Leptin levels in SARS-CoV-2 infection related respiratory failure: A cross-sectional study and a pathophysiological framework on the role of fat tissue

Abstract

Obesity is a risk factor for SARS-CoV-2 infected patients to develop respiratory failure. Leptin produced in visceral fat might play a role in the deterioration to mechanical ventilation. A cross sectional study was performed. The mean BMI was 31 kg/m 2 (range 24.8–48.4) for the 31 SARS-CoV-2 ventilated patients and 26 kg/m 2 (range 22.4–33.5) for 8 critically ill non-infected control patients. SARS-CoV-2 infected patients with a similar BMI as control patients appear to have significantly higher levels of serum leptin. The mean leptin level was 21.2 (6.0–85.2) vs 5.6 (2.4–8.2) ug/L for SARS-CoV-2 and controls respectively (p = 0.0007). With these findings we describe a clinical and biological framework that may explain these clinical observations. The ACE2 utilization by the virus leads to local pulmonary inflammation due to ACE2-ATII disbalance. This might be enhanced by an increase in leptin production induced by SARS-CoV-2 infection of visceral fat. Leptin receptors in the lungs are now more activated to enhance local pulmonary inflammation. This adds to the pre-existent chronic inflammation in obese patients. Visceral fat, lung tissue and leptin production play an interconnecting role. This insight can lead the way to further research and treatment.

A meta-analysis of the association between obesity and COVID-19

“…Moreover, studies show that obesity disrupts the immune system, limiting its capacity to deal with a new virus like SARS-CoV-2 [ 83 ]. In severe cases, patients may have a cytokine storm, characterised by the overproduction of IL-6, TNF- α , monocyte chemoattractant protein-1 and leptin, resulting in an increased risk of vascular hyperpermeability and multiorgan failure [ 84 , 85 ]. Besides, respiratory physiology is altered in patients with obesity, resulting in decreased functional residual capacity and expiratory reserve volume, leading to subsequent ventilation−perfusion abnormalities and hypoxaemia [ 86 , 87 ].…”

Resveratrol And Pterostilbene Potently Inhibit SARS-CoV-2 Replication In Vitro

“…Secondly, as an antioxidant, resveratrol is found to prevent the formation of reactive oxygen species (ROS), prevent airway epithelial remodeling by upregulation of SIRT1 and activate superoxide dismutase (SOD) (33,34). Lastly, resveratrol reduces the secretion of leptin (35), an adipokine that has been implicated to be a contributing factor in the development of respiratory failure and ARDS in SARS-CoV-2 infected patients (15). Therefore, resveratrol might not only be a promising candidate to inhibit viral replication early in infection it may also alleviate disease symptoms later in infection.…”

“…Next to the direct effect on virus replication, resveratrol was also reported to exhibit anti-inflammatory and anti-oxidant properties thereby having the potential to mitigate virus-induced disease pathogenesis (11,12). Based on these findings, we and others have postulated that resveratrol and its structural analog might be an advantageous treatment option for SARS-CoV-2 infected individuals (13)(14)(15).…”

Influence of obesity on serum levels of SARS-CoV-2-specific antibodies in COVID-19 patients

“…Obesity and associated inflammation lead to several debilitating chronic diseases such as type-2 diabetes, cancer, atherosclerosis, and inflammatory bowel disease [8][9][10][11][12][13][14][15]. Therefore, obesity has been identified as an additional risk factor for COVID-19 patients [16][17][18][19]. Also, the prevalence of the disease, and the occurrence of complications in obese individuals are increased compared to lean controls.…”