Insulin resistance (IR) is a pathophysiological abnormality characterized by abdominal obesity and ectopic fat deposition caused by the interaction of genetic and environmental factors. Recent studies have shown that adipose tissue can influence the energy metabolic balance of the body by secreting various cytokines or tissue factors, such as tumor necrosis factor-α (TNF-α), leptin, adiponectin, and resistin. Inflammatory mediators and adipose tissue factors may be associated with the development of IR or metabolic syndrome [1, 2]. Elevated levels of C-reactive protein (CRP), an acute phase inflammatory response marker, are closely related to IR and metabolic syndrome [3], and retrospective studies have shown that elevated CRP predicts the development of diabetes and cardiovascular disease, while lipocalin may improve insulin sensitivity by binding to receptors [4], and thiazolidinediones (TZDs) may enhance insulin sensitivity by upregulating lipocalin levels. Leptin, a type of adipokine, can regulate insulin secretion from pancreatic β-cells in addition to its effects on appetite suppression and reduction of energy intake, but its level is also elevated in IR patients due to leptin resistance. Human omentin (omentin) [5] is a protein expressed and secreted by visceral adipose tissue, which has the effect of increasing insulin sensitivity of adipocytes. The main free form in serum is omentin-1 [6], and its levels are negatively correlated with BMI, abdominal circumference, and leptin, and positively correlated with lipocalin and HDL-C levels. Glucose and lipid metabolism rely heavily on mitochondrial energy supply in cells, and it is possible that mitochondrial insufficiency also plays a role in IR development [7]. Although the cytokines and tissue factors mentioned above are closely related to IR, they have not been included as clinical indicators and are actually used in the assessment of IR. The following methods are still more accurate for assessing IR: 1) normoglycemic, hyperinsulinemic-euglycemic clamp technique: it refers to the measurement of tissue response to insulin (Ins) Glucose equilibrium situation to determine the sensitivity of the tissue to exogenous Ins. The method is: intravenous injection of short-acting Ins, so that the peripheral insulin level is rapidly increased and maintained, and arterial blood glucose is detected at regular intervals, and the glucose infusion rate (GIR) is adjusted by Harvard pump to keep the blood glucose normal (about 5 mmol/L), and after it is stabilized, the GIR at this time is equal to the glucose utilization rate (M) of peripheral tissues, and the smaller the GIR, the more serious the IR of the organism. This method is accurate and reproducible, and is considered the “gold standard” of IR, but it is expensive and time-consuming, and only applicable to small sample studies. 2) Hyperglycemic clamp method: It refers to the rapid intravenous injection of glucose to raise blood glucose and maintain it at about 10 mmol/L, without infusion of exogenous Ins, and blood is collected at intervals to measure Ins, at which time GIR is equal to peripheral tissue glucose utilization rate (M). M/I is used to indicate Ins sensitivity, the smaller the M/I, the more serious the IR of the organism. This method can simultaneously detect β-cell function and IR, but endogenous Ins unsuppressed will affect the results. 3) Short-time insulin tolerance test (ITT): Exogenous Ins is injected and the rate of decline of arterial blood glucose is used to determine Ins sensitivity. To avoid hypoglycemia in the body, the original dose of 0.1u/kg is reduced to 0.05u/kg, and the observation time is shortened from 30min to 15min. The test heats the arm to make venous blood arterialized. This method is simple and safe, but the specific site of IR cannot be judged and the slope of blood glucose decrease (KITT) is calculated. There are also micro model technique (MMT) etc. However, the above experimental methods are only applicable to small sample scientific research, and the following methods can be used for large sample epidemiological research: 1) Homeostasis model assessment (HOMA-IR): it is more widely used. Fasting insulin (FINS) and fasting glucose (FPG) are calculated as follows: HOMA-IR = FINS (mmol) x FPG (μU/mL) ÷ 22.5, and its normal value is 1. This value is non-normally distributed, and its natural logarithm is taken. cannot use the above linear formula to calculate IR, and the combination of many nonlinear formulas is called HOMA2-IR, and the results are calculated using relevant software [9]. 2)Insulin sensitivity index (ISI): the reciprocal of HOMA1-IR is the ISI, and the normal value is 100%. 3)FPG(mg/dL)/FINS(mU/L):