Journal
NATURE MICROBIOLOGY
Volume 3, Issue 5, Pages 622-631Publisher
NATURE PORTFOLIO
DOI: 10.1038/s41564-018-0146-2
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Funding
- National Natural Science Foundation of China [31370170]
- Natural Science Foundation of Beijing [7142119]
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Insulin resistance is a risk factor for obesity and diabetes and predisposes individuals to Staphylococcus aureus colonization; however, the contribution of S. aureus to insulin resistance remains unclear. Here, we show that S. aureus infection causes impaired glucose tolerance via secretion of an insulin-binding protein extracellular domain of LtaS, eLtaS, which blocks insulin-mediated glucose uptake. Notably, eLtaS transgenic mice (eLtaS(trans)) exhibited a metabolic syndrome similar to that observed in patients, including increased food and water consumption, impaired glucose tolerance and decreased hepatic glycogen synthesis. Furthermore, transgenic mice showed significant metabolic differences compared to their wild-type counterparts, particularly for the early insulin resistance marker ot-hydroxybutyrate. We subsequently developed a full human monoclonal antibody against eLtaS that blocked the interaction between eLtaS and insulin, which effectively restored glucose tolerance in eLtaS(trans) and S. aureus-challenged mice. Thus, our results reveal a mechanism for S. aureus-induced insulin resistance.
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