[메디게이트뉴스 서민지 기자] While obesity is known to increase the severity of COVID-19 infection and contribute to an increase in the incidence and mortality of complications, analysis suggests that this is due to the characteristics of obesity such as leptin resistance regulating the immune system, promoting insulin resistance, increasing ACE2 expression, and abnormal protein splicing. came out
Researcher Yoon Chang-ho of the Mayo Clinic recently revealed this through a report by the Korean Scientists and Engineers Network (KOSEN) on the subject of ‘obesity as a risk factor for COVID-19’.
The COVID-19 virus causes fever, cough, muscle pain, and fatigue, which can develop into hyperinflammation, cytokine storm, acute respiratory distress syndrome (ARDS), and COVID-associated coagulopathy (CAC).
A significant proportion of severely ill patients with COVID-19 arriving at the intensive care unit were found to be overweight or suffering from obesity. ) is known.
Researcher Yoon said, “There are clinical results that support the association between chronic inflammation, which is a characteristic of obesity, and COVID-19 severity. Of the 11 studies that investigated the association between BMI and mortality in COVID-19 inpatients, 10 studies were overweight or obese (BMI 30 The above) patients showed more severe disease symptoms,” he explained. “Patients admitted to the intensive care unit had 30% higher abdominal fat (VAT) and 30% lower subcutaneous fat tissue.”
In another study, compared to outpatients who did not require hospitalization, inpatients had no difference in BMI, but a higher percentage of abdominal fat, he added.
Therefore, understanding the association between COVID-19 severity and obesity is critical to advancing prevention strategies and developing treatments for high-risk populations.
Accordingly, researcher Yun analyzed potential mechanisms linking obesity and major disease complications as a result of infection with the COVID-19 virus (SARS-CoV-2), focusing on the metabolic and immune-related outcomes of obesity on the course of the COVID-19 disease.
Obesity has exploded in prevalence worldwide over the past 50 years. It is a major risk factor for the development of non-communicable diseases, and the World Health Organization (WHO) defines it as abnormal or excessive fat accumulation that can harm health.
Fat cells or adipose tissue, previously known as a simple energy-storing organ, have recently become known as an important endocrine organ. affects the whole body In particular, visceral fat does not accumulate much, but promotes systemic inflammation and is closely related to glucose and lipid metabolism disorders along with insulin resistance.
In addition, enlarged adipocytes produce several pro-inflammatory adipokines such as tumor necrosis factor-alpha (TNF-a), interleukin-6, and leptin. Hyperleptinemia causes central leptin resistance, which makes it difficult to control appetite and satiety, and can also cause chronic inflammation.
Researcher Yoon said, “First of all, coronaviruses bind to angiotensin-converting enzyme 2 (ACE2) to promote virus entry into target cells. In addition to the small intestine, kidney, and heart, adipose tissue also expresses ACE2.” “As a result, obese patients with chronic inflammation caused by pro-inflammatory cytokines are vulnerable to corona infection, and moreover, fat tissue stores the virus, and the combination of coronavirus and ACE2 causes abnormalities in immune system function and leads to severe disease. It will increase,” he explained.
In addition, the function of glucose control protein (GRP78), which acts as an anti-apoptosis regulator and misassembled protein decomposer in our body, is suppressed by the coronavirus. The problem is that when obesity causes endoplasmic reticulum stress and abnormal protein splicing (UPR) occurs, hypoxia, reactive oxygen species, insulin resistance, and nutritional imbalance cause GRP78 to be overexpressed and combine with coronavirus to promote entry into host cells. am.
In addition, obesity causes insulin resistance. When insulin resistance is promoted by excessive lipid accumulation in adipose tissue, hypoxia and inflammation are induced, and chronic elevation of proinflammatory cytokines directly affects the course of corona disease. In particular, obese people with elevated M1 macrophage TNF-a, which produces pro-inflammatory cytokines, are at greater risk of developing life-threatening complications.
“Chronic hyperleptinemia, which is often seen in obesity, also exacerbates COVID-19 disease,” said Yoon. In obese patients, infection or sepsis can further increase leptin levels, which further increases the risk of developing an imbalanced or hyperinflammatory response when infected with the coronavirus.”
“Corona infection increases the expression of a gene (SOCS3) encoding a suppressor of cytokine signaling in lung epithelium,” he said. “This gene is a key regulator of inflammation and a suppressor in the leptin signaling pathway. The expression of SOCS3 further impairs leptin signaling and negatively affects the immune response in obese patients.”
Therefore, “increased ACE2 and GRP78 into adipocytes increase viral entry, and the immune system cannot provide an appropriate immune response, resulting in virus elimination failure. Eventually, a pro-inflammatory overreaction can cause a cytokine storm, and high Leptinemia and dysfunction caused by adipocytes increase risks such as blood clot formation and bleeding, leading to higher rates of mortality and complications.” It cannot be defined as a simple excess of fat cells.”
Researcher Yoon said, “It is necessary to identify the causes of obesity and future severity and complications and use them for effective preventive measures and therapeutic intervention.” It is also important to practice a healthy lifestyle, such as restricting calorie foods, getting enough exercise and sleep, and avoiding chronic psycho-emotional stress.”
