LEPR and colitis: However, activation of ObR is an important pathogenic mechanism of UC, and ObR deficiency may confer resistance to 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis by inhibiting the nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB) and Ras homolog gene family member A (RhoA) signaling pathways [204].