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Recovering from toxemia-induced defective phagocytosis with high carb/high insulin diet
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0201878
Insulin treatment increases phagocytic activity after LPS stimulation
... acute insulin administration significantly increased phagocytosis. Similar to the longer condition, LPS reduced phagocytosis, which was reversed by insulin administration. TNFa, on the other hand, significantly increased phagocytosis, which was reversed by insulin.
Addition of insulin to the LPS(endotoxin) treated group partially alleviated this suppression, significantly increasing phagocytosis in comparison to the LPS group. n = 5/group. C)
Stress Hyperglycemia, Insulin Treatment, and Innate Immune Cells
https://www.hindawi.com/journals/ije/2014/486403/
To examine the effects of high glucose on macrophage proliferation, Liu et al. cultured monocyte/macrophage cell line WEHI-3 and splenic macrophages in hyperglycemic media with various concentrations (5.6–30 mM) of glucose. They found that macrophage proliferation increased with the greater concentrations of glucose [21]. The enhanced macrophage proliferation may result from increased CSF-1 receptor (CSF-1R) under these conditions [22]. In addition, hyperlipidemia has combined effect with hyperglycemia to stimulate the proliferation of macrophages since hypermetabolisms including hyperglycemia and hyperlipidemia are very common in critical illness [23]. In addition, hyperglycemia also enhances the immunological responses, as is shown in that hyperglycemia augmented increased cytokine production and phagocytosis in response to LPS [24]. This effect may be associated with elevated TLR expression [16].