84 CD14 is known to facilitate uptake of LPS, a function that might be independent of TLR4. 85 This implies that LPS is capable of enhancing its own uptake by promoting production of TNF-α ...

Furthermore, liver, but not whole-body, insulin resistance was detected in LPS-infused mice. CD14 mutant mice resisted most of the LPS and high-fat diet-induced features of metabolic diseases.

LPS receptor-deleted mice (i.e., CD14 mutants) are hypersensitive to insulin, and the occurrence of insulin resistance, obesity, and diabetes is delayed in response to high-fat feeding.