Metabolic syndrome: This concept was first proposed by Reaven in 1988 and later called insulin resistance syndrome or syndrome X. It is a group of syndromes with multiple syndromes associated with the risk of cardiovascular disease, often closely related to insulin resistance, and is a major problem in the prevention and treatment of cardiovascular disease and related diseases, as well as a current hot spot in clinical and basic research. The dyslipidemia in patients with metabolic syndrome is mainly characterized by elevated triglyceride-rich lipoproteins including very low density lipoprotein cholesterol and celiac particles and their remnants], reduced high density lipoprotein cholesterol and increased small and dense low density lipoproteins. I. Diagnosis of metabolic syndrome 1. Characteristics of metabolic syndrome: The main characteristics of metabolic syndrome are diabetes mellitus or hypoglycemia with dyslipidemia, hypertension and central obesity. In recent years, the research on metabolic syndrome has been intensified, and fibrinolytic coagulation abnormalities [plasma fibrinogen activator inhibitor C 1 and fibrinogen increase], hyperuricemia and microproteinuria are also included in the category of metabolic syndrome. 2. Diagnostic criteria of metabolic syndrome: There are no internationally accepted criteria for the diagnosis of metabolic syndrome. 1999, the World Health Organization had proposed a working definition of metabolic syndrome: diabetes mellitus or hypoglycemic tolerance and/or insulin resistance (glucose utilization below the lower 1/4th percentile as measured by the high insulin glucose clamp technique) with two or more of the following manifestations: hypertension (≥ 140/90 mmHg), high triglyceride (TG) [≥1.7 mmol/L (150 mg/dl)] and/or low HDL-C [<0.9 mmol/L (35 mg/dl) in men; <1.0 mmol/L (39 mg/dl) in women]; central obesity [waist/hip ratio, >0.90 in men women > 0.85 and/or body mass index (BMI) > 30], microalbuminuria (urinary albumin excretion rate ≥ 20 μg/min or albumin/creatinine ratio ≥ 30 mg/g). It is difficult to identify metabolic syndrome clinically using the above criteria. Therefore, the third guideline of the Adult Treatment Group of the U.S. Cholesterol Education Program in 2001 provides the definition and diagnostic criteria of metabolic syndrome: metabolic syndrome is defined as those who meet three or more of the following conditions: central obesity (waist circumference: men >2550px, women >2200px); high TG [≥1.69 mmol/L (150mg/dl)]; low HDL- C [<1.04 mmol/L (40 mg/dl) in men; <1.29 mmol/L (50 mg/dl) in women]; fasting glucose ≥6.1 mmol/L (110 mg/dl); blood pressure ≥130/85 mmHg (1 mmHg=0.133 kPa). the ATP III document is easy to operate, but for the diagnostic criteria of obesity, it is obviously not suitable for our population. For this reason, the Chinese diabetes branch suggested that the current temporary according to the 2002 "Chinese obesity working group" proposed standards, that is, BMI ≥ 28.0 or male waist circumference ≥ 2125px, female waist circumference ≥ 2000px as the central obesity diagnostic limit. 3, the epidemiology of metabolic syndrome: metabolic syndrome in different populations have a high incidence, mostly in adults over 50 years old, is the most common metabolic abnormalities in the middle-aged and elderly. However, studies on the epidemiological status of metabolic syndrome are limited. Meigs et al. reported that the prevalence of metabolic syndrome varied in different populations in the Framingham Offspring Study and the San? Meigs et al. reported that in the Framingham Offspring Study and the San Antonio Heart Study, approximately 24% of U.S. adults over the age of 20 had metabolic syndrome according to WHO/ATP III criteria, using obesity, dyslipidemia, hyperglycemia, and hypertension as diagnostic criteria for metabolic syndrome, and that the prevalence was higher among older adults and Mexican Americans, with a prevalence of 33% among Mexican Americans. Individuals with metabolic syndrome are two times more likely to develop cardiovascular disease and four times more likely to develop type 2 diabetes than non-metabolic syndrome individuals. In addition, according to the National Nutrition Survey (1988-1994), the prevalence of age-specific metabolic syndrome was 22.8% in men and 22.6% in women using the ATP III diagnostic criteria. 888 residents of Bruneck, Italy, aged 40-79 years were surveyed in the Bruneck study, and the prevalence of metabolic syndrome was 34.1% according to the WHO diagnostic criteria for metabolic syndrome. The prevalence of metabolic syndrome was 34.1% and 17.8% according to the ATP III criteria, and the prevalence was higher in the elderly and those who lacked exercise. There are not many large-scale epidemiological studies on the prevalence of metabolic syndrome in China. Chen Lei et al. recently reported an epidemiological survey of metabolic syndrome in Huayang and Cao Yang communities in Shanghai. According to the WHO diagnostic criteria for metabolic syndrome, the prevalence of metabolic syndrome in people aged 20-74 years was 17.14%, and the prevalence in men and women aged 45 years or older and 50 years or older was significantly higher, at 20.55% and 26.87%, respectively. The prevalence peaked at the age of 65-69, with 34.88% and 41.18% for men and women, respectively. Li Jianzhai et al. referred to the ATP III standard and obtained the age standardized Beijing population prevalence rate of 15.1% for males (9209 cases) and 13.0% for females (6990 cases) by using the Chinese waist circumference standard. The mechanism of dyslipidemia in metabolic syndrome is currently considered to be a disease caused by the combined effects of multiple genes and environmental factors, and insulin resistance is the common pathogenesis of a series of metabolic abnormalities in metabolic syndrome and is the central link of its dyslipidemia. Genetic abnormalities, obesity and lack of exercise, the role of antagonistic hormones, drugs and many other factors can lead to insulin resistance, and obesity, especially central obesity, is the initiating cause of insulin resistance, and its possible mechanisms are: 1. Obese people in vivo adipocyte hyperplasia and hypertrophy, the number of tissue cell insulin receptors is reduced or activity is reduced, while the Ca2+-ATPase activity on the tissue cell membrane is reduced, resulting in Intracellular calcium inhibits the role of insulin. 2, obese people have enhanced tumor necrosis factor-α converting enzyme activity in adipose tissue and elevated TNF-α level in vivo, which can inhibit the tyrosine kinase activity of insulin receptors in muscle tissue through endocrine and paracrine pathways, inhibit the phosphorylation of insulin receptor substrate-1 and the expression of glucose transporter 4, so that the insulin signal transduction process is blocked. 3, obese people peroxisome proliferator-activated receptor gene mutation. The main reason for dyslipidemia in patients with metabolic syndrome is that insulin resistance causes a large number of adipocytes that accumulate in the viscera of obese people to release excessive free fatty acids. Plasma FFA levels are mainly regulated by hormone-sensitive lipase and lipoprotein lipase in adipose tissue. hSL catalyzes the rate-limiting step of TG hydrolysis in adipose tissue to produce FFA, which regulates the release of FFA from adipose tissue, and LPL promotes the storage of FFA in adipose tissue in the form of TG. In insulin resistance, the inhibitory effect of insulin on HSL and the promotion of LPL synthesis are weakened, and fat mobilization in adipose tissue is enhanced, producing large amounts of FFA into the blood and being taken up by the liver as raw material for VLDL synthesis, resulting in increased synthesis and release of VLDL and TG from VLDL. Meanwhile, the activity of cholesteryl ester transfer protein and hepatic lipase (HL) is increased, and the former enhances the exchange of TG and cholesteryl ester between TRL and LDL and HDL, forming a large amount of TG-rich LDL and HDL, which are hydrolyzed by HL to form sLDL and small but dense HDL. In addition, insulin resistance may lead to the synthesis of hepatocyte apolipoprotein (CIII) The affinity of CM for LPL is higher than that of VLDL, and LPL preferentially degrades TG in CM particles, resulting in a more pronounced increase in VLDL than CM. Because of the slow clearance of VLDL and CM, the release of their surface components (such as apoA I, free cholesterol, phospholipids, etc.) decreases, leaving insufficient raw material for HDL synthesis and decreasing HDL levels. The decrease in HDL-C in patients with metabolic syndrome may also be related to the activity of adenosine triphosphate-binding frame transporter-1, whose main function is to participate in the assembly of HDL particles and reverse cholesterol transport. The reduced function of ABCA1 in patients with metabolic syndrome prevents apoA I from binding to intracellular lipids and is quickly cleared from plasma, resulting in lower HDL-C in blood. Dyslipidemia in metabolic syndrome significantly increases the risk of atherosclerotic cardiovascular disease in patients with metabolic syndrome, and its relationship with atherosclerosis is mainly manifested as follows: 1. In addition, the hypercoagulable state associated with elevated TRL also plays an important role in the development of AS. 2. sLDL has low affinity for LDL receptors, and its half-life in blood is prolonged, so it can enter the arterial wall and enter the subendothelium through the vascular endothelium more easily. sLDL has weak antioxidant capacity, so it is easily taken up by macrophages in the subendothelial space to form foam cells. 3. HDL is involved in cholesterol reversal and reduces cholesterol deposition in the vascular wall. HDL can also inhibit LDL oxidation and inhibit endothelial cells from expressing adhesion molecules, thus inhibiting macrophages and other cells from recruiting and adhering to the endothelium and entering the subendothelial space, which has an anti-AS effect. Therefore, dyslipidemia caused directly and indirectly by insulin resistance significantly increases the risk of atherosclerotic cardiovascular disease. Intervention for dyslipidemia in metabolic syndrome Patients with metabolic syndrome have a significantly increased risk of atherosclerotic cardiovascular disease, and studies have shown that intervention for dyslipidemia in metabolic syndrome can prevent and delay the onset and progression of atherosclerotic cardiovascular disease and reduce its morbidity and mortality. The latest targets for dyslipidemia in individuals with cardiovascular disease risk are TG < 1.69 mmol/L (150 mg/dl); HDL-C > 1.04 mmol/L (40 mg/dl); LDL-C < 2.6 mmol/L (100 mg/dl). Interventions for dyslipidemia in metabolic syndrome are comprehensive and include therapeutic lifestyle changes, medication to improve insulin sensitivity and lipid-lowering medication. 1. Therapeutic lifestyle changes: The latest recommendations for the treatment of hyperlipidemia put forward by ATP III in 2001 particularly emphasize the importance of therapeutic lifestyle changes. Therapeutic lifestyle changes mainly include diet control, exercise therapy, weight loss, etc. A good diet structure and regular exercise can improve central obesity, insulin sensitivity and dyslipidemia, reduce plasma TG and LDL, and increase HDL concentration. In addition, quitting smoking and avoiding excessive alcohol consumption can also help improve dyslipidemia. 2, drug treatment: the main drugs to improve the metabolic syndrome dyslipidemia include insulin sensitizers and lipid-lowering drugs. Thiazolidinediones (TZDs) are insulin sensitizers that can activate PPAR-γ, increase the expression of related genes in adipocytes, promote the uptake of glucose by adipose tissue and improve insulin sensitivity. TZDs can also inhibit TNF-α production, increase the body's sensitivity to insulin and improve the secretion function of pancreatic β-cells. TZDs reduce TG and FFA, increase HDL levels, and do not reduce total cholesterol, but can reduce sLDL. statins are competitive inhibitors of the enzyme 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase. Statins competitively inhibit HMG-CoA reductase, the rate-limiting step of cholesterol synthesis catalyzed by HMG-CoA reductase, resulting in reduced cholesterol synthesis. apoE and apoB are abundant in VLDL residues, and apoB is abundant in LDL, both of which bind to LDL receptors in the hepatocyte membrane and are cleared by the liver. Statins are able to upregulate LDL receptor activity and promote the clearance of VLDL residues and LDL from the blood circulation. Betablocker is a synthetic PPAR-α ligand, which decreases apoCIII concentration, increases LPL expression, promotes FFA uptake and β-oxidation by hepatocytes, and decreases TG concentration by activating PPAR-α. PPAR-α activation also promotes the expression of apoA I and apoA II, the major apolipoproteins of HDL, and increases HDL concentration. The incidence of metabolic syndrome is on the rise in both the West and China, and its dyslipidemia is mainly characterized by an atherogenic lipoprotein profile, i.e., elevated TRL, decreased HDL, and increased sLDL. Understanding the mechanisms of dyslipidemia in metabolic syndrome can help to actively intervene to reduce the occurrence and development of atherosclerotic cardiovascular disease in patients with metabolic syndrome. The selection of reasonable interventions is of great significance to achieve these goals. Firstly, therapeutic lifestyle changes should be emphasized, and patients with more severe dyslipidemia should be treated with a combination of multiple lipid-lowering drugs in addition to lifestyle changes, and the specific drug selection should be implemented specifically according to the characteristics of dyslipidemia. The mechanism of dyslipidemia in metabolic syndrome needs to be studied more extensively and deeply in the future to provide new directions for effective improvement of dyslipidemia and prevention and treatment of atherosclerotic cardiovascular diseases.