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From the Metabolism Section, Department of Veterans Affairs Medical Center, University of California, San Francisco, California
Malnutrition compromises immune function, reducing
resistance to infection. We examine whether the decrease in leptin
induced by starvation increases susceptibility to
lipopolysaccharide (LPS)- and tumor necrosis factor
(TNF)-induced lethality. In mice, fasting for 48 hours enhances
sensitivity to LPS. Decreasing the fasting-induced fall in leptin by
leptin administration markedly reduced sensitivity to LPS. Although
fasting decreases basal leptin levels, LPS treatment increased
leptin to the same extent as in fed animals. Fasting increased basal
serum corticosterone; leptin treatment blunted this increase. Fasting
decreased the ability of LPS to increase corticosterone; leptin
restored the corticosterone response to LPS. Serum glucose levels were
decreased in fasted mice and LPS induced a further decrease. Leptin
treatment affected neither basal glucose nor that after LPS. LPS
induced a fivefold greater increase in serum TNF in fasted
mice, which was blunted by leptin replacement. In
contrast, LPS induced lower levels of interferon-
and no
differences in interleukin-1ß in fasted compared to fed animals;
leptin had no effect on those cytokines. Furthermore, fasting
increased sensitivity to the lethal effect of TNF itself, which
was also reversed by leptin treatment. Thus, leptin seems to be
protective by both inhibiting TNF induction by LPS and by reducing TNF
toxicity.
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