en
Scientific article
English

Hyperoxia increases leptin production: a mechanism mediated through endogenous elevation of corticosterone

Publication date2001
Abstract

Leptin, a cytokine involved in the regulation of food intake, has been reported to be decreased in lung diseases such as chronic obstructive pulmonary disease and cystic fibrosis and increased in critically ill patients with sepsis. We investigated the role of leptin during hyperoxia in mice, which results in alveolar edema, severe weight loss, and death within 3-4 days. In oxygen-breathing mice, serum leptin was increased six- to sevenfold and its mRNA was upregulated in white adipose tissue. Leptin elevation could not be attributed to changes in circulating tumor necrosis factor-alpha but was completely dependent on endogenous corticosterone elevation because adrenalectomized mice did not exhibit any increase in leptin levels. Using leptin-deficient mice and wild-type mice treated with anti-leptin antibody, we demonstrate that weight loss was leptin independent. Lung damage was moderately attenuated in leptin-deficient mice but was not modified by anti-leptin antibody or leptin administration, suggesting that leptin does not play an essential role in the direct and short-term effects of oxygen-induced injury.

Keywords
  • Adipose Tissue/physiology
  • Animals
  • Body Weight
  • Corticosterone/metabolism
  • DNA Fragmentation
  • Female
  • Hyperoxia/metabolism/pathology
  • Immunoglobulin G/immunology
  • Interleukin-6/blood/metabolism
  • Leptin/blood/genetics/immunology/metabolism
  • Lung/pathology/physiopathology
  • Mice
  • Mice, Inbred C57BL
  • Mice, Obese
  • Organ Size
  • Oxygen/metabolism
  • RNA, Messenger/genetics/metabolism
  • Tumor Necrosis Factor-alpha/metabolism
Citation (ISO format)
BARAZZONE, Constance et al. Hyperoxia increases leptin production: a mechanism mediated through endogenous elevation of corticosterone. In: American journal of physiology. Lung cellular and molecular physiology, 2001, vol. 281, n° 5, p. L1150–1156.
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Article (Published version)
accessLevelRestricted
Identifiers
ISSN of the journal1040-0605
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