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Updated: Jun 4, 2026

Experimental Approach to Examine Leptin Signaling in the Carotid Bodies and its Effects on Control of Breathing
Published on: October 25, 2019
Airway and plasma leptin and adiponectin in lean and obese asthmatics and controls
Fernando Holguin1, Mauricio Rojas, Lou Anne Brown
1Division of Pulmonary, Allergy and Critical Care, Department of Medicine, Asthma Institute, University of Pittsburgh, Pittsburgh, PA 15213, USA. holguinf@upmc.edu
Introduction:
Obesity-mediated changes in plasma adipokines have been associated with increased systemic inflammation and oxidative stress. However, it is unknown whether obesity induces similar changes in airway levels of these adipokines and whether these changes are associated with increased airway biomarkers of inflammation and oxidative stress.
Methods:
Lean and obese asthmatics and controls underwent bronchoscopy with bronchoalveolar lavage (BAL), spirometry, and provided fasting plasma leptin and adiponectin. Biomarkers of oxidation and inflammation in the BAL included exhaled nitric oxide (NO), 8-isoprostanes, pH, and nitrogen oxide products (NOx).
Results:
Out of a total of 48 subjects, 44% had asthma and 56% were healthy controls. Among subjects with asthma, 66% were obese, 10% overweight, and 24% lean; in the controls these proportions were 63%, 11%, and 26%, respectively. After adjusting for age, sex, smoking history, ethnicity, and prebronchodilator forced exhalation in 1 second (FEV(1)), obesity was associated with higher BAL and plasma leptin levels in asthmatics and controls. Increasing BMI was associated with increased BAL leptin and was marginally and inversely associated with BAL adiponectin. Significant associations between BAL and plasma levels were only observed for leptin. No significant associations were observed between BAL and plasma adipokines with the airway biomarkers of oxidation and inflammation.
Conclusion:
Increasing BMI is associated with changes in the concentrations of airway adipokines in asthmatics and healthy controls; however, these associations are not related with biomarkers of airway oxidation or inflammation.
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