Hyperglycemia enhances the cytokine production and oxidative responses to a low but not high dose of endotoxin in rats.

Denne beskriver hvordan hyperglycemi (regnes som blodsukker over 7 mmol/L i lengre perioder, eller fastende blodsukker over 7) gir økt cytokin-aktivitet i flere timer etter en stressende episode. Om man spiser en snickers går blodsukkeret opp til over 10, og om man kontinuerlig spiser mat som øker blodsukkeret er det en stor sjangse for at man har en kronisk betennelsesreaskjon med økt cytokin aktivitet.

Kobler vi det med denne, som nevner at cytokiner tilført fra utenfor muskelen kan gi hyperalgesi, så begynner bildet å bli klarere: «One mechanism of action, the immune-to-brain communication through activation of brain and spinal cord glial cells was reviewed by Wieseler-Frank et al. (2005). Activation of CNS glia and subsequent production of inflammatory cytokines can lead to hyperalgesia.» http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1552097/

Abstract

OBJECTIVE:

The aim of this study was to investigate whether hyperglycemia enhances the systemic inflammatory response and oxidative stress induced by endotoxin.

DESIGN:

Laboratory investigation.

SETTING:

University medical school.

SUBJECTS:

Forty-one male Sprague-Dawley rats.

INTERVENTIONS:

A hyperglycemic condition was produced in rats by glucose clamp for 3 hrs. Immediately on stopping the glucose infusion, animals received different doses of endotoxin injection (0, 0.2, or 1 mg/kg), and then blood glucose concentration was monitored over the ensuing 2 hrs. At the end of 2 hrs, levels of tumor necrosis factor-alpha, interleukin-1beta, interleukin-6, corticosterone, and alpha-1 acid glycoprotein were determined in serum, and malondialdehyde and total glutathione content were determined in the liver.

MEASUREMENTS AND MAIN RESULTS:

Over the 2-hr period, blood glucose concentrations returned to normal in initially hyperglycemic rats. However, the levels of cytokines, corticosterone, and alpha-1 acid glycoprotein were significantly higher in these animals compared with nonhyperglycemic controls, demonstrating an extended effect of prior hyperglycemia on markers of systemic inflammation. With low-dose (0.2 mg/kg) but not high-dose (1 mg/kg) endotoxin administration, hyperglycemic animals had significantly higher levels of cytokines compared with controls, indicating that prior hyperglycemia can enhance the systemic inflammatory response to a moderate endotoxin dose, but that the maximum effects of endotoxin on production of inflammatory cytokines are not altered by transient high glucose exposure.

CONCLUSIONS:

Systemic inflammation persists for a period following hyperglycemia, and this can enhance the systemic inflammatory response to a subsequent moderate stress.

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