Evidence that lipopolysaccharide-induced anorexia depends upon central, rather than peripheral, inflammatory signals
Abstract
Systemic inflammatory stimuli cause anorexia and weight loss by disrupting the physiological regulation of energy balance. Mice lacking MyD88, an intracellular mediator of signal transduction activated by Toll-like receptor 4 or IL-1beta receptors, are resistant to anorexia induced by the bacterial endotoxin lipopolysaccharide (LPS), despite a significant circulating cytokine response. Thus, we hypothesized that induction of a peripheral inflammatory response is insufficient to cause LPS-induced anorexia when MyD88 signaling in the central nervous system and other tissues is absent. To test this hypothesis, we used bone marrow transplantation (BMT) to determine if LPS-induced anorexia can be restored to MyD88-deficient mice by reconstituting their bone marrow with wild-type (WT) immune cells. We found that restoring WT circulating immune cells to mice lacking MyD88 conferred only a mild, short-lived anorexia in response to LPS, such that food intake was fully normalized by 20 h post injection (LPS 4.1 +/- 0.5 g vs. vehicle 4.3 +/- 0.3 g), whereas LPS-induced anorexia was profound and sustained in WT controls after either autologous BMT or sham BMT. Similarly, LPS-mediated induction of hypothalamic mRNA encoding IL-1beta and TNFalpha was robust in both WT control groups but was absent in chimeric MyD88 mice, despite comparable peripheral inflammatory responses across the three groups. We conclude that LPS reduces food intake via a mechanism dependent on MyD88 signaling within brain and/or other tissues and that in the absence of this effect, robust stimulation of circulating immune cells cannot induce sustained anorexia.
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Some animal data suggest that lipopolysaccharide directly initiates an anorexic response by activating the Toll-like receptor 4/MyD88 signaling pathway in the central nervous system, although it has also been proven otherwise.
“some animal data suggest that LPS directly initiates an anorexic response (i.e., inflammation-induced anorexia) by activating the Toll-like receptor 4/MyD88 signaling pathway in the central nervous system [42,43], although it has also been proven otherwise [44].”
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- Authors
- Wisse, B. E., Ogimoto, K., Tang, J., Harris, M. K., Raines, E. W., & Schwartz, M. W.
- Affiliations
- University of Washington (US)
- Corresponding author
- Wisse, Brent E.
- Venue
- Endocrinology
- Publisher
- The Endocrine Society
- Published
- 2007-11-01
- Volume
- 148
- Issue
- 11
- Pages
- 5230-5237
- ISSN
- 0013-7227 (ISSN-L)
- 1945-7170
- OpenAlex
- W2033218360
- Cited by
- 85
- References
- 39
- Citations by year
- 2026: 1 · 2025: 4 · 2024: 9 · 2023: 1 · 2022: 2 · 2021: 4 · 2019: 6 · 2018: 2 · 2017: 7 · 2016: 6 · 2015: 3 · 2014: 8 · 2013: 3 · 2012: 5
- FWCI
- 2.59
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- M.J. Murdock Charitable Trust
- University of Washington
- National Institutes of Health (2r01dk012829-36)
- National Heart, Lung, and Blood Institute (P01HL018645)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK074758, P30-DK 17047, DK 12829, DK 61384, P01DK068384, K08DK061384, P30DK035816, P30DK017047)
- National Institute of Neurological Disorders and Stroke (NS-32273)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Keywords
- lipopolysaccharide, anorexia, MyD88, TLR4, IL-1β, TNF-α, hypothalamus, bone marrow transplantation, chimeric mice, energy balance, dietary intake, immune cells, endotoxin
- MeSH terms
- Animals, Anorexia, Body Composition, Body Weight, Cells, Cultured, Eating, Female, Hypothalamus, Immune System, Lipopolysaccharides, Male, Mice, Inbred C57BL, Spleen, Signal Transduction, Bone Marrow Transplantation, Mice, Knockout, Inflammation Mediators, Mice, Myeloid Differentiation Factor 88
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