Leptin and the control of pharyngeal patency during sleep in severe obesity

Steven D. Shapiro, Chien Hung Chin, Jason P. Kirkness, Brian M. McGinley, Susheel P. Patil, Vsevolod Y. Polotsky, Paolo Jose Cesare Biselli, Philip L. Smith, Hartmut Schneider, Alan R. Schwartz

Research output: Contribution to journalArticlepeer-review

Abstract

Rationale: Obesity imposes mechanical loads on the upper airway, resulting in flow limitation and obstructive sleep apnea (OSA). In previous animal models, leptin has been considered to serve as a stimulant of ventilation and may prevent respiratory depression during sleep. We hypothesized that variations in leptin concentration among similarly obese individuals will predict differences in compensatory responses to upper airway obstruction during sleep. Methods: An observational study was conducted in 23 obese women [body mass index (BMI): 46 ± 3 kg/m2, age: 41 ± 12 yr] and 3 obese men (BMI: 46 ± 3 kg/m2, age: 43 ± 4 yr). Subjects who were candidates for bariatric surgery were recruited to determine upper airway collapsibility under hypotonic conditions [pharyngeal critical pressure (passive PCRIT)], active neuromuscular responses to upper airway obstruction during sleep, and overnight fasting serum leptin levels. Compensatory responses were defined as the differences in peak inspiratory airflow (AVImax), inspired minute ventilation (AVI), and pharyngeal critical pressure (APCRIT) between the active and passive conditions. Results: Leptin concentration was not associated with sleep disordered breathing severity, passive PCRIT, or baseline ventilation. In the women, increases in serum leptin concentrations were significantly associated with increases in AVImax (r2 = 0.44, P < 0.001), AVI (r2 = 0.40, P < 0.001), and APCRIT (r2 = 0.19, P < 0.04). These responses were independent of BMI, waist-to-hip ratio, neck circumference, or sagittal girth. Conclusion: Leptin may augment neural compensatory mechanisms in response to upper airway obstruction, minimizing upper airway collapse, and/or mitigating potential OSA severity. Variability in leptin concentration among similarly obese individuals may contribute to differences in OSA susceptibility.

Original languageEnglish (US)
Pages (from-to)1334-1341
Number of pages8
JournalJournal of applied physiology
Volume116
Issue number10
DOIs
StatePublished - May 15 2014

Keywords

  • Leptin
  • Obesity
  • Obstructive sleep apnea
  • Upper airway control

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

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