general practice. MetS was defined as occurrence of at least three of the following: obesity, type 2 diabetes, hypertension, and high cholesterol. Odds ratios (OR) and 95% confidence intervals (CI) were estimated using conditional logistic regression. MetS was marginally associated with BE (OR = 1.12, 95%CI 1.00⿿1.25). Similar effects were found for the individual component factors of obesity, hypertension, and high cholesterol. History of GERD modified the association (P-_{effect modification} <1E⿿5), with the MetS-BE association confined to patients without a history of GERD (OR = 1.33, 95%CI 1.12⿿1.58). No association between MetS and risk of EA was detected in the main or stratified analyses. In this large population-based case-control study, individuals with MetS had a marginally increased risk of BE in the absence of GERD. The systemic inflammatory state (MetS) may represent a reflux-independent inflammatory pathway that increases the risk of BE. MetS did not increase risk of EA in this study population.     

Protective mechanisms of the Mediterranean diet in obesity and type 2 diabetes

The prevalence of obesity has grown to an alarming level of at least 300 million people worldwide. Additionally, a diabetes epidemic is underway, with an estimate of 217 million people with diabetes worldwide. There are many links between excessive body weight and type 2 diabetes, and one common and fundamental cause of both epidemics is an unhealthy diet. Research to identify and promote diets that protect individuals from obesity and type 2 diabetes is urgently needed. The Mediterranean diet, a concept developed in the 1950s, refers to dietary habits of individuals from the Mediterranean basin. The Mediterranean diet is an eating pattern that successfully combines pleasant taste and positive health effects. The Mediterranean diet does not stand for a homogenous and exclusive model among the Mediterranean basin population but rather represents a set of healthy dietary habits, including high consumption of vegetables and fresh fruits and the use of olive oil as the main source of fat. Evidence from epidemiological studies supports a protective effect of this dietary pattern on weight gain and the development of type 2 diabetes. Several mechanistic explanations link characteristic components of the Mediterranean diet with obesity and type 2 diabetes. This review will discuss potential mechanisms by which the Mediterranean diet protects individuals from both diseases.     

Genome-wide linkage scan for the metabolic syndrome: the GENNID study

In the United States, the metabolic syndrome (MetS) constitutes a major public health problem with over 47 million persons meeting clinical criteria for MetS. Numerous studies have suggested genetic susceptibility to MetS. The goals of this study were (i) to identify susceptibility loci for MetS in well-characterized families with type 2 diabetes (T2D) in four ethnic groups and (ii) to determine whether evidence for linkage varies across the four groups. The GENNID study (Genetics of NIDDM) is a multicenter study established by the American Diabetes Association in 1993 and comprises a comprehensive, well-characterized resource of T2D families from four ethnic groups (whites, Mexican Americans, African Americans, and Japanese Americans). Principal component factor analysis (PCFA) was used to define quantitative phenotypes of the MetS. Variance components linkage analysis was conducted using microsatellite markers from a 10-cM genome-wide linkage scan, separately in each of the four ethnic groups. Three quantitative MetS factors were identified by PCFA and used as phenotypes for MetS: (i) a weight/waist factor, (ii) a blood pressure factor, and (iii) a lipid factor. Evidence for linkage to each of these factors was observed. For each ethnic group, our results suggest that several regions harbor susceptibility genes for the MetS. The strongest evidence for linkage for MetS phenotypes was observed on chromosome 2 (2q12.1-2q13) in the white sample and on chromosome 3 (3q26.1-3q29) in the Mexican-American sample. In conclusion, the results suggest that several regions harbor MetS susceptibility genes and that heterogeneity may exist across groups.     

Serum Adiponectin Confers Little Protection Against Diabetes and Hypertension in Turkish Men

We determined serum adiponectin's role as a biomarker of metabolic syndrome (MetS), type 2 diabetes (DM) and hypertension among Turkish adults who have a high prevalence of MetS. Individuals with measured serum adiponectin concentrations, constituting a random sample of Turkish adults, were studied cross‐sectionally. MetS was identified by criteria of the Adult Treatment Panel‐III modified for male abdominal obesity. Median age of 547 men and 652 women was 54 years. MetS was identified in 46%. Linear regression analysis among nine variables revealed homeostatic model assessment (HOMA) index in both sexes and C‐reactive protein (CRP) only in men as inversely associated covariates of adiponectin, and sex hormone‐binding globulin (SHBG) as positive covariate in women. Age‐adjusted sex‐specifically dichotomized high vs. low adiponectin levels were significantly associated with DM (odds ratio (OR) 0.55, P = 0.01) and hypertension (OR 0.64, P = 0.012) in women, but not in men. Further adjustment for smoking status and presence of high/low BMI did not alter this sex‐based relationship. As regards association with MetS, low adiponectin and high BMI interacted significantly in each sex. Yet adiponectin was associated only in men additively to the simultaneously adjusted five MetS components. We conclude that adiponectin concentrations, clearly linked to metabolic disorders, may diverge among sexes regarding protection against cardiometabolic risk through anti‐inflammatory or antioxidative function, Turkish men alone revealing significant dysfunction independent of obesity. This dysfunction may underlie also the association of adiponectin levels with MetS in men to be independent of the MetS components.     

Butyrylcholinesterase interactions with amylin may protect pancreatic cells in metabolic syndrome

The metabolic syndrome (MetS) is a risk factor for type 2 diabetes mellitus (T2DM). However, the mechanisms underlying the transition from MetS to T2DM are unknown. Our goal was to study the potential contribution of butyrylcholinesterase (BChE) to this process. We first determined the hydrolytic activity of BChE in serum from MetS, T2DM and healthy individuals. The ‘Kalow’ variant of BChE (BChE‐K), which has been proposed to be a risk factor for T2DM, was genotyped in the last two groups. Our results show that in MetS patients serum BChE activity is elevated compared to T2DM patients and healthy controls (P < 0.001). The BChE‐K genotype showed similar prevalence in T2DM and healthy individuals, excluding this genotype as a risk factor for T2DM. However, the activity differences remained unexplained. Previous results from our laboratory have shown BChE to attenuate the formation of β‐amyloid fibrils, and protect cultured neurons from their cytotoxicity. Therefore, we next studied the in vitro interactions between recombinant human butyrylcholinesterase and amylin by surface plasmon resonance, Thioflavine T fluorescence assay and cross‐linking, and used cultured pancreatic β cells to test protection by BChE from amylin cytotoxicity. We demonstrate that BChE interacts with amylin through its core domain and efficiently attenuates both amylin fibril and oligomer formation. Furthermore, application of BChE to cultured β cells protects them from amylin cytotoxicity. Taken together, our results suggest that MetS‐associated BChE increases could protect pancreatic β‐cells in vivo by decreasing the formation of toxic amylin oligomers.     

Serum amyloid A is found on ApoB‐containing lipoproteins in obese humans with diabetes

Objective:

In murine models of obesity/diabetes, there is an increase in plasma serum amyloid A (SAA) levels along with redistribution of SAA from high‐density lipoprotein (HDL) to apolipoprotein B (apoB)‐containing lipoprotein particles, namely, low‐density lipoprotein and very low‐density lipoprotein. The goal of this study was to determine if obesity is associated with similar SAA lipoprotein redistribution in humans.

Design and Methods:

Three groups of obese individuals were recruited from a weight loss clinic: healthy obese (n = 14), metabolic syndrome (MetS) obese (n = 8), and obese with type 2 diabetes (n = 6). Plasma was separated into lipoprotein fractions by fast protein liquid chromatography, and SAA was measured in lipid fractions using enzyme‐linked immunosorbent assay and Western blotting.

Results:

Only the obese diabetic group had SAA detectable in apoB‐containing lipoproteins, and SAA reverted back to HDL with active weight loss.

Conclusions:

In human subjects, SAA is found in apoB‐containing lipoprotein particles only in obese subjects with type 2 diabetes, but not in healthy obese or obese subjects with MetS.     

Comparison of accuracy of diabetes risk score and components of the metabolic syndrome in assessing risk of incident type 2 diabetes in Inter99 cohort

Background

Given the increasing worldwide incidence of diabetes, methods to assess diabetes risk which would identify those at highest risk are needed. We compared two risk-stratification approaches for incident type 2 diabetes mellitus (T2DM); factors of metabolic syndrome (MetS) and a previously developed diabetes risk score, PreDx® Diabetes Risk Score (DRS). DRS assesses 5 yr risk of incident T2DM based on the measurement of 7 biomarkers in fasting blood.

Methodology/Principal Findings

DRS was evaluated in baseline serum samples from 4,128 non-diabetic subjects in the Inter99 cohort (Danes aged 30–60) for whom diabetes outcomes at 5 years were known. Subjects were classified as having MetS based on the presence of at least 3 MetS risk factors in baseline clinical data. The sensitivity and false positive rate for predicting diabetes using MetS was compared to DRS. When the sensitivity was fixed to match MetS, DRS had a significantly lower false positive rate. Similarly, when the false positive rate was fixed to match MetS, DRS had a significantly higher specificity. In further analyses, subjects were classified by presence of 0–2, 3 or 4–5 risk factors with matching proportions of subjects distributed among three DRS groups. Comparison between the two risk stratification schemes, MetS risk factors and DRS, were evaluated using Net Reclassification Improvement (NRI). Comparing risk stratification by DRS to MetS factors in the total population, the NRI was 0.146 (p = 0.008) demonstrating DRS provides significantly improved stratification. Additionally, the relative risk of T2DM differed by 15 fold between the low and high DRS risk groups, but only 8-fold between the low and high risk MetS groups.

Conclusions/Significance

DRS provides a more accurate assessment of risk for diabetes than MetS. This improved performance may allow clinicians to focus preventive strategies on those most in need of urgent intervention.