The pivotal relation between glucagon‐like peptides, NFκB and inflammatory bowel disease

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Abstract
Glucagon‐like peptides (GLPs), GLP‐1 and GLP‐2, are released from intestinal enteroendocrine cells (L cells) in response to ingested nutrients. GLP‐1 plays a crucial role in lowering blood glucose and controlling body weight, through stimulating the islet ß cells of pancreas to secrete insulin, inhibiting gastric emptying, and reducing food ingestion. Therefore, GLP‐1 receptor agonists are now used in the treatment of obese patients with type 2 diabetes mellitus (T2DM). GLP‐2, on the other hand, is used as a novel therapy for short bowel syndrome (SBS) through its ability to restore intestinal homeostasis and induce epithelial proliferation. GLPs and the inhibitors of their degradation enzymes, dipeptidyl peptidase‐IV (DPP‐IV) inhibitors, have many anti‐inflammatory actions. Many animal‐based clinical trials have proved that GLP‐based therapy has a pivotal role in the management of inflammatory bowel disease (IBD), possibly through regulating the transcription factor nuclear factor kappa‐ligand B (NFκB). NFκB controls the production and secretion of many cytokines and chemokines encountered in the pathophysiology of IBD such as interleukin (IL‐1β‐IL‐12, IL‐13, IL‐21, IL‐22, IL‐6) and tumour necrosis factor‐alpha (TNF‐α) and hence, may provide a promising therapeutic option.

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