Diet gun

Obesity is a state of chronic low-grade inflammation, termed “meta-inflammation” (metabolically driven inflammation), which results from complex interactions between the immune system, adipose tissue, and metabolic organs.

This persistent inflammation creates a persistent immune activation that contributes to insulin resistance, dyslipidemia, and an increased risk of cardiovascular, renal, hepatic, and metabolic diseases.

Adipose Tissue

Excess adipose tissue, unfortunately, plays a central role in the immune dysfunction caused by obesity.

When fat cells grow and expand, they trigger the infiltration of immune cells that secrete substances that disrupt insulin signaling, promote oxidative stress, and perpetuate systemic inflammation.

In people who do not have a large amount of adipose tissue, adipose tissue is composed primarily of anti-inflammatory molecules that help maintain metabolic homeostasis.

Inflammatory and anti-inflammatory

In obesity, the balance between pro-inflammatory and anti-inflammatory molecules is disrupted, exacerbating metabolic dysfunction.

Leptin, which regulates appetite and energy homeostasis, is elevated in obesity, but paradoxically fails to exert its anorectic effects due to the body’s creation and resistance to leptin.

In contrast, the substance adiponectin, an anti-inflammatory and insulin-sensitizing substance, is significantly reduced in obesity, further contributing to insulin resistance and chronic inflammation.

Other similar substances promote endothelial dysfunction, increase oxidative stress and enhance inflammatory signaling, with the result that these systemic alterations enhance the post-inflammatory state and lead, as mentioned above, to cardiovascular, renal, hepatic and metabolic diseases associated with obesity.

Gut microbiome

The gut microbiome is also increasingly recognized as a key factor contributing to obesity-induced post-inflammation as you experience an increase in pro-inflammatory pathogens in the gut.

This altered composition of the microbiome promotes intestinal permeability, allowing bacteria to enter the circulation, a phenomenon known as metabolic endotoxemia.

In addition, the altered composition of the microbiome produces short-chain fatty acids (SCFAs) that affect immune function and also contribute to increased inflammation and metabolic dysfunction.

Restoring the intestinal microbial balance through prebiotics, probiotics, and nutritional interventions is of great importance in mitigating post-inflammation in obesity.

Hypothalamus

The hypothalamus is inflamed during obesity, inflammation that plays a critical role in the dysfunction of energy balance and metabolic homeostasis.

In obesity, inflammatory signaling within the hypothalamus is increased, impairing neuronal function leading to leptin and insulin resistance in the central nervous system.

As a result, satiety signals are blunted, hunger increases, and energy expenditure decreases, perpetuating weight gain and metabolic dysfunction.

White blood cells

Extreme obesity alters the functions of white blood cells, particularly T cells, increasing the number of senescent and exhausted cells, which negatively affects the body’s adaptive immunity.

Hematopoiesis

The chronic post-inflammatory state in obesity also disrupts hematopoiesis, leading to impaired neutrophil function and reduced activity of antigen-presenting cells. This type of immune dysfunction translates into an increased risk of serious viral infections, such as influenza, and delayed healing of possible wounds.

In conclusion, obesity, since it can create major alterations in the immune system, can lead to serious health problems if not treated promptly and with a permanent plan to prevent recurrent flare-ups in the long term.

Source of the article