CCKAR

CCKAR (cholecystokinin A receptor, CCK1R) is a class A G protein-coupled receptor that preferentially recognizes sulfated cholecystokinin peptides and functions as a major physiological regulator of pancreatic enzyme secretion, gallbladder contraction, gastrointestinal motility, and satiety signaling^[1]. Mechanistically, CCKAR primarily couples to G_q-dependent signaling pathways, linking nutrient-derived cholecystokinin release to digestive and metabolic responses across the gastrointestinal tract and peripheral nervous system^[1][2]. In experimental and disease-related contexts, CCKAR has been associated with lipid absorption, glucose and energy metabolism, obesity, diabetes, metabolic syndrome, and cholesterol gallstone disease, making the receptor a relevant target for studies of gastrointestinal and metabolic regulation^[2]. Compared with the related isoform CCKBR (CCK2R), which is enriched in the central nervous system and displays high affinity for both gastrin and cholecystokinin peptides, CCKAR is predominantly localized in peripheral digestive tissues and exhibits a marked preference for sulfated CCK ligands^[1][3][4]. This distinction underlies their different physiological functions, with CCKAR primarily mediating digestive and satiety responses, whereas CCKBR contributes more prominently to neurotransmission, anxiety-related behaviors, memory processes, and gastrin signaling^[1][3][4]. For experimental applications, selective CCKAR agonists and antagonists have been widely used to investigate receptor-mediated control of gastrointestinal secretion, gallbladder function, feeding behavior, and metabolic homeostasis^[1][4].