Leptin levels in SARS-CoV-2 infection related respiratory failure: A cross-sectional study and a pathophysiological framework on the role of fat tissue
Peter H.J. van der Voort,
Jill Moser,
Durk F. Zandstra,
Anneke C. Muller Kobold,
Marjolein Knoester,
Cornelis F. Calkhoven,
Inge Hamming,
Matijs van Meurs
Affiliations
Peter H.J. van der Voort
Department of Critical Care, University of Groningen, University Medical Center Groningen, 9700, RB, Groningen, the Netherlands; Corresponding author.
Jill Moser
Department of Critical Care, University of Groningen, University Medical Center Groningen, 9700, RB, Groningen, the Netherlands
Durk F. Zandstra
Department of Critical Care, University of Groningen, University Medical Center Groningen, 9700, RB, Groningen, the Netherlands
Anneke C. Muller Kobold
Department of Laboratory Medicine, University of Groningen, University Medical Center Groningen, 9700, RB, Groningen, the Netherlands
Marjolein Knoester
Department of Clinical Microbiology and Infection Prevention, University of Groningen, University Medical Center Groningen, 9700, RB, Groningen, the Netherlands
Cornelis F. Calkhoven
European Research Institute for the Biology of Ageing (ERIBA), University Medical Center Groningen, University of Groningen, 9700, AD, Groningen, the Netherlands
Inge Hamming
Department of Critical Care, University of Groningen, University Medical Center Groningen, 9700, RB, Groningen, the Netherlands
Matijs van Meurs
Department of Critical Care, University of Groningen, University Medical Center Groningen, 9700, RB, Groningen, the Netherlands
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/m2 (range 24.8–48.4) for the 31 SARS-CoV-2 ventilated patients and 26 kg/m2 (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.
