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Inflammatory mediators have an established role in inducing insulin resistance and promoting hyperglycemia. In turn, hyperglycemia has been argued to drive immune cell dysfunction as a result of mitochondrial dysfunction. Here, the authors review the evidence challenging this view. First, it is pointed out that inflammatory mediators are known to induce altered mitochondrial function. In this regard, critical care patients suffer both an elevated inflammatory tone as well as hyperglycemia, rendering it difficult to distinguish between the effects of inflammation and hyperglycemia. Second, emerging evidence indicates that a decrease in mitochondrial respiration and an increase in reactive oxygen species (ROS) production are not necessarily manifestations of pathology, but adaptations taking shape as the mitochondria is abdicating its adenosine triphosphate (ATP)-producing function (which is taken over by glycolysis) and instead becomes "retooled" for an immunological role. Collectively, these observations challenge the commonly held belief that acute hyperglycemia induces mitochondrial damage leading to immune cell dysfunction.

Original publication




Journal article


BioEssays : news and reviews in molecular, cellular and developmental biology

Publication Date





Department of Physiological Sciences, Stellenbosch University, 7602, Stellenbosch, South Africa.


Mitochondria, Humans, Hyperglycemia, Inflammation, Reactive Oxygen Species, Insulin