Inflammation or inflammatory reaction is a stereotypical, complex, developmentally acquired ability of living organisms to respond to various damages, the symptoms of which are: erythema (redness), lump (swelling), inflammation (heat), tenderness (pain) and functio laesa (impaired function) . In the case of chronic metabolic diseases, such as type 2 diabetes or obesity, similar mechanisms and signaling molecules are used at the cellular level as in classic inflammation, but the above symptoms do not occur. The designation “low-grade inflammation” or chronic inflammation has therefore been proposed for these chronic conditions.
The role of adipose tissue in inflammation
Adipose tissue has been shown to play a significant role in low-level inflammation. The relationship between excessive accumulation of adipose tissue and the development of insulin resistance or type 2 diabetes has been known for a long time, but knowledge about the mutual dependencies was provided by the study of clinical cases of lipodystrophy, i.e. a condition in which lipodystrophy (congenital or acquired) occurs, significant dysfunction of adipose tissue or is completely absent ( lipoatrophy).
An apparent paradox – inflammation and insulin resistance
People affected in this way suffer from severe insulin resistance with all the typical symptoms, including type 2 diabetes. These are therefore identical disorders that are commonly found in the condition associated with chronic nutrient excess – obesity.
This apparent paradox can be explained by the ability of adipose tissue to appropriately process the flow of nutrients, i.e. to store lipids in the event of their increased (but not permanent) supply and release them in the process of lipolysis (decomposition of fats accumulated in fat cells).
In the case of complete absence of adipose tissue (lipoatrophy) or limitation of its function and quantity (lipodystrophy), it is obvious that the body has lost this “absorption” capacity of adipose tissue, and lipids are deposited in other tissues, where they significantly interact with intermediate metabolism and participate in the development of insulin resistance.
What is the relationship between obesity and insulin resistance and diabetes?
In obese people, the situation is different: chronic excess energy leads to a gradual increase in the volume of fat cells (adipocytes), and only after reaching a certain critical level of fat cell size does activation and proliferation of preadipocytes occur, and new fat cells are created.
It has been proven that the larger the fat cell, the greater the insulin resistance and the risk of developing diabetes.
Cytokine production in mild inflammation
Chronic, mild inflammation is characterized by increased production of a number of cytokines (protein-like substances used to interact with cells and transmit information) from adipose tissue, especially TNF-α, IL-6, IL-1, IL -8, while the production of cytokines the anti-inflammatory adiponectin and leptin is reduced.
Macrophages that are physiologically present in adipose tissue and are recruited to a greater extent into adipose tissue during the development of obesity are responsible for the production of these cytokines.
Macrophages in adipose tissue cluster mainly around large, hypertrophic, dying or dead fat cells.
Changes in cellular metabolism
A phenomenon called “endoplasmic reticulum stress” plays an important role in the process of cell death of hypertrophied fat cells. This intracellular organelle performs an essential function in protein synthesis.
Excess nutrients are one of the factors causing an increased demand for the endoplasmic reticulum in fat cells. Part of the response to this stress is extensive changes in cell metabolism that can lead to cell death.
The emergence of insulin resistance, what are its causes?
At today’s level of knowledge, the emergence of insulin resistance due to the pro-inflammatory state of the body can be summarized by the following sequence of events: excess nutrients and insufficient physical activity lead to hypertrophy of fat cells and disturbances in the insulin sensitivity of target tissues, especially muscles.
Hypertrophic fat cells, and therefore altered adipose tissue, further cause a mild pro-inflammatory state through the production of inflammatory cytokines and higher levels of free fatty acids released during lipolysis in fat cells.
As the disease progresses, macrophages in adipose tissue increase and macrophages are summoned to the adipose tissue to eliminate dying fat cells.
These macrophages produce low-intensity pro-inflammatory substances and lead to insulin resistance. This creates both basic conditions for the development of type 2 diabetes.
Atherosclerosis, what are its causes and its relationship with inflammation?
Because chronic mild inflammation is one aspect of abdominal obesity, it is likely that sustained exposure to inflammatory cytokines from macrophages leads to the development of atherosclerosis.
Obese patients had higher levels of circulating amyloid (a part of the protein that builds up in the intercellular space during disease states).
Therefore, some authors place obesity, diabetes and Alzheimer’s disease at least indirectly. Diseases associated with this type of inflammation include atherosclerosis, diabetes, thrombosis, myocardial infarction, stroke, metabolic disorders, and dementia.
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