Insulin resistance and adipokines: the endocrine pathway of obesity-induced metabolic syndrome

Insulin resistance (IR) refers to a decreased sensitivity and responsiveness of the body to insulin, meaning that normal doses of insulin produce less of a normal biological effect. In the early stages of insulin resistance, the body compensates by increasing insulin secretion to maintain normal blood glucose levels. However, if this continues for a long period, with insulin levels remaining consistently high, pancreatic beta cell function will eventually be impaired, leading to type 2 diabetes.

Insulin resistance is central to metabolic syndrome and is associated with various metabolic diseases. Obesity is the most common cause of insulin resistance. In fact, obesity is a symptom, with its root cause in adipose tissue. Adipose tissue is the initiating site of insulin resistance, and its formation is mainly related to metabolic disorders of adipose tissue. Obese patients have elevated levels of free fatty acids, which is also an important reason for resistance. Obesity and insulin resistance are mutually causal: obesity leads to resistance, and resistance, in turn, exacerbates obesity.

Adiponectin is a special protein secreted by adipocytes and is present in high concentrations in blood plasma. It participates in glucose and lipid metabolism by binding to its receptors, and is highly beneficial for weight loss. Unlike other adipokines, adiponectin is significantly negatively correlated with the degree of obesity. Obese patients have lower levels of adiponectin, which increases after weight loss. Increasing adiponectin levels can increase insulin sensitivity, which is beneficial for preventing type 2 diabetes.

Adiponectin also has the effects of regulating blood lipids and preventing atherosclerosis. It can increase fatty acid oxidation and reduce triglyceride levels in the body. As an important substance connecting adipose tissue and overall metabolism, adiponectin plays a key role in the prevention of metabolic syndrome.

Leptin is a protein product encoded by the obesity gene and primarily acts on the hypothalamus. It controls fat storage by suppressing appetite, reducing food intake, and increasing energy expenditure. Normally, elevated leptin levels suppress appetite. However, in most obese patients, although serum leptin levels are higher than normal, it fails to exert its effects; this phenomenon is called "leptin resistance." Leptin resistance and insulin resistance often coexist, together forming the pathological basis of obesity.

Adipose tissue is no longer considered a simple energy storage device, but rather a metabolically active endocrine organ. It secretes dozens of protein factors, such as leptin, adiponectin, tumor necrosis factor, and resistin. These substances play important roles in the body's endocrine and metabolic processes, participating in the regulation of energy homeostasis.

Clinically, blood glucose measurement is a crucial indicator for diagnosing diabetes. In the early stages of diabetes, postprandial blood glucose is often elevated, while fasting blood glucose levels are not significantly elevated. Focusing solely on fasting blood glucose can lead to numerous hidden risks. Postprandial hyperglycemia is an independent risk factor for cardiovascular events. If both fasting and postprandial blood glucose are high, priority should be given to lowering fasting blood glucose through exercise and diet, as a decrease in fasting blood glucose will generally lead to a decrease in postprandial blood glucose.

Exercise, through a series of complex processes, can significantly improve insulin sensitivity and resistance. Studies show that exercising three times a week for half an hour each time is effective, but this effect only lasts for about five days. Therefore, it is essential to persist with long-term exercise.