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Related Experiment Video

Updated: Jun 25, 2026

Experimental Approach to Examine Leptin Signaling in the Carotid Bodies and its Effects on Control of Breathing
05:45

Experimental Approach to Examine Leptin Signaling in the Carotid Bodies and its Effects on Control of Breathing

Published on: October 25, 2019

Leptin receptor polymorphisms and lung function decline in COPD.

N N Hansel1, L Gao, N M Rafaels

  • 1Department of Medicine, School of Medicine, Johns Hopkins University, Baltimore, MD, USA.

The European Respiratory Journal
|February 7, 2009
PubMed
Summary
This summary is machine-generated.

Genetic variants in the leptin receptor (LEPR) gene are associated with lung function decline in smokers with chronic obstructive pulmonary disease (COPD). This suggests LEPR may be a novel genetic factor in COPD development.

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Last Updated: Jun 25, 2026

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05:45

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Published on: October 25, 2019

Phenotyping Mouse Pulmonary Function In Vivo with the Lung Diffusing Capacity
07:13

Phenotyping Mouse Pulmonary Function In Vivo with the Lung Diffusing Capacity

Published on: January 6, 2015

Area of Science:

  • Genetics
  • Pulmonology
  • Molecular Biology

Background:

  • Chronic obstructive pulmonary disease (COPD) affects only a subset of smokers, indicating a significant genetic susceptibility component.
  • The leptin receptor (LEPR) is expressed in lung tissue and may be involved in the mechanisms underlying COPD.
  • Understanding genetic factors influencing COPD progression is crucial for identifying at-risk individuals and developing targeted therapies.

Purpose of the Study:

  • To investigate the association between genetic variations in the LEPR gene and the rate of lung function decline in individuals with COPD.
  • To explore the potential role of LEPR in COPD pathogenesis through genetic association and in vivo expression studies.

Main Methods:

  • Genotyping of 36 single nucleotide polymorphisms (SNPs) in the LEPR gene in 429 European American participants from the Lung Health Study.
  • Calculation of mean annual decline in forced expiratory volume in 1 second (% predicted) over a 5-year period using linear regression.
  • Immunohistochemistry analysis of LEPR gene expression in lungs of smoke-exposed inbred mice to assess in vivo relevance.

Main Results:

  • Significant associations (p<0.05) were found between 21 LEPR SNPs and lung function decline.
  • Haplotype analyses corroborated the associations identified with individual SNPs.
  • Immunohistochemistry results in mice supported a potential role for LEPR in the pathogenesis of COPD.

Conclusions:

  • Genetic variants within the LEPR gene are significantly associated with lung function decline in a population of smokers with COPD.
  • These findings identify LEPR as a novel candidate gene for COPD.
  • The study highlights the importance of genetic factors in determining COPD susceptibility and progression.