Crocin stimulates insulin secretion via the activation of K+ and Ca2+ channels, and inhibits carbohydrate digestion and absorption, and DPPH

This study investigated crocin’s role in promoting insulin secretion and explored the underlying mechanisms involved. Insulin secretory effects of crocin were assessed in a perfused rat pancreas. To investigate the pathways involved in insulin release, experiments were conducted with 11 mM glucose, 50 μM verapamil, 8 mM diazoxide, and 200 μM IBMX. Sucrose malabsorption was measured in six GI tract segments of rats after administering an oral sucrose load. Glucose absorption was evaluated through in situ intestinal perfusion (from duodenum to 40 cm); in vitro starch digestion using α-amylase and α-glucosidase enzymes and glucose diffusion via a cellulose ester dialysis membrane. Crocin’s antioxidant potential was tested through DPPH radical inhibition assays. Gastrointestinal motility was assessed using the BaSO4 milk transit test. Crocin induced a fourfold rise in insulin secretion in the perfused rat pancreas. Crocin, combined with 11 mM glucose, significantly increased insulin release. Insulin secretion induced by crocin was significantly reduced by diazoxide (KATP opener) and verapamil (Ca²+ channel blocker), indicating involvement of glucose metabolism, calcium signaling, and KATP channels. Insulin release was not increased by crocin in the presence of IBMX, suggesting a mechanism independent of the adenylate cyclase–cAMP signaling pathway. Crocin reduced glucose absorption and increased residual sucrose levels in the intestine after oral administration. It also decreased glucose absorption during in situ intestinal perfusion with glucose and in the in vitro glucose diffusion assay. Significant enhancement in gut motility was also observed. Crocin lowered glucose release from starch digestion in vitro and demonstrated antioxidant activity by inhibiting DPPH.