The Function and\nMechanism of Laminaripentaose Prepared\nfrom Curdlan for the Amelioration of the Cognitive Dysfunctions in\nObese Mice

Functional oligosaccharides induce\nspecific alterations in gut\nmicrobiota, potentially providing physiological benefits. However,\nthe effects of laminaripentaose (LPA) on metabolic syndrome and the\nmechanism underlying it have not been intensively investigated yet.\nThis study aimed to determine the effects of LPA on obesity and obesity-induced\ncognition impairment in mice. C57BL/6N mice fed with a high-fat diet\nreceived an LPA treatment for 12 weeks. An antibiotic intervention\nwas further applied to evaluate the effects of the gut microbiota\non cognitive functions. LPA treatment (500 mg/kg) reduced the weight\ngain by 32.4%. Furthermore, LPA improved memory functions and reduced\nhippocampal insulin resistance and neuronal injury. LPA markedly reduced\nsystemic low-grade inflammation and intestinal barrier injury. Moreover,\nLPA increased gut beneficial bacteria, and <i>Butyricimonas</i> and <i>Bifidobacterium</i> were increased by 94.0 and\n422.7%, respectively, accompanied by increased fecal short-chain fatty\nacids. Interestingly, antibiotic cocktail treatment abrogated the\nbeneficial effects of LPA on cognition, which further suggests that\nLPA may attenuate obesity-induced cognition impairment via the gut-brain\naxis. Our findings provide the first evidence for the potential of\ndietary LPA to prevent obesity and obesity-associated complications.