TLR4 and Insulin resistance: Chronic inflammation originating in the gut—exemplified by lipopolysaccharide (LPS) leakage—can infiltrate adipose depots via TLR4-dependent activation of resident macrophages, triggering local cytokine production that induces adipose insulin resistance and disrupts adipokine secretion, which have been suggested to promote adipose browning and to activate the TLR4–NF-κB pathway in adipose macrophages, but robust human evidence for these effects is lacking [95,96].