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Cited by 1,251

The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.

Leptin regulates proinflammatory immune responses

Loffreda, S., Yang, S. Q., Lin, H. Z., Karp, C. L., Brengman, M. L., Wang, D. J., Klein, A. S., Bulkley, G. B., Bao, C., Noble, P. W., Lane, M. D., Diehl, A. M.·1998·The FASEB Journal
DOI 10.1096/fasebj.12.1.57
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Abstract

Obesity is associated with an increased incidence of infection, diabetes, and cardiovascular disease, which together account for most obesity-related morbidity and mortality. Decreased expression of leptin or of functional leptin receptors results in hyperphagia, decreased energy expenditure, and obesity. It is unclear, however, whether defective leptin-dependent signal transduction directly promotes any of the conditions that frequently complicate obesity. Abnormalities in tumor necrosis factor alpha expression have been noted in each of the above comorbid conditions, so leptin deficiency could promote these complications if leptin had immunoregulatory activity. Studies of rodents with genetic abnormalities in leptin or leptin receptors revealed obesity-related deficits in macrophage phagocytosis and the expression of proinflammatory cytokines both in vivo and in vitro. Exogenous leptin up-regulated both phagocytosis and the production of proinflammatory cytokines. These results identify an important and novel function for leptin: up-regulation of inflammatory immune responses, which may provide a common pathogenetic mechanism that contributes to several of the major complications of obesity.

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Citations

Cites

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Metadata

Authors
Loffreda, S., Yang, S. Q., Lin, H. Z., Karp, C. L., Brengman, M. L., Wang, D. J., Klein, A. S., Bulkley, G. B., Bao, C., Noble, P. W., Lane, M. D., & Diehl, A. M.
Venue
The FASEB Journal
Publisher
Wiley
Published
1998-01
Volume
12
Issue
1
Pages
57-65
ISSN
  • 0892-6638 (ISSN-L)
  • 1530-6860
DOI
10.1096/fasebj.12.1.57
OpenAlex
W2142431039
Cited by
1,251
References
5
FWCI
31.51
Type
journal article
Language
en
Open access
closed

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