10.08.2017

Hier geht's zur zu Grunde liegenden Arbeit:
https://www.ncbi.nlm.nih.gov/pubmed/26926996

Abstract:
Abnormal glucose metabolism and enhanced oxidative stress accelerate cardiovascular disease, a chronic inflammatory condition causing high morbidity and mortality. Here, we report that in monocytes and macrophages of patients with atherosclerotic coronary artery disease (CAD), overutilization of glucose promotes excessive and prolonged production of the cytokines IL-6 and IL-1β, driving systemic and tissue inflammation. In patient-derived monocytes and macrophages, increased glucose uptake and glycolytic flux fuel the generation of mitochondrial reactive oxygen species, which in turn promote dimerization of the glycolytic enzyme pyruvate kinase M2 (PKM2) and enable its nuclear translocation. Nuclear PKM2 functions as a protein kinase that phosphorylates the transcription factor STAT3, thus boosting IL-6 and IL-1β production. Reducing glycolysis, scavenging superoxide and enforcing PKM2 tetramerization correct the proinflammatory phenotype of CAD macrophages. In essence, PKM2 serves a previously unidentified role as a molecular integrator of metabolic dysfunction, oxidative stress and tissue inflammation and represents a novel therapeutic target in cardiovascular disease.

 

Die Rede ist also von einer abnormen Glukoseaufnahme und-verwertung, nicht zwangsweise von einem übermäßigen Glukoseangebot.

 

In der Originalarbeit heißt es u.A.:
"Further evidence for mitochondrial dysfunction came from uncoupling experiments, which revealed a robust respiratory reserve capacity in patient-derived cells. Insufficient uncoupling is a primary mechanism driving mtROS
production and essentially indicates that mitochondria in CAD cells have lost a major protective mechanism. Possible causes include chronic glucose overload, in line with the surplus glucose uptake shown in Fig. 5 and the up-regulation of
glucose transporters shown in Fig. 7. The defect was present in nondiabetic patients, eliminating elevated blood glucose as the sole cause. Persistent up-regulation of the glucose transporters and the glycolytic machinery suggest a fundamental abnormality in glucose handling."

 

Übrigens ist eine Entzündung per se erst mal nichts Böses/Schlechtes, sondern Teil der körpereignen Immunreaktion. Entzündung bedeutet, dass Gewebe durchlässiger werden für Fress- und Reparaturzellen, damit die an ihren Einsatzort gelangen können. Problematisch wird es immer nur bei einem chronischen Zuviel; egal von was (Entzündung, Zucker, Fett, Sport, etc.).

LG,
Thorsten