The Function and Mechanism of Laminaripentaose Prepared from Curdlan for the Amelioration of the Cognitive Dysfunctions in Obese Mice

Functional oligosaccharides induce specific alterations in gut microbiota, potentially providing physiological benefits. However, the effects of laminaripentaose (LPA) on metabolic syndrome and the mechanism underlying it have not been intensively investigated yet. This study aimed to determine the effects of LPA on obesity and obesity-induced cognition impairment in mice. C57BL/6N mice fed with a high-fat diet received an LPA treatment for 12 weeks. An antibiotic intervention was further applied to evaluate the effects of the gut microbiota on cognitive functions. LPA treatment (500 mg/kg) reduced the weight gain by 32.4%. Furthermore, LPA improved memory functions and reduced hippocampal insulin resistance and neuronal injury. LPA markedly reduced systemic low-grade inflammation and intestinal barrier injury. Moreover, LPA increased gut beneficial bacteria, and <i>Butyricimonas</i> and <i>Bifidobacterium</i> were increased by 94.0 and 422.7%, respectively, accompanied by increased fecal short-chain fatty acids. Interestingly, antibiotic cocktail treatment abrogated the beneficial effects of LPA on cognition, which further suggests that LPA may attenuate obesity-induced cognition impairment via the gut-brain axis. Our findings provide the first evidence for the potential of dietary LPA to prevent obesity and obesity-associated complications.