Figure 2.

A, image of Caenorhabditis elegans and schematic magnification of the intestinal epithelium. The nematode's head faces to the top and arrowheads mark the intestinal lumen. The scheme focuses on epithelial cells with the basolateral side to the left and the apical side to the right side. B, interplay of peptide transporter PEPT-1 and sodium–proton exchanger NHX-2 in enterocytes. Ba, in the wild-type situation, both proteins are active in the apical membrane and stabilize amino acid homeostasis and intracellular pH (pHin). Bb, loss of PEPT-1 protein stops the peptide and proton influx, leading to lower intracellular amino acid concentrations and an increase in pHin. Uptake of fatty acids via the fatty acid flip–flop mechanism is supported and induces obesity. Bc, when NHX-2 is missing, proton export stops and pHin decreases. Uptake of fatty acids via the flip–flop mechanism is decreased, leading to nematodes with empty body fat depots.