Does tLR4 Expression by Liver Resident Cells mediate the Development of Glucose Intolerance and Insulin Resistance in Experimental Periodontitis?
We observed that GFPWT:WT, but not GFPWT:KO chimeras, treated with LPS developed GI/IR despite similar degrees of gingival inflammation, circulating cytokine levels, and LPS concentrations. We conclude that LPS from periodontitis sites has a pivotal role in triggering the development of GI/IR through a mechanism that involves TLR4 expression by resident macrophages/Kupffer cells in the liver.
Visibility of the LSW on B mode appears to be a better indicator than other structures for M1 evaluation.