Opposing Effects of Fasting Metabolism on Tissue Tolerance in Bacterial and Viral Inflammation.
Level 5 - mechanism / opinion, no new human data
Preclinical animal experimental research on metabolic mechanisms of tissue tolerance.
PubMed 27610573 · doi:10.1016/j.cell.2016.07.026
What was done
The authors investigated the physiological role of sickness-induced anorexia and nutritional supplementation in experimental animal models of bacterial sepsis, viral sepsis, and influenza infection. They assessed the impact of nutritional status and glucose availability on survival, pathogen burden, inflammation levels, and tissue tolerance mechanisms.
What was found
The abstract reports no numerical values or sample sizes. Qualitatively, anorexia was protective and nutritional supplementation (specifically glucose) was detrimental in bacterial sepsis models. Conversely, nutritional supplementation protected against mortality during influenza infection and viral sepsis, whereas inhibiting glucose utilization was lethal. These divergent outcomes occurred largely independently of pathogen load or inflammatory magnitude.
Why it matters
This study provides evidence that sickness anorexia is an adaptive host defense mechanism with pathogen-specific trade-offs, demonstrating that tissue tolerance requires distinct metabolic states during bacterial versus viral infections.
Limits
The findings are derived entirely from preclinical animal models, and translation to human clinical feeding practices during acute infection is unproven. The abstract does not provide sample sizes, effect sizes, survival percentages, or specific details regarding experimental regimens.
Cited by
- supports Ruslan Medzhitov published a Cell study showing that force-feeding mice or restoring glucose levels to normal concentrations made an otherwise survivable bacterial infection lethal.