Definition of insulin resistance
insulin resistance refers to the reduced sensitivity of surrounding tissues to insulin in the body. That is to say, when the body secretes a certain amount of insulin, its biological effect is lower than the normal level, and the tissues are not sensitive to insulin. Peripheral tissues such as muscle and fat are resistant to the role of insulin in promoting glucose uptake. In order to maintain the normal metabolic level, It is necessary to secrete more than normal amount of insulin.
At this time, the blood insulin level increases, so insulin resistance is often complicated with hyperinsulinemia. The phenomenon of insulin resistance has been found more than 50 years ago. In the past 20 to 30 years, it has been found that this phenomenon generally exists in type 1 diabetes, accounting for more than 90%, and may be one of the pathogenesis factors of type 1 diabetes.
One study on insulin resistance was conducted by the Department of Molecular and Clinical Medicine at the University of Gothenburg, Sweden. This research focused on understanding the molecular mechanisms underlying insulin resistance, a key pathological feature of type 2 diabetes and metabolic syndrome.
The study employed a comprehensive approach, utilizing both in vitro cell culture models and in vivo animal studies, to investigate how various factors such as obesity, inflammation, and genetic predispositions contribute to the development of insulin resistance. Researchers examined the signaling pathways involved in insulin action, particularly those leading to glucose uptake in skeletal muscle and adipose tissue. They also explored the role of adipokines, cytokines, and other inflammatory mediators in disrupting insulin signaling.
The study employed a comprehensive approach, utilizing both in vitro cell culture models and in vivo animal studies, to investigate how various factors such as obesity, inflammation, and genetic predispositions contribute to the development of insulin resistance. Researchers examined the signaling pathways involved in insulin action, particularly those leading to glucose uptake in skeletal muscle and adipose tissue. They also explored the role of adipokines, cytokines, and other inflammatory mediators in disrupting insulin signaling.
This study contributes to the growing body of knowledge on the pathophysiology of insulin resistance, guiding the development of more targeted therapeutic strategies for type 2 diabetes and related metabolic disorders.
etiology of insulin resistance
There are many causes of insulin resistance. Medically speaking, they include the following aspects:
- Abnormal structure of insulin receptor: insulin and its receptor can produce biological effects only after binding. The relationship between insulin and its receptor is like a key and a lock. When a key opens a lock, the receptor will appreciate differently. If insulin cannot bind with it, it cannot open the door of blood glucose entering the tissue, thus inhibiting the utilization of glucose. In recent years, medical research has found that the receptor defect is related to insulin receptor gene mutation types 1, 2, 4 and 5. It causes receptor protein synthesis, displacement of the receptor from the cytoplasm back to the cell membrane and changes in receptor components β Impairment of subunit phosphorylation, and acceleration of receptor degradation.
- Decrease in the number of insulin receptors: when insulin receptors decrease, insulin cannot fully play its physiological role.
- Post insulin receptor defect: after insulin binds to the receptor, any link of intracellular signal transmission is blocked, which can lead to reduced insulin responsiveness, such as abnormal glucose transport, abnormal glucokinase level, etc. these changes are related to abnormal changes in some genes.
- Insulin receptor antibody: studies suggest that the body can spontaneously produce insulin receptor antibody, which may be the most important factor in the decline of tissue sensitivity to insulin. It does not directly block the binding of insulin and its receptor, but can inhibit the biological effect of insulin, accelerate the degradation of insulin receptor, and reduce the number of insulin receptors.
- Too many substances antagonize insulin: it can also induce insulin resistance, which will be described in detail later.
- Abnormal insulin structure can lead to obstacles in binding with the receptor. Like the above metaphor, because the “key” has changed, it cannot open the door for ordinary sugar to enter the cell, thus affecting the utilization of sugar. Strictly speaking, this kind of situation does not belong to insulin resistance.
