肥胖与代谢综合征─中国之现状

目的复习肥胖的定义、危害、诊断及治疗原则,回顾近年来有关代谢综合征的新进展,并根据作者1996年全国糖尿病流行病学资料,对我国南、北方体重、腰臀比、血压及IGT和糖尿病发生率进行比较。方法利用自然人群,采取分层随机抽样方法,直接测OGTT服糖后2小时血糖。结果北方受试者的平均BMI、腰臀比、收缩压/舒张压略高于南方,糖尿病患病率有较高的趋势,但缺乏统计学意义,然而南方受试者腰围随年龄增加的趋势较为明显,IGT的发生率高于北方受试者。结论我国肥胖、糖耐量损害及糖尿病患者较1980年及1990年显著增多。阳性家族史、年龄、受教育程度、体力活动量、体质指数、腰臀比及吸烟指数是糖尿病及糖耐量损害的危险因子。其中年龄40岁、具有糖尿病家族史、体质指数25以上及腰臀比0.9以上人群糖尿病及糖耐量损害患病率剧增。     

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.     

Abdominal obesity and the metabolic syndrome.

Abdominal obesity in man is an integrated part of the Metabolic Syndrome, and is associated with a complex neuroendocrine disturbance. Its consequences for the metabolism of the periphery seems to be insulin resistance caused by a combination of a relative hypercortisolaemia and a relative deficiency of sex steroid hormones. This hormonal aberration, in combination with a relative insufficiency of growth hormone secretion, might also direct depot triglycerides to visceral adipose tissues, a consequence at least partly due to varying densities of the specific receptors for these hormones. Visceral fat accumulation may thus be a consequence of the neuroendocrine aberrations, and may amplify the metabolic symptoms via effects on the liver of free fatty acids released in abundance from the lipolytically sensitive enlarged visceral fat depots. The origin of the neuroendocrine disturbance is not known, but epidemiological and cross-sectional information suggest that psychosocial factors are intimately involved. Animal and human studies indicate that the mediating factor(s) may be stress-sensitivity, leading to the neuroendocrine consequences observed.     

Obesity and the metabolic response to severe multiple trauma in man.

In the obese state profound metabolic disturbances exist and it is not known how this disrupted metabolism in obese subjects (body mass index greater than 30) may change their ability to respond to the superimposed, injury-induced stress. Understanding the mechanisms that modify the metabolic parameters in traumatized obese patients is essential in their nutritional assessment and further treatment. We have investigated in 7 obese and 10 nonobese multiple trauma patients, on a whole-body level, the energy metabolism, protein kinetics, and lipolysis in the early catabolic "flow phase" of severe injury when they were receiving maintenance fluids without calories or nitrogen. Traumatized obese patients mobilized relatively more protein and less fat compared with nonobese subjects. A relative block both in lipolysis and fat oxidation is experienced by injured obese patients that results in a shift to preferential use of proteins and carbohydrates. Reduced endogenous protein synthetic efficiency observed in obese patients implies increased protein recycling. Thus obese patients could not effectively use their most abundant fat fuel sources and have to depend on other fuel sources. The nutritional management of obese trauma victims should therefore be tailored towards provision of enough glucose calories to spare protein.     

Obesity and the polycystic ovary syndrome

Polycystic ovarian syndrome (PCOS) is extremely common among reproductive-aged women, but often goes undiagnosed. PCOS is associated with the metabolic syndrome and carries a greatly increased risk of impaired glucose tolerance and type 2 diabetes mellitus, and cardiovascular risks. Treatment of PCOS may provide relief of cosmetic problems and depression by improving patient self-esteem. In addition, because of its association with the metabolic syndrome, type 2 diabetes mellitus, and cardiovascular disease, its recognition and treatment can potentially be life saving. This article reviews the impact, pathophysiology, and associated risks of obesity and the metabolic syndrome in PCOS.     

Obesity and metabolic syndrome: association with chronodisruption, sleep deprivation, and melatonin suppression

Obesity has become an epidemic in industrialized and developing countries. In 30 years, unless serious changes are made, a majority of adults and many children will be classified as overweight or obese. Whereas fatness alone endangers physiological performance of even simple tasks, the associated co-morbidity of obesity including metabolic syndrome in all its manifestations is a far more critical problem. If the current trend continues as predicted, health care systems may be incapable of handling the myriad of obesity-related diseases. The financial costs, including those due to medical procedures, absenteeism from work, and reduced economic productivity, will jeopardize the financial well-being of industries. The current review summarizes the potential contributions of three processes that may be contributing to humans becoming progressively more overweight: circadian or chronodisruption, sleep deficiency, and melatonin suppression. Based on the information provided in this survey, life-style factors (independent of the availability of abundant calorie-rich foods) may aggravate weight gain. Both epidemiological and experimental data support associations between disrupted physiological rhythms, a reduction in adequate sleep, and light-at-night-induced suppression of an essential endogenously produced molecule, melatonin. The implication is that if these problems were corrected with life-style changes, body-weight could possibly be more easily controlled.     

肥胖低通气综合征

随着人们生活水平的提高,肥胖患者越来越多,因肥胖引起的一系列相关疾病如高脂血症、糖尿病、呼吸系统疾病等也越来越被重视。但其中最常被忽略又非常具有临床诊治意义的一种疾病是肥胖低通气综合征（obesity hypoventilation syndrome, OHS）,可严重影响患者的呼吸、心脑血管及内分泌代谢系统,若不及时纠正,可进一步引发呼吸衰竭、心律失常、心功能衰竭等,预后恶劣。本文将就OHS的相关概念、发病机制、临床表现及最新诊治进展等方面的内容做逐一阐述,希望能引起相关临床医师的重视。     

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。     

Obesity in adults is associated with reduced lung function in metabolic syndrome and diabetes: the Strong Heart Study

OBJECTIVE

The purposes of this study were to investigate whether reduced lung function is associated with metabolic syndrome (MS) and diabetes (DM) in American Indians (AIs) and to determine whether lower pulmonary function presents before the development of DM or MS.

RESEARCH DESIGN AND METHODS

The Strong Heart Study (SHS) is a multicenter, prospective study of cardiovascular disease (CVD) and its risk factors among AI adults. The present analysis used lung function assessment by standard spirometry at the SHS second examination (1993–1995) in 2,396 adults free of overt lung disease or CVD, with or without DM or MS. Among MS-free/DM-free participants, the development of MS/DM at the SHS third examination (1996–1999) was investigated.

RESULTS

Significantly lower pulmonary function was observed for AIs with MS or DM. Impaired pulmonary function was associated with MS and DM after adjustment for age, sex, abdominal obesity, current smoking status, physical activity index, hypertension, and SHS field center. Both forced vital capacity (FVC) and forced expiratory volume in 1 s (FEV1) were negatively associated with insulin resistance or DM severity and with serum markers of inflammation (P < 0.05). FVC and FEV1-to-FVC ratio both predicted DM in unadjusted analyses but not when adjusted for covariates, including waist circumference. In the adjusted model, abdominal obesity predicted both MS and DM.

CONCLUSIONS

Reduced lung function is independently associated with MS and with DM, and impaired lung function presents before the development of MS or DM; these associations may result from the effects of obesity and inflammation.Pulmonary dysfunction has been reported in type 2 diabetes (T2DM) (1–4), and prospective studies suggest that reduced lung function may be associated with the development of diabetes (DM) and inflammation may contribute to incident DM (5,6); however, the underlying mechanism remains unclear. Studies also indicate a possible association among obesity, metabolic syndrome (MS), and pulmonary impairment in a restrictive pattern (7–9), but no study of lung function has included both DM and MS.American Indians (AIs) have the highest prevalence of DM of any segment of the U.S. population (10). The aims of this study were to test the hypotheses that reduced lung function is independently associated with MS and DM and to test whether impaired lung function presents before the development of MS or DM in AIs.     

Treating the metabolic syndrome

The metabolic syndrome (MS), a cluster of metabolic abnormalities with insulin resistance as its central component, is increasing in prevalence and is associated with an increased risk of cardiovascular disease and Type 2 diabetes mellitus (T2DM). Current evidence supports an aggressive intervention approach that comprises lifestyle modification in conjunction with drug treatment of the MS components. Healthier eating and regular exercise greatly reduce waistline and body mass index, lower blood pressure and improve lipid profile. Lifestyle modification has been proven to prevent T2DM development. Nevertheless, appropriate treatment of MS components often requires pharmacologic intervention with insulin-sensitizing agents, such as metformin and thiazolidinediones, while statins and fibrates, or angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers are the first-line lipid-modifying or antihypertensive drugs. Only severely obese patients require specific drug treatments. Very often, drug combinations will be necessary to manage multiple risk factors. As we progress in the understanding of the pathophysiology of the MS, new targets for therapies will probably be identified and new treatments will prove to be even more efficacious than those currently available for the management of this life-threatening condition.     

Childhood weight and metabolic syndrome in adults.

Metabolic syndrome is a clustering of many insulin resistance-associated cardiovascular risk factors such as hypertension, hypertriglyceridaemia, low high-density lipoprotein (HDL) cholesterol, abnormal glucose metabolism and hyperinsulinaemia. Furthermore, it is known that obesity is the most common clinical state characterized by insulin resistance. Central adiposity, in particular, has been shown to be the most distinctive feature of this syndrome. Some studies have also suggested that obesity per se would be necessary for the expression of metabolic defects associated with centrally distributed fat. It has been presented that undernutrition in utero might 'programme' blood pressure, insulin resistance, blood coagulation and cholesterol metabolism and would thus have a role in the aetiology of cardiovascular disease and type 2 diabetes in adult life. Some studies have also found associations between low birthweight and metabolic syndrome in adulthood. However, criticism on this hypothesis of fetal programming has recently been presented. It has been suggested that the origins of adulthood risk of cardiovascular disease and type 2 diabetes can be related to somatic growth as a child, not necessarily to intrauterine growth. In westernized countries, the relative proportion of underweight newborn children is decreasing, and thus considering entire populations low birthweight has lost its theoretical role in the aetiology of type 2 diabetes and cardiovascular disease. On the other hand, as obesity is known to be increasing in the industrialized countries among all age groups, the association between weight gain in childhood and metabolic syndrome in adulthood is more than noteworthy. Instead of undernutrition during pregnancy, sedentary lifestyle and lack of physical exercise pose a new threat. This results in an increased occurrence of overweight in childhood, which may be the first sign of insulin resistance and future metabolic syndrome.     

Treating the metabolic syndrome

The metabolic syndrome (MS), a cluster of metabolic abnormalities with insulin resistance as its central component, is increasing in prevalence and is associated with an increased risk of cardiovascular disease and Type 2 diabetes mellitus (T2DM). Current evidence supports an aggressive intervention approach that comprises lifestyle modification in conjunction with drug treatment of the MS components. Healthier eating and regular exercise greatly reduce waistline and body mass index, lower blood pressure and improve lipid profile. Lifestyle modification has been proven to prevent T2DM development. Nevertheless, appropriate treatment of MS components often requires pharmacologic intervention with insulin-sensitizing agents, such as metformin and thiazolidinediones, while statins and fibrates, or angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers are the first-line lipid-modifying or antihypertensive drugs. Only severely obese patients require specific drug treatments. Very often, drug combinations will be necessary to manage multiple risk factors. As we progress in the understanding of the pathophysiology of the MS, new targets for therapies will probably be identified and new treatments will prove to be even more efficacious than those currently available for the management of this life-threatening condition.     

PPAR agonists and the metabolic syndrome

Cardiovascular disease is significantly increased in patients with the metabolic syndrome and type 2 diabetes. A clustering of risk factors, including dyslipidemia, insulin resistance, hypertension, inflammation and coagulation disorders are likely to promote cardiovascular events in these patients. Peroxisome proliferator-activated receptors (PPARs) represent one important pathway that influence vascular function both directly and indirectly by altering gene expression. Indeed, PPAR activation induces beneficial effects not only on glucose homeostasis and lipid metabolism but also on endothelial function and vessel wall inflammation. PPAR agonists such as fibrates (PPARalpha) and insulin-sensitizing thiazolidinediones (PPARgamma) are in clinical use and may alter the process of atherosclerosis, especially in subjects with the metabolic syndrome and type 2 diabetes. This review will highlight the emerging evidence for the beneficial effects of PPAR agonists in the prevention and treatment of atherosclerosis in such high-risk patients.