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. 2022 Jan 25;12:833544. doi: 10.3389/fendo.2021.833544

Figure 2.

Figure 2

Specific and diverse roles of IECs in HFD-induced metabolic disease. The roles of intestinal epithelial cells (IECs) in body weight gain and glucose homeostasis can be categorized into immune crosstalk/chemokine signaling (90), pathways involving the endocannabinoid system (166), pathways involving microbial metabolites (167, 168) and signaling pathways related to LPS signaling (63, 66, 124). While most pathways exerted adverse effects on glucose metabolism and weight gain in response to HFD feeding, IEC specific knockout of CCL2 and MyD88 decreased body weight gain and improved glucose metabolism during high-fat diet feeding (90, 124). CCL2 and MyD88 knockout improved intestinal barrier function by increasing claudin 1 levels and decreased expression of inflammatory cytokines, respectively (highlighted in red). AMPs, antimicrobial peptides; CCL2, C-C motif chemokine ligand 2; HDAC3, histone deacetylase 3; HFD, high fat diet; IAP, intestinal alkaline phosphatase; IDO, Indolamine 2;3-dioxygenase; IEC, intestinal epithelial cells; KO, knockout; LPS, lipopolysaccharides; Mφ, macrophages; MyD88, myeloid differentiation primary response gene 88; NAPE PLD, N-acylphosphatidylethanolamine phospholipase D; POMC, pro-opiomelanocortin; SCFA, short chain fatty acids; TLR4, toll-like receptor 4; Treg, regulatory T cells.