Homeostasis model assessment of insulin resistance in relation to the incidence of cardiovascular disease: the San Antonio Heart Study

OBJECTIVE: The prospective association between insulin levels and risk of cardiovascular disease (CVD) is controversial. The objective of the present study was to investigate the relationship of the homeostasis model assessment of insulin resistance (HOMA-IR), as well as insulin levels, with risk of nonfatal and fatal CVD over the 8-year follow-up of the San Antonio Heart Study. RESEARCH DESIGN AND METHODS: Between 1984 and 1988, randomly selected Mexican-American and non-Hispanic white residents of San Antonio participated in baseline examinations that included fasting blood samples for glucose, insulin, and lipids, a glucose tolerance test, anthropometric measurements, and a lifestyle questionnaire. Between 1991 and 1996, 2,569 subjects who were free of diabetes at baseline were reexamined using the same protocol. RESULTS: Over the follow-up period, 187 subjects experienced an incident cardiovascular event (heart attack, stroke, heart surgery, angina, or CVD death). Logistic regression analysis indicated that risk of a CVD event increased across quintiles of HOMA-IR after adjustment for age, sex, and ethnicity (P for trend <0.0001; quintile 5 vs. quintile 1, odds ratio [OR] 2.52, 95% CI 1.46-4.36). Additional adjustment for LDL, triglyceride, HDL, systolic blood pressure, smoking, alcohol consumption, exercise, and waist circumference only modestly reduced the magnitude of these associations (P for trend 0.02; quintile 5 vs. quintile 1, OR 1.94, 95% CI 1.05-3.59). Furthermore, there were no significant interactions between HOMA-IR and ethnicity, sex, hypertension, dyslipidemia, glucose tolerance (impaired glucose tolerance versus normal glucose tolerance), or obesity. The magnitude and direction of the relationship between insulin concentration and incident CVD were similar. CONCLUSIONS: We found a significant association between HOMA-IR and risk of CVD after adjustment for multiple covariates. The topic remains controversial, however, and additional studies are required, particularly among women and minority populations.     

All-cause and cardiovascular mortality among diabetic participants in the San Antonio Heart Study: evidence against the "Hispanic Paradox"

OBJECTIVE: The observation that Hispanics have lower all-cause and cardiovascular mortality, despite increased diabetes and obesity, lower socioeconomic status (SES), and barriers to health care, has been termed the "Hispanic Paradox." We examined the relationship between ethnicity and all-cause and cardiovascular mortality in Mexican Americans (MAs) and non-Hispanic whites (NHWs) with diabetes. RESEARCH DESIGN AND METHODS: In the San Antonio Heart Study, a prospective cohort, we compared the mortality in 554 U.S.-born MAs, 95 Mexico-born MAs, and 178 NHW participants with diabetes aged 25-72 years. Over an average of 10.4 years, 188 deaths occurred: 115 from cardiovascular disease (CVD) [death certificate ICD-9 codes 401-414 or 420-447 (excluding 427.5)]. Because of potential differences between migrants and nonmigrants, hazard ratios (HRs) were calculated comparing U.S.-born MAs and Mexico-born MAs with NHWs. RESULTS: The age- and sex-adjusted HR for all-cause mortality comparing U.S.-born MAs with NHWs was 1.66 (95% CI 1.15-2.40), while comparing Mexico-born MAs with NHWs was 1.14 (95% CI 0.63-2.06). Cardiovascular mortality HRs were 1.66 (95% CI 1.04-2.65) and 0.89 (95% CI 0.40-2.01), respectively. After adjusting for possible confounders, such as fasting glucose and diabetes duration, the hazard of all-cause and cardiovascular mortality (although not statistically significant) appeared higher in U.S.-born MAs than in the other two groups. CONCLUSIONS: We found it important to differentiate MAs by birthplace. Among diabetic participants, contrary to the prediction of the "Hispanic Paradox," compared with NHWs, U.S.-born MAs were at greater risk of all-cause and cardiovascular mortality, while Mexico-born MAs appeared to be at similar risk.     

The metabolic syndrome as predictor of type 2 diabetes: the San Antonio heart study

OBJECTIVE: The oral glucose tolerance test identifies high-risk subjects for diabetes, but it is costly and inconvenient. To find better predictors of type 2 diabetes, we evaluated two different definitions of the metabolic syndrome because insulin resistance, which is commonly associated with this clustering of metabolic factors, frequently precedes the onset of type 2 diabetes. RESEARCH DESIGN AND METHODS: We compared the ability of the National Cholesterol Education Program (NCEP) definition, a modified version of the 1999 World Health Organization (WHO) definition that excludes the 2-h glucose requirement, and impaired glucose tolerance (IGT) to predict incident type 2 diabetes. In the San Antonio Heart Study, 1734 participants completed a 7- to 8-year follow-up examination. RESULTS: IGT and the NCEP definition had higher sensitivity than the modified WHO definition (51.9, 52.8, and 42.8%, respectively). IGT had a higher positive predictive value than the NCEP and modified WHO definitions (43.0, 30.8, and 30.4%, respectively). The combination of the IGT and NCEP definitions increased the sensitivity to 70.8% with an acceptable positive predictive value of 29.7%. Risk for incidence of type 2 diabetes using the NCEP definition was independent of other risk factors, including IGT and fasting insulin (odds ratio 3.30, 95% CI 2.27-4.80). The NCEP definition performed better with fasting glucose >or=5.4 mmol/l (sensitivity 62.0% and positive predictive value 30.9%). CONCLUSIONS: The metabolic syndrome predicts diabetes independently of other factors. However, the NCEP definition performs better than the modified 1999 WHO definition. Lowering the fasting glucose cutoff to 5.4 mmol/l improves the prediction of diabetes by the metabolic syndrome.     

The metabolic syndrome and cardiovascular disease

The metabolic syndrome, which is very common in the general population, is defined by the clustering of several classic cardiovascular risk factors, such as type 2 diabetes, hypertension, high triglycerides and low high-density lipoprotein cholesterol (HDL). Central obesity and insulin resistance, which are the two underlying disorders of the syndrome, are further risk factors for cardiovascular disease. Moreover, a panel of novel (non-traditional) risk factors are ancillary features of the metabolic syndrome. They include biomarkers of chronic mild inflammation (e.g. C-reactive protein, CRP), increased oxidant stress (e.g. oxidized low density lipoprotein, LDL), thrombophilia (e.g. plasminogen activator inhibitor-1, PAI-1) and endothelial dysfunction (e.g. E-selectin). Therefore, subjects with the metabolic syndrome are potentially at high risk of developing atherosclerosis and clinical cardiovascular events.In recent years several longitudinal studies have confirmed that subjects with the metabolic syndrome present with atherosclerosis and suffer from myocardial infarction and stroke at rates higher than subjects without the syndrome. The risk of cardiovascular disease (CVD) is particularly high in women with the syndrome and in subjects with pre-existing diabetes, CVD and/or high CRP. However, an increased risk is already present in subjects with a cluster of multiple mild abnormalities. The risk related to the metabolic syndrome is definitely higher when subjects affected are compared to subjects free of any metabolic abnormality.     

The metabolic syndrome in older individuals: prevalence and prediction of cardiovascular events: the Cardiovascular Health Study

OBJECTIVE: The prevalence of the metabolic syndrome, a potent risk factor for cardiovascular diseases (CVDs), has not been adequately explored in older individuals. Moreover, two sets of criteria have been proposed for the definition of metabolic syndrome, one by the World Health Organization (WHO) and one by the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATPIII). We therefore investigated the prevalence of this syndrome in a subgroup of older participants from the Cardiovascular Health Study (CHS) who were free of CVD at baseline. We also compared the prognostic significance of the two definitions of the metabolic syndrome. RESEARCH DESIGN AND METHODS: A total of 2,175 subjects from the CHS who were free of CVD at baseline and not taking antihypertensive or lipid-lowering medications were studied. Prevalence of the metabolic syndrome was assessed with both the WHO and ATPIII criteria. The incidence of coronary or cerebrovascular disease was ascertained during a median follow-up time of 4.1 years. RESULTS: Prevalence of the metabolic syndrome was 28.1% by ATPIII criteria and 21.0% by WHO criteria. The two sets of criteria provided concordant classification for 80.6% of participants. Multivariate Cox propotional hazard models showed that the metabolic syndrome defined with the ATPIII criteria, but not with the WHO criteria, was an independent predictor of coronary or cerebrovascular events and was associated with a 38% increased risk (hazard ratio 1.38 [95% CI 1.06-1.79], P < 0.01). CONCLUSIONS: Prevalence of the metabolic syndrome in older individuals is approximately 21-28% (depending on the definition used). The two sets of criteria have 80% concordance in classifying subjects. As defined by the ATPIII criteria, the metabolic syndrome yields independent prognostic information, even after adjusting for traditional cardiovascular risk factors and the individual domains of the metabolic syndrome.     

Insulin resistance,the metabolic syndrome,and risk of incident cardiovascular disease in nondiabetic american indians: the Strong Heart Study

OBJECTIVE: Insulin resistance (IR) and the metabolic syndrome (MS) are associated with type 2 diabetes and adverse cardiovascular disease (CVD) risk factor profiles. Whether IR and MS predict CVD independently of diabetes and other CVD risk factors is not known. This study examines whether IR and/or presence of MS are independently associated with CVD in nondiabetic American Indians (AI). RESEARCH DESIGN AND METHODS: We examined 2283 nondiabetic AI who were free of CVD at the baseline examination of the Strong Heart Study (SHS). CVD risk factors were measured, IR was quantified using the homeostasis model assessment (HOMA), and MS as defined by the National Cholesterol Education Program Adult Treatment Panel (ATP III) was assessed for each participant. Incident CVD and diabetes were ascertained during follow-up. RESULTS: MS was present in 798 individuals (35%), and 181 participants (7.9%) developed CVD over 7.6 +/- 1.8 years of follow-up. Age, BMI, waist circumference, and triglyceride levels increased and HDL cholesterol decreased across tertiles of HOMA-IR. Risk of diabetes increased as a function of baseline HOMA-IR (6.3, 14.6, and 30.1%; P < 0.001) and MS (12.8 vs. 24.5%). In Cox models adjusted for CVD risk factors, risk of CVD did not increase either as a function of baseline HOMA-IR or MS, but individual CVD risk factors predicted subsequent CVD. CONCLUSIONS: Among nondiabetic AI in the SHS, HOMA-IR and MS both predict diabetes, but neither predicts CVD independently of other established CVD risk factors.     

Adiponectin: linking the metabolic syndrome to its cardiovascular consequences

Obesity and its related disorders, glucose intolerance, hypertension and hyperlipidemia, collectively named the metabolic syndrome, result in substantial cardiovascular morbidity and mortality. Recent data point to several underlying regulatory mechanisms through which obesity links these various outcomes. Adipose tissue is now understood to function not merely as a passive energy storage depot but as an active endocrine organ, producing a variety of bioactive substances termed adipocytokines. Adiponectin, an adipocytokine first described as the most abundant protein produced by adipocytes, appears to serve as a central regulatory protein in many of the physiologic pathways controlling lipid and carbohydrate metabolism, and to mediate various vascular processes. Adiponectin displays both anti-inflammatory and antiatherogenic properties. Unlike other adipocytokines, its levels are paradoxically decreased in obesity and insulin-resistance states including metabolic syndrome and diabetes, as well as hypertension and coronary artery disease. This review will detail the relationship of adiponectin to various features of obesity and insulin-resistance syndromes, as well as its relationship to the cardiovascular complications of these disorders.     

Adiponectin: linking the metabolic syndrome to its cardiovascular consequences

Obesity and its related disorders, glucose intolerance, hypertension and hyperlipidemia, collectively named the metabolic syndrome, result in substantial cardiovascular morbidity and mortality. Recent data point to several underlying regulatory mechanisms through which obesity links these various outcomes. Adipose tissue is now understood to function not merely as a passive energy storage depot but as an active endocrine organ, producing a variety of bioactive substances termed adipocytokines. Adiponectin, an adipocytokine first described as the most abundant protein produced by adipocytes, appears to serve as a central regulatory protein in many of the physiologic pathways controlling lipid and carbohydrate metabolism, and to mediate various vascular processes. Adiponectin displays both anti-inflammatory and antiatherogenic properties. Unlike other adipocytokines, its levels are paradoxically decreased in obesity and insulin-resistance states including metabolic syndrome and diabetes, as well as hypertension and coronary artery disease. This review will detail the relationship of adiponectin to various features of obesity and insulin-resistance syndromes, as well as its relationship to the cardiovascular complications of these disorders.     

Obesity and metabolic syndrome as related to cardiovascular disease

The metabolic syndrome (MetS) constitutes a multifaceted disorder, including obesity, dyslipidemia, hyperglycemia and hypertension, associated with an increased propensity towards cardiovascular disease (CVD). Besides this, accumulating data suggest the involvement of nontraditional, novel, cardiovascular risk factors in MetS. Among them, insulin resistance seems to possess a predominant role in MetS-related CVD in obese patients. Furthermore, adipose tissue fatty acid metabolism, increased incidence of oxidative stress and endothelial dysfunction, and excessive production of adipocyte derivatives, known as adipokines, have all been proposed to contribute to the pathogenesis of CVD in obese patients with MetS. Lifestyle interventions, such as weight loss and increased physical activity, have long been the cornerstone for the treatment of obesity-related disorders. With the exception of obesity, pharmaceutical interventions targeting each disorder of MetS have yielded considerable improvement in cardiovascular morbidity and mortality. The long-term management of obesity and its complications seems promising but requires further investigation.     

Hepatic insulin resistance,metabolic syndrome and cardiovascular disease

BackgroundThe metabolic syndrome is a constellation of common metabolic disorders that is associated with cardiovascular disease. Insulin resistance has a central role in the pathophysiology of metabolic syndrome.Recent advancesIt is now commonly accepted that chronic inflammation associated with visceral obesity induces insulin resistance in the liver. Chronic inflammation is characterized by the production of abnormal adipokines and cytokines such as TNF-α, FFA, IL-1, IL-6, leptin and resistin. These factors inhibit insulin signalling in hepatocytes by activating SOCS proteins, several kinases such as JNK, IKK-β and PKC and protein tyrosine phosphatases such as PTP1B and PTEN, that in turn impair insulin signalling at insulin receptor and insulin receptor substrate (IRS) level. Hepatic insulin resistance in turn causes impaired suppression of glucose production by insulin in hepatocytes leading to hyperglycemia. An important and early complication of hepatic insulin resistance is the induction of hepatic VLDL production, via changes in the rate of apoB synthesis and degradation and de novo lipogenesis, or increased FFA flux from adipose tissue into the liver. Insulin resistance also stimulates the production of CRP and PAI-1, both markers of an inflammatory state. All metabolic abnormalities related to hepatic insulin resistance have been shown to directly or indirectly promote atherosclerosis. Hyperglycemia induces a series of alterations including endothelial dysfunction, cellular proliferation, changes in extracellular matrix conformation and impairment of LDL receptor-mediated uptake decreasing the in vivo clearance of LDL. Small dense LDLs associated with high circulating VLDL have higher affinity to the intimal proteoglycans leading to the penetration of more LDL particles into the arterial wall. CRP can also accelerate atherosclerosis by increasing the expression of PAI-1 and adhesion molecules in endothelial cells, inhibition of nitric oxide formation and increasing LDL uptake into macrophages.ConclusionsOverall, growing evidence suggests that hepatic insulin resistance is sufficient to induce several components of the metabolic syndrome and promote progression to cardiovascular disease. Many unresolved questions remain however on the molecular and cellular mechanisms that trigger hepatic insulin resistance and promote the development of clinical metabolic syndrome.     

Low prevalence of metabolic syndrome and its components in rural Japan

Tsunan, Niigata is a non-westernized rural Japanese town, known for heavy snowfalls and as a rice-producing area, whose inhabitants have a long life expectancy. We investigated the prevalence of obesity, metabolic syndrome (MetS) and its components in Tsunan. A total of 1,155 men and women, 40-69 years of age were recruited from participants in the 2005 public-health program in Tsunan. Obesity was defined as body-mass index (BMI) >or= 25 kg/m(2). MetS was defined as BMI >or= 25 kg/m(2) as well as at least two of the following three items: (1) high glycosylated hemoglobin (HbA1c >or= 5.5%); (2) high blood pressure (HBP: systolic blood pressure >or= 130 mmHg or diastolic blood pressure >or= 85 mmHg), and (3) low high-density lipoprotein cholesterol (HDL-C < 40 mg/dL). If an individual was diagnosed with diabetes, hypertension, or dyslipidemia, each item was recorded as a positive finding. The prevalence of MetS and its components among Tsunan inhabitants were compared to the results of the 2005 Japanese nationwide survey. The prevalence of MetS was 4.6% in males and 4.2% in females. The prevalence of obesity, high HbA1c, HBP, and low HDL-C were 22.1/22.2%, 13.4/16.4%, 46.6/40.0%, and 9.2/3.9% in males/females, respectively. All values were significantly lower than the national results, except for the rate of female obesity. The lower prevalence of MetS and its components in Tsunan may be due to the consumption of traditional Japanese food, which is still commonly eaten there, and the higher levels of regular physical activity of farmers.     

Increased oxidative stress in obesity and its impact on metabolic syndrome

Obesity is a principal causative factor in the development of metabolic syndrome. Here we report that increased oxidative stress in accumulated fat is an important pathogenic mechanism of obesity-associated metabolic syndrome. Fat accumulation correlated with systemic oxidative stress in humans and mice. Production of ROS increased selectively in adipose tissue of obese mice, accompanied by augmented expression of NADPH oxidase and decreased expression of antioxidative enzymes. In cultured adipocytes, elevated levels of fatty acids increased oxidative stress via NADPH oxidase activation, and oxidative stress caused dysregulated production of adipocytokines (fat-derived hormones), including adiponectin, plasminogen activator inhibitor-1, IL-6, and monocyte chemotactic protein-1. Finally, in obese mice, treatment with NADPH oxidase inhibitor reduced ROS production in adipose tissue, attenuated the dysregulation of adipocytokines, and improved diabetes, hyperlipidemia, and hepatic steatosis. Collectively, our results suggest that increased oxidative stress in accumulated fat is an early instigator of metabolic syndrome and that the redox state in adipose tissue is a potentially useful therapeutic target for obesity-associated metabolic syndrome.     

Gender differences in the metabolic syndrome and their role for cardiovascular disease

Summary Women live longer than men and develop cardiovascular disease (CVD) at an older age. The metabolic syndrome represents a major risk factor for the development of CVD, and gender¹ differences in this syndrome may contribute to gender differences in CVD. In recent years, the metabolic syndrome has been more prevalent in men than in women. Prevalence is increasing and this increase has been steeper in women, particularly in young women, during the last decade. The contributions of the different components of the metabolic syndrome differ between genders and in different countries. In a recent survey in Germany, 40% of the adult population had been diagnosed with disturbed glucose tolerance or type 2 diabetes. Undiagnosed diabetes was more frequent in men than in women, and risk factors for undiagnosed diabetes differed between the sexes. Worldwide, in individuals with impaired glucose tolerance, impaired fasting glucose was observed more frequently in men, whereas impaired glucose tolerance occurred relatively more often in women. Lipid accumulation patterns differ between women and men. Premenopausal women more frequently develop peripheral obesity with subcutaneous fat accumulation, whereas men and postmenopausal women are more prone to central or android obesity. In particular, android obesity is associated with increased cardiovascular mortality and the development of type 2 diabetes. Visceral adipocytes differ from peripheral adipocytes in their lipolytic activity and their response to insulin, adrenergic and angiotensin stimulation and sex hormones. Visceral fat is a major source of circulating free fatty acids and cytokines, which are directly delivered via the portal vein to the liver inducing insulin resistance and an atherogenic lipid profile. Inflammation increases cardiovascular risk particularly in women. A relatively greater increase in cardiovascular risk by the appearance of diabetes in women has been reported in many studies. Thus, the presently available data suggest that the pathophysiology of the metabolic syndrome and its contribution to the relative risk of cardiovascular events and heart failure show gender differences, which might be of potential relevance for prevention, diagnostics, and therapy of the syndrome. ¹ "Gender" is used to include biological sex as well as gender in its strict sense Supported by the DFG (grants to V. Regitz–Zagrosek) and the BMBF (Competence Network Heart Failure) An erratum to this article can be found at     

Management of cardiovascular disease in African-American women: utility of the metabolic syndrome guidelines

Cardiovascular disease (CVD) is the leading cause of death in the Unites States and is disproportionately more prevalent among African-American women than members of other ethnic groups. The National Cholesterol Education Adult Treatment Panel III (ATP III) metabolic syndrome guidelines are useful in clinical practice to identify individuals who are at risk for developing CVD. Amendments to the ATP III criteria might be indicated to enhance early identification of CVD risk factors among African-American women, even when only one or two of the criteria are met. The addition of body mass index (BMI) and the identification of acanthosis nigricans as a marker of insulin resistance to the ATP III metabolic syndrome guidelines might facilitate early CVD risk identification, strategy implementation, and reduction of premature morbidity and mortality within this population.     

代谢综合征与糖尿病和心血管疾病

1999年世界卫生组织(WHO)公布了代谢综合征(metabolic syndrome,MS)的工作定义(简称WHO定义)。此后6～7年间,世界各国及多个学术组织对其相继提出了不同定义。众多不同定义在一定程度上造成了对MS的认识及临床应用上的混乱;也造成了MS的国际间交流和比较上的     

合肥市成人代谢综合征患病现状及危险因素分析

目的了解合肥市成年常住居民代谢综合征(MS)的患病现状及相关危险因素,为MS的防治提供帮助。方法 2016年9—10月采用分层整群抽样方法在合肥部分城乡地区抽取2772例成年常住居民,通过现场调查的方式对调查对象进行问卷调查、身体测量和实验室检测。合肥市MS的患病情况依照2007年《中国成人血脂异常防治指南》中MS的诊断标准进行分析,对MS相关影响因素运用多因素logistic回归分析。结果合肥市18岁及以上成年常住居民MS的粗患病率为21.97%,标化后患病率为16.71%。随着年龄增加,合肥市MS患病率呈升高趋势(χ~2=117.663,P 0.001),男性居民高于女性(χ~2=49.288,P 0.001),城市居民高于农村(χ~2=8.999,P=0.003)。logistic回归分析显示,高密度脂蛋白胆固醇是MS保护因素,高血压、高血糖、腰围、三酰甘油是MS危险因素。结论合肥地区成年人群MS的患病率较高,应针对MS的相关危险因素尽早采取干预措施,从而减少MS的发生,提高生活质量。     

Impaired Glucose Tolerance and Obesity as Effect Modifiers of Ethnic Disparities of the Progression to Diabetes: The San Antonio Heart Study

OBJECTIVE

The Diabetes Prevention Program (DPP) reported no racial/ethnic differences in the incidence of diabetes in individuals with impaired glucose tolerance (IGT). Therefore, it has been hypothesized that factors associated with racial/ethnic disparities act prior to the development of IGT. Because impaired fasting glucose (IFG) and obesity were also very prevalent in the DPP, we examined IGT, IFG, and obesity as effect modifiers of ethnic disparities in the San Antonio Heart Study.

RESEARCH DESIGN AND METHODS

Participants were 3,015 Mexican Americans and non-Hispanic whites aged 25–64 years. The median follow-up period was 7.8 years. IGT, IFG, and diabetes were defined by the 2003 American Diabetes Association criteria, and obesity was defined as BMI ≥30 kg/m².

RESULTS

Mexican Americans had an excess risk of incident IGT (odds ratio 1.48 [95% CI 1.16–1.89]) and incident IFG (1.71 [1.31–2.23]) compared with non-Hispanic whites. Mexican Americans also had a higher incidence of diabetes among individuals who had normal 2-h glucose (2.20 [1.48–3.29]) and IGT (1.72 [1.08–2.74]) at baseline. There was an interaction of obesity on the relationship between ethnicity and progression to IGT or diabetes (P = 0.034), with Mexican Americans having a greater risk among the nonobese (1.73 [1.36–2.21]) and a comparable risk among the obese (1.08 [0.75–1.56]).

CONCLUSIONS

Ethnic differences can be detected at both the early and later stages of the diabetes disease process. However, non-Hispanic whites lose much of the ethnic advantage once they have developed obesity.Minority populations are at increased risk of developing diabetes (1–4). Obesity and fat distribution do not fully account for racial/ethnic disparities in the development of diabetes (1,2). Obesity and ethnicity influence the development of diabetes in individuals with impaired glucose tolerance (IGT) (5). However, the rate of conversion from IGT to type 2 diabetes was similar across racial/ethnic groups in the Diabetes Prevention Program (DPP) (6). The DPP was designed as a large, randomized clinical trial involving adults who were at very high risk of future diabetes (rate of conversion to diabetes was 11.0% per year). Consequently, Dagogo-Jack et al. (7) recently hypothesized that factors associated with racial/ethnic disparities act prior to the development of IGT (i.e., at early stages). A longitudinal study is underway to explore this hypothesis in African Americans and non-Hispanic whites (7).A closer look at the DPP eligibility criteria suggests that factors other than IGT may also have contributed to the very high rate of progression to diabetes (6). DPP criteria for enrollment included fasting plasma glucose 5.3–6.9 mmol/L (≤6.9 mmol/L in Native Americans) and BMI ≥24 kg/m² (≥22 kg/m² in Asians). Therefore, it is also plausible that the lack of racial/ethnic differences in the risk of diabetes could have been influenced by the fact that mean fasting glucose was 5.92 mmol/L and mean BMI was 34.2 kg/m². To clarify these assumptions, the objective of this study was to assess ethnic disparities proximal to and during the IGT and impaired fasting glucose (IFG) stages in nonobese and obese participants in the San Antonio Heart Study (SAHS).     

成人代谢综合征的不同组分与其发病的关系

目的了解成人代谢综合征(MS)不同组分与其发病的相关关系。方法随机抽取广西南宁市区部分事业单位工作人员共7 917人,按标准测定血压、体重、腰围,采血检测血糖及血脂等生化项目。结果(1)本组人群中MS标化患病率为7.90%。MS各组分标化患病率从高到低依次为腹型肥胖、高TG、高血压、IGR、低HDL、DM和肥胖。(2)本组人群中检出1项、2项及≥3项MS组分者分别占33.30%、24.33%和16.20%;检出MS者,疾病组(包括高血压、DM和肥胖)明显高于相应正常组或正常高值组,而正常高值组亦明显高于相应正常组。(3)主成分分析表明,4个公因子的累积贡献率达到全部的65.02%。其中因子1“血糖”为20.04%,因子2“血压”为16.05%,通过合计因子3和4“血脂”为28.93%。结论在不同血糖、血压和BMI水平人群中,随血糖、血压和BMI的水平增高,检出MS多项组分及MS者比例明显增多。MS与其组分中血脂、血糖、血压有密切关系。     

Occupation-related differences in the prevalence of metabolic syndrome

OBJECTIVE—To investigate the prevalence of metabolic syndrome in the Spanish working population and determine how the prevalence varies according to occupation and sex.RESEARCH DESIGN AND METHODS—This was a cross-sectional study of 259,014 workers (mean age 36.4 years, range [16–74]; 72.9% male) who underwent a routine medical checkup. The Adult Treatment Panel III (2001) definition for metabolic syndrome was used.RESULTS—The prevalence of metabolic syndrome was 11.6% (95% CI 11.5–11.7) in male subjects and 4.1% (4.0–4.2) in female subjects and increased with age. The prevalence of metabolic syndrome varied in the different categories of occupational activity depending on the sex considered. Among female subjects, the age-adjusted prevalence of metabolic syndrome was higher in blue-collar than in white-collar workers, but this difference was not evident among male workers.CONCLUSIONS—The prevalence of metabolic syndrome varies in the different categories of occupational activity in the Spanish working population. This variation also depends on sex.There is little information about the prevalence of metabolic syndrome or its components in workers (1). The overall prevalence of the metabolic syndrome is ∼25% in general populations from the U.S. and Europe, including Spain (1–3). Some studies have shown a sex-specific inverse association between measures of socioeconomic status and the prevalence of the metabolic syndrome (2–4). This study aimed to investigate the prevalence of metabolic syndrome in the Spanish working population and determine whether prevalence differed according to occupational activity and sex.