Insulin resistance and metabolic syndrome

Introduction to insulin resistance and metabolic syndrome Insulin resistance is one of the hot issues of concern. As early as the 1960s, impaired glucose tolerance (IGT) was observed. Diabetes, obesity, lipid metabolism disorders and high blood pressure often appeared in the same individual. It is a prosperous syndrome, but for a long time it is not known why the various components of the syndrome appear in the same individual or in the same family, so it is also called X syndrome. Until 1988, Reaven first proposed After insulin resistance syndrome, the above-mentioned multiple manifestations were linked to insulin resistance, and the common pathological basis of their onset was insulin resistance. Insulin resistance is defined as a decrease in the body's reactivity to the physiological effects of insulin or a decrease in sensitivity. Narrowly defined insulin resistance refers to a decrease in the reactivity of tissue cells to insulin-mediated glucose utilization. The main sites that produce insulin resistance are in the liver, muscle and adipose tissue. basic knowledge The proportion of sickness: 0.6% Susceptible people: no special people Mode of infection: non-infectious Complications: hyperinsulinemia, obesity, hypertension

Insulin resistance and the cause of metabolic syndrome

Hereditary factors (30%):

There are many causes of insulin resistance, including genetic factors or structural abnormalities of primary insulin resistance such as insulin, presence of insulin antibodies in the body, mutations in the insulin receptor or insulin receptor (eg Glut4 gene mutation, glucokinase gene) Mutations and mutations in insulin receptor substrate genes, etc., the vast majority (more than 90%) of primary insulin resistance is due to multiple gene mutations, and often multiple gene mutations synergistically lead to insulin resistance.

Environmental factors (30%):

In addition to the above genetic factors, many environmental factors also participate in or lead to insulin resistance, called secondary insulin resistance such as obesity (the most important cause of insulin resistance, especially central obesity, which is mainly related to long-term lack of exercise and diet Related to excessive energy intake, 80% of patients with type 2 diabetes are diagnosed with obesity), long-term hyperglycemia, and high free fatty acidemia.

Drugs (30%):

Certain drugs (such as glucocorticoids), certain trace element deficiency (such as chromium and vanadium deficiency), pregnancy and in vivo insulin antagonistic hormones.

Pathogenesis

Increased tumor necrosis factor alpha (TNF-), enhanced TNF- activity can promote lipolysis caused by elevated plasma FFA levels, inhibit tyrosine kinase activity of muscle tissue insulin receptor, inhibit IRS-1 phosphorylation and Glut4 Expression, which leads to insulin resistance and hyperinsulinemia. In recent years, it has been found that fat cells can secrete resistin. Resistin can reduce glucose uptake after insulin stimulation, neutralize glucose uptake after neutralizing resistin, and others are thin. The decrease in the level of resistance and adiponectin or the decrease in activity is also related to insulin resistance. The increase of triglyceride (TG) content in skeletal muscle cells is also considered to be one of the causes of insulin resistance, and excessive accumulation of TG in B cells may cause Its function is reduced.

Insulin resistance and prevention of metabolic syndrome

Strengthen exercise, control diet, and reduce weight: Obese people emphasize a reasonable diet plan, while carrying out long-term scientific and regular exercise, so that weight loss, maintaining weight within the ideal range is the basis for reducing insulin resistance and treating metabolic syndrome. Exercise itself can also enhance the body's sensitivity to insulin, especially skeletal muscle, which helps to correct a variety of metabolic disorders, and is beneficial for lowering blood sugar and blood pressure and improving lipid metabolism.

Insulin resistance and complications of metabolic syndrome Complications hyperinsulinemia obesity hypertension

Mainly have hyperglycemia, hyperinsulinemia, dyslipidemia (blood free fatty acids, cholesterol, triglyceride and low-density lipoprotein cholesterol, high-density lipoprotein cholesterol), overweight or obesity (body mass index over 25), high Blood pressure and so on.

Insulin resistance and metabolic syndrome symptoms Common symptoms Diabetes visceral obesity proteinuria hyperuricemia

The traditional components of metabolic syndrome mainly include central obesity, impaired diabetes or impaired glucose tolerance, hypertension, lipid abnormalities and cardiovascular diseases. However, with the in-depth study of this syndrome, its composition is expanding continuously. In addition to the above ingredients, it also includes polycystic ovary syndrome, hyperinsulinemia or hyperinsulinemia, hyperfibrinogenemia and plasminogen activator inhibitor-1 (PAI-1), hyperuricemia Symptoms, endothelial cell dysfunction - microalbuminuria and inflammation (blood CRP, IL-6 and metalloproteinase-9 increased).

Insulin resistance and metabolic syndrome examination

Laboratory inspection:

There is a physiological variation in insulin sensitivity. The timing and extent of insulin resistance occur in different tissues of the same individual. Glucocorticoid and prolactin, sex hormones, sex hormone binding globulin, androgen's physiological neuroendocrine rhythm and daily insulin sensitivity variation Relatedly, the effect of insulin decreased by 27% at night, and the sensitivity of insulin in the elderly decreased. In healthy people, there is no seasonal change in insulin sensitivity. The range of change is small within a certain period of time, and the changes between individuals and individuals themselves are small. Individuals with type 2 diabetes have higher insulin resistance than those without weight-type type 2 diabetes. The means and indicators for evaluating insulin resistance are related to glucose metabolism.

1. Estimating insulin resistance status by fasting blood glucose and plasma insulin

The following methods cannot be used for the assessment of individual insulin resistance status and can be used for population studies.

(1) FINS/FPG, INSlh/PGlh and the area under the insulin curve.

(2) Steady-state model method: Homa's insulin resistance index (Homa-IR) = FINS × FPG / 22.5.

(3) 1/(Fins×FPG), which has a good correlation with the classical clamp method and can reflect the sensitivity of individuals to insulin-mediated glucose metabolism. It is a practical and effective index in population research.

2. Experiment on the sensitivity of the body to insulin by applying an external load

(1) Clamp technology (including high blood glucose clamp technology, normal blood glucose high insulin clamp technology), normal blood glucose high insulin clamp technology is currently the gold standard for detecting insulin sensitivity, which can be used to judge the individual's insulin resistance status.

(2) The minimum model method: the blood is cumbersome, time-consuming, and application promotion is limited, and can be used to judge the individual's insulin resistance state.

3. Six parameters can be used clinically - hypertension, waist-to-hip ratio, triglyceride and HDL cholesterol levels, family history of type 2 diabetes, and glycemic control is a simple estimate of the presence of insulin resistance in diabetic patients.

Diagnostic Identification of Insulin Resistance and Metabolic Syndrome

diagnosis

1. WHO diagnosis of metabolic syndrome

(1) Basic conditions: Impaired glucose regulation or diabetes and/or insulin resistance (in the normal population, hyperinsulinemia in the normal blood glucose clamp test, the glucose uptake rate is below the quartile).

(2) Additional conditions: Have the following 2 or more components:

1 blood pressure increased 140/90 mmHg.

2 plasma TG 1.7mmol / L and / or HDL-C male <0.9mmol / L, female <1.0mmol / L.

3 central obesity [waist to hip ratio: male > 0.9, female > 0.85, and / or BMI > 30].

4 microalbuminuria ( 20g / min or urinary albumin / creatinine > 30mg / g).

2. NCEP-ATPIII diagnostic criteria for metabolic syndrome have the following three or more conditions for clinical diagnosis:

(1) Fasting blood glucose 5.6 mmol / L (100 mg / dl).

(2) Blood pressure 130/85 mmHg.

(3) Plasma TG 1.69 mmol / L (150 mg / dl).

(4) HDL-C male <1.04 mmol/L (40 mg/dl), female <1.29 mmol/L (50 mg/dl).

(5) Central obesity (or visceral obesity): waist circumference men > 102 cm, women > 88 cm.

3. American Endocrinology Society (ACE) and American Clinical Endocrinology Association (AACE) Diagnostic Criteria for Metabolic Syndrome

Diagnosis based on clinical assessment of risk factors: overweight or obesity BMI 25; TG1.70 mmol/L (150 mg/dl); HDL-C: male <1.04 mmol/L (40 mg/dl), female< 1.29 mmol/L (50 mg/dl); blood pressure 130/85 mmHg; blood glucose >7.8 mmol/L (140 mg/dl) at 2 h after glucose load, fasting blood glucose 6.1-7.0 mmol/L (110-126 mg/ Dl), other risk factors: type 2 diabetes, family history of hypertension or CVD, polycystic ovary syndrome, sitting lifestyle, old age, type 2 diabetes or high risk of cardiovascular disease.

4. China's criteria for diagnosing metabolic syndrome

(1) Overweight or obesity: body mass index 25.

(2) Hyperglycemia: fasting blood glucose 6.1 mmol / L (110 mg / dl) and / or glucose load 7.8 mmoL / L (140 mg / dl); and / or have been diagnosed with diabetes and treatment .

(3) Hypertension: systolic/diastolic blood pressure 140/90mmHg, and/or those who have been diagnosed with hypertension and treated.

(4) dyslipidemia: fasting TG 1.70mmol / L (50mg / dl); and / or fasting blood HDL-C: male <0.9mmol / L (35 mg / dl), female <1.0mmol / L (39mg /dl).

Any of the above 4 items can be diagnosed.

Differential diagnosis

Insulin resistance and metabolic syndrome should be differentiated from diabetes.

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