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Departments of 1 Medicine and 2 Environmental Health, Johns Hopkins University, Baltimore, Maryland 21205; and 3 Department of Medicine, Cornell University Medical College and Strang Cancer Prevention Center, New York, New York 10021
Obesity is a
complex syndrome that involves defective signaling by a number of
different factors that regulate appetite and energy homeostasis.
Treatment with exogenous leptin reverses hyperphagia and obesity in
ob/ob
mice, which have a mutation that causes leptin deficiency, proving the
importance of this factor and its receptors in the obesity syndrome.
Cells with leptin receptors have been identified outside of the
appetite regulatory centers in the brain. Thus leptin has peripheral
targets. Because macrophages express signaling-competent leptin
receptors, these cells may be altered during chronic leptin deficiency.
Consistent with this concept, the present study identifies several
phenotypic abnormalities in macrophages from
ob/ob
mice, including decreased steady-state levels of uncoupling protein-2
mRNA, increased mitochondrial production of superoxide and hydrogen
peroxide, constitutive activation of CCAAT enhancer binding protein
(C/EBP)-
, an oxidant-sensitive transcription factor, increased
expression of interleukin-6 and cyclooxygenase (COX)-2, two C/EBP-
target genes, and increased COX-2-dependent production of
PGE2. Given the importance of
macrophages in the general regulation of inflammation and immunity,
these alterations in macrophage function may contribute to
obesity-related pathophysiology.
obesity; uncoupling proteins; cytokines; cyclooxygenase-2; superoxide
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