Abstract
Type 2 diabetes (T2D) is associated with chronic exposure to increases in tumor necrosis factor alpha (TNFα), which contributes to insulin resistance and the development of foot ulcers in 25% of affected individuals. The mechanism by which TNFα leads to insulin resistance and poor wound healing is unclear. We hypothesized that glycosphingolipid GM3 is a critical mediator of TNFα-induced pathology in diabetic skin. In undifferentiated, cultured normal human epidermal keratinocytes (NHEKs), chronic TNFα treatment (100 pM x 4 days) increased the expression of both GM3 (8-fold increase, P<0.001) and its synthesizing enzyme GM3 synthase (GM3S) (4-fold increase, P<0.01), as shown by lipidomics, flow-cytometry and RT-qPCR.
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