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For example, anorexia of infection is part of the acute phase response ( APR ) to infection.
The APR response can be triggered by lipopolysaccharides and peptidoglycans from bacterial cell walls, bacterial DNA, double-stranded viral RNA, and viral glycoproteins, which can trigger production of a variety of proinflammatory cytokines.
These can have an indirect effect on appetite by a number of means, including peripheral afferents from their sites of production in the body, by enhancing production of leptin from fat stores.
Inflammatory cytokines can also signal to the central nervous system more directly by specialized transport mechanisms through the blood – brain barrier, via circumventricular organs ( which are outside the barrier ), or by triggering production of eicosanoids in the endothelial cells of the brain vasculature.
Ultimately the control of appetite by this mechanism is thought to be mediated by the same factors normally controlling appetite, such as neurotransmitters ( serotonin, dopamine, histamine ), corticotropin releasing factor, neuropeptide Y, and α-melanocyte-stimulating hormone.

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