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Cited by 862

The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.

Endotoxin and cytokines induce expression of leptin, the ob gene product, in hamsters.

Open access
Grunfeld, C, Zhao, C, Fuller, J, Pollack, A, Moser, A, Friedman, J, Feingold, K R·1996·Journal of Clinical Investigation

Abstract

The expression of leptin, the ob gene product, is increased in adipose tissue in response to feeding and energy repletion, while leptin decreases food intake. Because adipose tissue gene expression is regulated by cytokines induced during infection and because infection is associated with anorexia, we tested whether induction of leptin might occur during the host response to infection. Administration of endotoxin (LPS), a model for gram negative infections, induces profound anorexia and weight loss in hamsters. In fasted adipose tissue to levels similar to fed control animals. There is a strong inverse correlation between mRNA levels of leptin and subsequent food intake. TNF and IL-1, mediators of the host response to LPS, also induced anorexia and increased levels of leptin in mRNA in adipose tissue. As assessed by immuknoprecipitation and Western blotting, circulating leptin protein is regulated by LPS and cytokines in parallel to regulation of adipose tissue leptin mRNA. Induction of leptin during the host response to infection may contribute to the anorexia of infection.

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Crossref · 10.1172/jci118653

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Metadata

Authors
Grunfeld, C., Zhao, C., Fuller, J., Pollack, A., Moser, A., Friedman, J., & Feingold, K. R.
Venue
Journal of Clinical Investigation
Published
1996-05-01
Volume
97
Issue
9
Pages
2152-2157
ISSN
0021-9738 (ISSN-L)
OpenAlex
W1993203791
Cited by
862
References
4
FWCI
17.03
Type
journal article
Language
en
Open access
bronze

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.