Ghrelin Arg51Gln mutation is a risk factor for Type 2 diabetes and hypertension in a random sample of middle-aged subjects

AIMS/HYPOTHESIS: Experimental studies have suggested that ghrelin, a novel gastrointestinal peptide hormone, could play a role in glucose homeostasis. In addition, ghrelin has been associated with beneficial haemodynamic effects in experimental settings. Since the Arg51Gln mutation changes the carboxyterminal amino acid of the mature hormone and is associated with low ghrelin concentrations, we assessed the hypothesis that Arg51Gln mutation is a risk factor for Type 2 diabetes, impaired glucose tolerance, and hypertension. METHODS: Blood pressure recordings and oral glucose tolerance test were carried out in the hypertensive ( n=519) and control cohorts ( n=526) of our well-defined OPERA study. The genotypes and plasma IGF-I and IGFBP-1 concentrations of 1031 subjects were analysed. RESULTS: The ghrelin 51Gln allele was a risk factor for Type 2 diabetes, and the effect remained significant after adjustment for age, BMI, and study group (OR=2.53, CI: 1.11-5.75, p=0.027). In addition, the 51Gln allele was a risk factor for hypertension (OR=2.63, CI: 1.37-5.08, p=0.003). 51Gln carriers had lower concentrations of IGF-I and higher concentrations of IGFBP-1 compared to non-carriers. CONCLUSION/INTERPRETATION: The ghrelin 51Gln allele could increase the risk for Type 2 diabetes and hypertension. The low IGF-I concentrations in 51Gln carriers suggest that the mechanism might be associated with low GH concentrations.     

What does postprandial hyperglycaemia mean?

AIMS: The potential importance of postprandial glucose (PPG) control in the development of complications in Type 2 diabetes is much debated. The recent American Diabetes Association (ADA) consensus statement discussed the role of postprandial hyperglycaemia in the pathogenesis of diabetic complications and concluded that the relationship between PPG excursions and the well-established risk factors for cardiovascular disease (CVD) should be further examined. Using the ADA statement as a starting point and including the more recent American College of Endocrinology guidelines on glycaemic control, a panel of experts in diabetes met to review the role of PPG within the context of the overall metabolic syndrome, in the development of complications in Type 2 diabetes. RESULTS: Post-prandial hyperglycaemia is a risk indicator for micro- and macrovascular complications, not only in patients with Type 2 diabetes but also in those with impaired glucose tolerance. In addition, the metabolic syndrome confers an increased risk of CVD morbidity and mortality. The debate focused on the relative contributions of postprandial hyperglycaemia, the metabolic syndrome and, in particular, raised triglyceride levels in the postprandial state, to the development of cardiovascular complications of diabetes. CONCLUSIONS: The panel recommended that in the prevention and management of microvascular complications of Type 2 diabetes, targeting both chronic and acute glucose fluctuations is necessary. Lowering the macrovascular risk also requires control of (postprandial) triglyceride levels and other components of the metabolic syndrome.     

Synergism between mutant HNF1A and the metabolic syndrome in Oji-Cree Type 2 diabetes.

AIMS: To determine the prevalence of the metabolic syndrome in the Sandy Lake Oji-Cree and to examine its interaction with HNF1A in association with impaired glucose tolerance and Type 2 diabetes. METHODS: Using data collected from the Sandy Lake Health and Diabetes Project (1993-1995), the presence or absence of the metabolic syndrome was determined in 515 Oji-Cree subjects, > or = 18 years of age. In the original study, fasting plasma analytes were measured, a 75-g oral glucose tolerance test was administered, and subjects were genotyped for HNF1A G319S. RESULTS: The unadjusted prevalence of the metabolic syndrome in the Oji-Cree adults was 29.9%. The adjusted odds ratio (OR) and 95% confidence interval for Type 2 diabetes among subjects who carried the HNF1A G319S mutation and had the modified metabolic syndrome (excluding hyperglycaemia) was 20.3 (6.94, 59.6). Adjusted ORs for Type 2 diabetes for subjects with either the HNF1A G319S mutation alone or the modified metabolic syndrome alone were 5.56 (2.85, 10.9) and 4.84 (2.53, 9.27), respectively. The risk of having impaired glucose tolerance was not influenced by the presence of either factor. CONCLUSIONS: The risk of Type 2 diabetes was similar (approximately five-fold increased) for subjects with either the presence of the modified metabolic syndrome or the private HNF1A G319S mutation. Interestingly, when present in combination, the two independent risk factors appeared to act synergistically to confer an even greater increased risk of Type 2 diabetes.     

Ghrelin与阻塞性睡眠呼吸暂停低通气综合征并代谢综合征

Ghrelin是迄今发现的体内唯一的生长激素促分泌物质受体的内源性配体,它不仅是生长激素的强烈促分泌剂,还促进摄食,对调节能量代谢也有重要作用,并可能参与肥胖和2型糖尿病的发病过程,在体内还可以促进机体慢波睡眠,在阻塞性睡眠呼吸暂停低通气综合征（obstructive sleep apnea-hyponea syndrome,OSAHS）患者中尤其明显。本文主要阐述Ghrelin的一般特点及其与OSAHS及代谢综合征的关系。     

The ghrelin/GOAT/GHS-R system and energy metabolism

Ghrelin is a brain-gut peptide that was discovered through reverse pharmacology and was first isolated from extracts of porcine stomach. Ghrelin binds to growth hormone secretagogue receptor (GHS-R) and is acylated on its serine 3 residue by ghrelin O-acyltransferase (GOAT). Several important biological functions of ghrelin have been identified, which include its growth hormone-releasing and appetite-inducing effects. Ghrelin exerts its central orexigenic effect mainly by acting on the hypothalamic arcuate nucleus via the activation of the GHS-R. Peripherally ghrelin has multiple metabolic effects which include promoting gluconeogenesis and fat deposition. These effects together with the increased food intake lead to an overall body weight gain. AMP-activated protein kinase, which is a key enzyme in energy homeostasis, has been shown to mediate the central and peripheral metabolic effects of ghrelin. The hypothalamic fatty acid pathway, hypothalamic mitochondrial respiration and uncoupling protein 2 have all been shown to act as the downstream targets of AMPK in mediating the orexigenic effects of ghrelin. Abnormal levels of ghrelin are associated with several metabolic conditions such as obesity, type 2 diabetes, Prader-Willi syndrome and anorexia nervosa. The ghrelin/GOAT/GHS-R system is now recognised as a potential target for the development of anti-obesity treatment.     

Metabolic syndrome: "common soil" for diabetes and atherosclerosis. Novel approaches to an integrated therapy

Type 2 diabetes and atherosclerotic vascular disease develop in parallel. Prospective epidemiologic studies have shown a striking communality of major risk factors for both diseases. This raises the question of a "common soil". The traits of the metabolic syndrome including dyslipidemia, visceral obesity and hypertension are predictors of type 2 diabetes as well as coronary heart disease. The same applies to the environmental factors: overnutrition, physical inertia and smoking. Visceral obesity, insulin resistance and low-grade inflammation are known as major components of the common soil for metabolic syndrome and coronary heart disease. Depending on the quality of metabolic control diabetes will accelerate the progression of atherosclerosis via unstable plaque formation.The "common soil" concept provides a paradigm for an integrated therapeutic approach. This applies to a lifestyle intervention as well as a rational use of drugs in diseases of the metabolic syndrome.The medication should consider coexisting disorders of the metabolic syndrome to use pleiotropic effects. On the other hand, side effect such as the worsening of blood glucose levels caused by beta-blockers and diuretics should be avoided.The following medication should be preferred in context of the metabolic syndrome: oral antidiabetics such as acarbose, metformin and thiazolidinediones, antihypertensives such as ACE inhibitors and ARBs (angiotensin receptor blockers) and lipid-lowering drugs such as atorvastatin, rosuvastatin, and the modern nicotinic acid derivative Niaspan, respectively.The strategy using synergies in drug treatment can reduce polypharmacy and costs and improve the patients' compliance.     

The metabolic syndrome: prevalence, CHD risk, and treatment

An increased risk of coronary heart disease (CHD) morbidity and mortality is associated with the metabolic syndrome, a condition characterized by the concomitant presence of several abnormalities, including abdominal obesity, dyslipidemia, hypertension, insulin resistance (with or without glucose intolerance or diabetes), microalbuminuria, prothrombotic, and proinflammatory states. Estimates of the prevalence of the metabolic syndrome indicate that this condition is now common and likely to increase dramatically over the coming decades, in parallel with greater rates of obesity and Type 2 diabetes. Risk factors for the metabolic syndrome are already present in obese children and adolescents. Thus, identifying and treating all affected individuals promptly and optimally are critical to ensure that this potentially challenging healthcare burden is minimized. Here, we review the prevalence of the metabolic syndrome, dyslipidemias, and CHD risk. Although changes in lifestyle are fundamental to reducing many of the CHD risk factors associated with the metabolic syndrome, pharmacologic interventions also play an important role. Retrospective subanalyses of the effects of statins on coronary event rates and lipid levels in patients with the metabolic syndrome included in clinical trials indicate that these agents are beneficial in correcting the extensive lipid abnormalities that are frequently present in these individuals. However, the optimal management of metabolic syndrome dyslipidemia will depend on the outcomes of future prospective clinical trials. This review examines the underlying causes and prevalence of the metabolic syndrome and its impact on CHD morbidity and mortality and discusses the role of statins in optimizing its management.     

Role of sleep duration in the regulation of glucose metabolism and appetite

Sleep curtailment has become a common behavior in modern society. This review summarizes the current laboratory evidence indicating that sleep loss may contribute to the pathophysiology of diabetes mellitus and obesity. Experimentally induced sleep loss in healthy volunteers decreases insulin sensitivity without adequate compensation in beta-cell function, resulting in impaired glucose tolerance and increased diabetes risk. Lack of sleep also down-regulates the satiety hormone leptin, up-regulates the appetite-stimulating hormone ghrelin, and increases hunger and food intake. Taken together with the epidemiologic evidence for an association between short sleep and the prevalence or incidence of diabetes mellitus and/or obesity, these results support a role for reduced sleep duration in the current epidemic of these metabolic disorders. Screening for habitual sleep patterns in patients with "diabesity" is therefore of great importance. Studies are warranted to investigate the putative therapeutic impact of extending sleep in habitual short sleepers with metabolic disorders.     

Plasma endothelin in postmenopausal women with type 2 diabetes mellitus and metabolic syndrome: a comparison of oral combined and transdermal oestrogen-only replacement therapy

SUMMARY
Aim   Type 2 diabetes and metabolic syndrome are major cardiovascular risk factors in postmenopausal women, but the role of vasoconstrictive endothelin-1 (ET-1) in these conditions is not known. We studied the levels of ET-1 and the effect of postmenopausal hormonal therapy on ET-1 levels in postmenopausal women.
Methods   We compared plasma levels of ET-1 in 22 postmenopausal type 2 diabetic women and 14 postmenopausal women with metabolic syndrome with plasma levels in 10 healthy postmenopausal control women. The basal values for ET-1 were measured for all groups. These women were then randomised to receive in a double-dummy, crossover trial: either oral continuous oestradiol (2.0 mg) + norethisterone acetate (1.0 mg) per day or continuous transdermal oestrogen-only (50 μg/day) for 3 months. Between the active therapy there were 3-month wash-out periods. ET-1-values were measured again at the end of each treatment period.
Results   The type 2 diabetic women had significantly (p < 0.003) elevated ET-1 levels (4.8 ± 1.0 pg/ml) whereas those with metabolic syndrome (4.4 ± 1.7 pg/ml) had non-significantly (NS) elevated ET-1 levels compared to controls (3.6 ± 0.3 pg/ml). Both oral and transdermal hormone replacement therapy (HRT) failed to affect plasma ET-1 except in 14 hypertensive women from the diabetes and metabolic syndrome groups who were on angiotensin convertase enzyme (ACE) inhibitors. These women's ET-1 levels before oral HRT (4.6 ± 1.1 pg/ml) fell to 4.1 ± 0.9 pg/ml (p < 0.05).
Conclusions   Type 2 diabetes in postmenopausal women is associated with elevated ET-1 levels. Oestrogen replacement therapy does not affect the levels of ET-1 in postmenopausal women with type 2 diabetes or metabolic syndrome.     

Analysis the significant risk factors on type 2 diabetes perspective of Bangladesh

Millions of people in Bangladesh and the world have a metabolic disease named diabetes. It is also responsible for occurring different kinds of diseases such as heart attack, kidney disease, blindness and renal failure. Diabetes is a deadly, disabling disease whose risk is increasing at an alarming rate day by day perspective to Bangladesh. The detection process of diabetes is a tedious and multilayered task from some important risk factors. Like other diseases, Type2 diabetes also depends on some factors that are known as risk factors of Type2 diabetes. Risk factors are divided into four categories like Scio-economic condition, Habits, Family History and Hard Diseases etc. in proposed system. Initially 731 diabetes and non-diabetes patient’s data have been collected from different diagnostic centers, pre-processed and clustered for identifying relevant and non-relevant data. Significant factors are discovered according to four categories. Next correlation is assessment among significant factors. Finally highly significant factors are discovered whose are directly or indirectly associated with type2 diabetes. Results indicate that Age, Area of Residence, Education Level, Social Status, Family Income, Expense, Tobacco, BMI, Family History, Physical Exercise and Hard Diseases have worst impact on Quality of Life (QoL) among all factors of type2 diabetes respectively.     

Metabolic syndrome is not associated with markers of subclinical atherosclerosis, serum adiponectin and endogenous androgen concentrations in Japanese men with Type 2 diabetes.

AIMS: Metabolic syndrome is characterized by its association with certain cardiovascular disease risk factors. The aim of this study was to investigate the relationships between metabolic syndrome and markers of subclinical atherosclerosis, serum adiponectin and endogenous androgen concentrations in Japanese men with Type 2 diabetes. METHODS: Using the 2005 International Diabetes Federation (IDF) definition, we assessed the prevalence of the metabolic syndrome in 424 consecutive men with Type 2 diabetes aged 40-75 years in a cross-sectional study. We compared characteristics including ultrasonographic carotid atherosclerosis markers, pulse-wave velocity (PWV), and serum adiponectin, free testosterone, and dehydroepiandrosterone sulphate (DHEA-S) concentrations in diabetic patients with and without the metabolic syndrome. RESULTS: The prevalence of the metabolic syndrome in Japanese men with Type 2 diabetes was 46.9%. Men with the metabolic syndrome had higher urinary albumin excretion rate than those without. Carotid intima-media thickness (0.97 +/- 0.26 vs. 0.91 +/- 0.18 mm), plaque score [3.3 (1.5-8.1) vs. 3.8 (1.3-6.2)], PWV (1818 +/- 331 vs. 1749 +/- 331 cm/s) and ankle-brachial index (1.10 +/- 0.14 vs. 1.08 +/- 0.16) did not differ significantly between patients with and without the metabolic syndrome. Similarly, serum adiponectin [3.70 (2.06-6.09) vs. 4.65 (3.09-7.02) microg/ml], free testosterone (36.4 +/- 10.7 vs. 34.7 +/- 11.1 pmol/l), and DHEA-S concentrations (3.29 +/- 1.83 vs. 3.17 +/- 1.63 micromol/l) did not differ significantly between groups, CONCLUSIONS: The metabolic syndrome, as defined by the IDF, is not significantly associated with subclinical atherosclerosis markers, serum adiponectin, or endogenous androgen concentrations in Japanese men with Type 2 diabetes.     

Ghrelin, obesity and diabetes

The high prevalence of obesity and diabetes will lead to higher rates of morbidity and mortality. The search for drugs to treat these metabolic disorders has, therefore, intensified. The stomach-derived peptide ghrelin regulates food intake and body weight. Recent work suggests that ghrelin also controls glucose metabolism. In addition, current evidence suggests that most of the actions of ghrelin could contribute to the metabolic syndrome. The ghrelin signaling system is, therefore, a promising target for the development of new drugs for the treatment of obesity and diabetes. Agents that block the ghrelin signaling system might be especially useful targets. This Review summarizes the potential and the limitations of ghrelin as a tool to better understand, prevent and treat obesity and diabetes.     

Thiazolidinediones-benefits on microvascular complications of type 2 diabetes

Type 2 diabetes is associated with serious microvascular complications, such as nephropathy, retinopathy, and neuropathy, which have a significant impact on patients' quality of life, morbidity, and mortality. Type 2 diabetes management strategies to reduce the risk of microvascular complications include treatment of hyperglycaemia, hypertension, and other vascular risk factors. The importance of glycaemic control in reducing the risk of microvascular complications of diabetes is well established. However, many antihyperglycaemic therapies fail to provide adequate glycaemic control and do not prevent complications in the long term. The thiazolidinediones (TZDs) are a class of agents that provide sustained glycaemic control, mediated primarily by reductions in insulin resistance. Evidence reviewed suggests that the TZDs may have the potential to reduce microvascular complications through benefits that go beyond glycaemic control. Insulin resistance underlies a range of metabolic abnormalities, collectively known as the metabolic syndrome (MS), which are cardiovascular (CV) risk factors. Components include visceral obesity, hyperglycaemia, hypertension, dyslipidaemia, low-grade inflammation and microalbuminuria (an early manifestation of target organ damage). Reducing insulin resistance, therefore, has the potential to reduce both microvascular and macrovascular complications.     

Peroxisome proliferator-activated receptor (PPAR) in metabolic syndrome and type 2 diabetes mellitus

Type 2 diabetes mellitus, a global epidemic, is largely attributed to metabolic syndrome and its clustering of cardiovascular risk factors including abdominal obesity, dyslipidemia, hypertension and hyperglycemia. The two primary approaches to optimally control risk factors associated with metabolic syndrome are lifestyle changes and medications. Although many pharmacological targets have been identified, clinical management of cardiovascular risk factors associated with metabolic syndrome and type 2 diabetes is still dismal. Recent evidence suggests premises of the peroxisome proliferator-activated receptor (PPAR) ligands in the combat against type 2 diabetes and metabolic syndrome including obesity and insulin resistance. Three subtypes of the PPAR nuclear fatty acid receptors have been identified: alpha, beta/delta and gamma. PPARalpha is believed to participate in fatty acid uptake (beta- and omega-oxidation) mainly in the liver and heart. PPARbeta/delta is involved in fatty acid oxidation in muscle. PPARgamma is highly expressed in fat to facilitate glucose and lipid uptake, stimulate glucose oxidation, decrease free fatty acid level and ameliorate insulin resistance. Synthetic ligands for PPARalpha and gamma such as fibric acid and thiazolidinediones have been used in patients with type 2 diabetes and pre-diabetic insulin resistance with significantly improved HbA(1c) and glucose levels. In addition, nonhypoglycemic effects may be elicited by PPAR agonists or dual agonists including improved lipid metabolism, blood pressure control and endothelial function, as well as suppressed atherosclerotic plaque formation and coagulation. However, issues of safety and clinical indication remain undetermined for use of PPAR agonists for the incidence of heart disease in metabolic syndrome and type 2 diabetes.     

Epidemiology of diabetes mellitus and associated cardiovascular risk factors: focus on human immunodeficiency virus and psychiatric disorders

Type 2 diabetes mellitus and obesity have reached epidemic proportions in many developing and developed nations, leading to talk of the "twin epidemics." The latest projections from the International Diabetes Federation suggest that 190 million people worldwide currently have type 2 diabetes. In addition, > or = 300 million people worldwide have impaired glucose tolerance (IGT). These statistics represent an epidemic of major proportions--possibly the largest epidemic in human history--in terms of glucose intolerance and cardiovascular disease (CVD) risk because individuals with IGT are at substantially higher risk for diabetes and CVD than are members of the general population. Along with IGT, the metabolic syndrome comprises other major CVD risk factors, including insulin resistance, central obesity, and dyslipidemia; insulin resistance has been implicated as the single most common cause of the syndrome. Although the exact prevalence of the metabolic syndrome is unknown, the syndrome is widespread among adults in developed nations, becoming more prevalent with age. Epidemiologic data suggest that in patients with schizophrenia or affective disorders, both diabetes and obesity are 1.5 to 2.0 times more prevalent than in the general population. Furthermore, because adverse effects of certain therapies for human immunodeficiency virus (HIV) infection and psychiatric disorders increase the risk for developing diabetes, obesity, and the metabolic syndrome, such therapies should be carefully chosen, particularly considering CVD risk. Appropriate therapy may be determined via screening of patients for levels of fasting blood glucose and lipids, as well as other CVD risk factors, before initiating use of second-generation antipsychotic agents or highly active antiretroviral therapy.     

C-reactive protein and the development of the metabolic syndrome and diabetes in middle-aged men

Aims/hypothesis Low-grade inflammation has been implicated in the development of Type 2 diabetes and cardiovascular disease, but its role in the pathogenesis of the metabolic syndrome is unclear. We investigated the association between C-reactive protein (CRP) levels and the development of the metabolic syndrome and diabetes in men.Methods Serum CRP concentrations and factors related to insulin resistance were determined in middle-aged Finnish men who participated in a population-based cohort study and were free of diabetes at baseline.Results At the 11-year follow-up, 143 of 680 men had developed the metabolic syndrome as defined by the National Cholesterol Education Program (NCEP) and 103 of 598 men had developed the metabolic syndrome as defined by the World Health Organization (WHO). Our analyses excluded men with the metabolic syndrome by the respective definition at baseline. In all, 78 of 762 men developed diabetes over the same period. Men with CRP concentrations 3 mg/l had a several-fold higher age-adjusted risk of developing the metabolic syndrome (NCEP definition: odds ratio [OR]=3.2, 95% CI 1.9–5.5; WHO definition: OR=3.4, 95% CI 2.0–6.1) or diabetes (OR=4.1, 95% CI 2.1–8.0) than men whose CRP levels were <1.0 mg/l. Even after further adjustment for potentially confounding lifestyle factors and factors related to insulin resistance, the risk of diabetes (OR=2.3, 95% CI 1.0–5.1) was still increased in men with CRP concentrations 3 mg/l, but the association with the metabolic syndrome was no longer significant.Conclusions/interpretation Low-grade inflammation may increase the risk of the metabolic syndrome and diabetes in middle-aged men, but some of the risk is mediated through obesity and factors related to insulin resistance.Abbreviations CRP C-reactive protein - KIHD Kuopio Ischaemic Heart Disease Risk Factor Study - NCEP National Cholesterol Education Program - WHO World Health Organization     

Clinical significance of high-sensitivity C-reactive protein in lifestyle-related disease and metabolic syndrome

OBJECTIVES: High-sensitivity C-reactive protein (hs-CRP), a biochemical marker of subclinical inflammation, is associated with atherosclerosis and cardiovascular disease. The present study evaluated the clinical usefulness of hs-CRP in lifestyle-related diseases and metabolic syndrome. METHODS: Hs-CRP was measured in 407 subjects who underwent a checkup at our Medical Office of Cardiology. Levels of hs-CRP were compared between various clinical conditions associated with lifestyle-related diseases and metabolic syndrome. RESULTS: Levels of hs-CRP were significantly high in the subjects with hypertension, hyperlipidemia, diabetes, obesity, and metabolic syndrome (p < 0.001). Both diabetes and metabolic syndrome were strongly associated with hs-CRP levels (diabetes: p = 0.0001, beta = 0.184; metabolic syndrome: p < 0.00001, beta = 0.264). In addition, hs-CRP levels were strongly associated with number of risk factors, and hs-CRP levels were significantly increased with increased number of risk factors. In patients with many risk factors, levels of hs-CRP were significantly higher in subjects with abdominal obesity than in normal subjects (p < 0.001). Waist circumference and hemoglobin A1c levels represented independent predictors for hs-CRP levels in subjects with metabolic syndrome (waist circumference: p < 0.00001, beta = 0.256; hemoglobin A1c: p < 0.00001, beta = 0.242). CONCLUSIONS: Levels of hs-CRP were strongly associated with lifestyle-related diseases, metabolic syndrome, and increased number of risk factors. These results suggest that measurement of hs-CRP may be useful in risk management for clinical practice.     

2型糖尿病家族史是糖耐量正常个体发生代谢综合征的独立危险因素

目的研究糖耐量正常（NGT）的2型糖尿病（T2DM）一级亲属中代谢综合征（MS）的相关危险因素。方法采用横断面研究，比较182例T2DM家族史阳性（FH^＋）与126例家族史阴性（FH^-）NGT个体的人体测量指标和代谢参数的差异，分析MS的相关危险因素。结果FH^＋个体的腰围和OGTT血糖曲线下面积显著高于FH^-个体，而胰岛β细胞功能指数则显著低于FH^-个体。Logistic分析显示，T2DM家族史是MS和中心性肥胖的独立危险因素，OR值分别为3．33和2．59；中心性肥胖是高血压、高TG血症及低HDL-C血症的独立危险因素，OR值分别为1．41、1．43及1、07。结论T2DM家族史可能是NGT的一级亲属发生中心性肥胖和MS的独立危险因素。早期生活方式干预可使该人群避免发生中心性肥胖，从而减少发生MS甚或心血管疾病的风险。     

Lifestyle management in the metabolic syndrome

Type 2 diabetes and metabolic syndrome are two of the fastest growing public health problems in both developed and developing countries. Cardiovascular disease is the most prevalent complication of type 2 diabetes and the metabolic syndrome. Overweight, obesity, or weight gain has been shown to be an important risk factor for the development of type 2 diabetes and an important component of the metabolic syndrome. Physical inactivity is another important risk factor for the development of type 2 diabetes. Data from prospective studies have shown that at least 30 min/day of moderate to vigorous physical activity can prevent type 2 diabetes. Moderate or high levels of physical fitness are effective in preventing type 2 diabetes. Results from clinical trials have indicated that lifestyle changes, including dietary modification and increase in physical activity, can prevent type 2 diabetes. Analyses from prospective studies have confirmed that healthy diets are effective and safe ways to prevent type 2 diabetes and the metabolic syndrome. Public health messages, health care professionals, and the health care system should aggressively promote physical activity and responsible nutritional habits during occupation, leisure time, and daily life and prevent overweight and obesity.     

Exercise, fitness, and cardiovascular disease risk in type 2 diabetes and the metabolic syndrome

This article highlights research supporting the concept that increased physical activity and cardiorespiratory fitness attenuate risk of cardiovascular disease, type 2 diabetes, and the metabolic syndrome. Increased activity and fitness also attenuate risk of developing cardiovascular disease in persons who have type 2 diabetes or the metabolic syndrome. Although controversial, relationships between physical activity/physical fitness and type 2 diabetes/metabolic syndrome are largely independent of body weight. Thus, physical inactivity and poor cardiorespiratory fitness are not only important determinants of cardiovascular and metabolic diseases, but they can also be considered common features of these conditions, much like traditional risk factors such as obesity and insulin resistance.