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Opposing Effects of Fasting Metabolism on Tissue Tolerance in Bacterial and Viral Inflammation

Kyla

ᴀɴɴɪᴇ ɢꜱᴀᴍᴩᴇʟ
Messages
721
Location
Canada
Atlantic article here:
http://www.theatlantic.com/science/archive/2016/09/glucose-inflammation/498965/

study here:
http://www.cell.com/cell/fulltext/S0092-8674(16)30972-2

Some excerpts from article:
Do you feed a fever and starve a cold? Or is it the opposite? I can never remember. I never cared to. I thought it was just something people said when they didn’t know what else to say.
Ruslan Medzhitov cares. He’s a distinguished professor of immunobiology at Yale. And in the journal Cell today, his team showed some dramatic benefits to starving a bacterial illness—but feeding a viral illness...



...Ketogenesis limits the body's formation of substances known as reactive oxygen species, which can damage cells. When you introduce glucose (as in, if you eat sugar, or any carbohydrate that breaks down into sugar), that switch to a fasting metabolism is undone. The sugar triggers the release of the hormone insulin, which tells the body that we don't need to use our fat reserves, bringing ketogenesis to a grinding halt. So when the mice were given glucose, the inflammatory process caused damage to neurons in the brain, causing the mice to convulse and die.

Meanwhile the virus triggered a different type of sepsis, in which removing glucose was uniformly lethal. In that case, glucose seemed to be necessary for adapting to the stress of viral inflammation, by preventing stress-mediated apoptosis (cell death). Without that, an area in the brainstem was destroyed by inflammation, and the mice would stop breathing...

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Opposing Effects of Fasting Metabolism on Tissue Tolerance in Bacterial and Viral Inflammation


DOI: http://dx.doi.org/10.1016/j.cell.2016.07.026

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Highlights


  • •Fasting metabolism is protective in bacterial, but not viral, inflammation
  • •Ketone bodies limit ROS-induced neuronal damage during bacterial inflammation
  • •Glucose utilization prevents UPR-mediated neuronal damage during viral inflammation


Summary
Acute infections are associated with a set of stereotypic behavioral responses, including anorexia, lethargy, and social withdrawal. Although these so-called sickness behaviors are the most common and familiar symptoms of infections, their roles in host defense are largely unknown. Here, we investigated the role of anorexia in models of bacterial and viral infections. We found that anorexia was protective while nutritional supplementation was detrimental in bacterial sepsis. Furthermore, glucose was necessary and sufficient for these effects. In contrast, nutritional supplementation protected against mortality from influenza infection and viral sepsis, whereas blocking glucose utilization was lethal. In both bacterial and viral models, these effects were largely independent of pathogen load and magnitude of inflammation. Instead, we identify opposing metabolic requirements tied to cellular stress adaptations critical for tolerance of differential inflammatory states.


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