Background “Western” style dietary patterns are characterized by a high proportion of highly processed foods rich in fat and low in fiber. This diet pattern is associated with a myriad of metabolic dysfunctions, including neuroinflammation and cognitive impairment. β-glucan, the major soluble fiber in oat and barley grains, is fermented in the lower gastrointestinal tract, potentially impacting the microbial ecosystem and thus may improve elements of cognition and brain function via the gut-brain axis. The present study aimed to evaluate the effect of β-glucan on the microbiota gut-brain axis and cognitive function in an obese mouse model induced by a high-fat and fiber-deficient diet (HFFD). Results After long-term supplementation for 15 weeks, β-glucan prevented HFFD-induced cognitive impairment assessed behaviorally by object location, novel object recognition, and nesting building tests. In the hippocampus, β-glucan countered the HFFD-induced microglia activation and its engulfment of synaptic puncta, and upregulation of proinflammatory cytokine (TNF-α, IL-1β, and IL-6) mRNA expression. Also, in the hippocampus, β-glucan significantly promoted PTP1B-IRS-pAKT-pGSK3β-pTau signaling for synaptogenesis, improved the synaptic ultrastructure examined by transmission electron microscopy, and increased both pre- and postsynaptic protein levels compared to the HFFD-treated group. In the colon, β-glucan reversed HFFD-induced gut barrier dysfunction increased the thickness of colonic mucus (Alcian blue and mucin-2 glycoprotein immunofluorescence staining), increased the levels of tight junction proteins occludin and zonula occludens-1, and attenuated bacterial endotoxin translocation. The HFFD resulted in microbiota alteration, effects abrogated by long-term β-glucan supplementation, with the β-glucan effects on Bacteroidetes and its lower taxa particularly striking. Importantly, the study of short-term β-glucan supplementation for 7 days demonstrated pronounced, rapid differentiating microbiota changes before the cognitive improvement, suggesting the possible causality of gut microbiota profile on cognition. In support, broad-spectrum antibiotic intervention abrogated β-glucan’s effects on improving cognition, highlighting the role of gut microbiota to mediate cognitive behavior. Conclusion This study provides the first evidence that β-glucan improves indices of cognition and brain function with major beneficial effects all along the gut microbiota-brain axis. Our data suggest that elevating consumption of β-glucan-rich foods is an easily implementable nutritional strategy to alleviate detrimental features of gut-brain dysregulation and prevent neurodegenerative diseases associated with Westernized dietary patterns.

A high-fat (HF) diet is a major predisposing factor of neuroinflammation and cognitive deficits. Recently, changes in the gut microbiota have been associated with neuroinflammation and cognitive impairment, through the gut-brain axis. Curdlan, a bacterial polysaccharide widely used as food additive, has the potential to alter the composition of the microbiota and improve the gut-brain axis. However, the effects of curdlan against HF diet-induced neuroinflammation and cognitive decline have not been investigated. We aimed to evaluate the neuroprotective effect and mechanism of dietary curdlan supplementation against the obesity-associated cognitive decline observed in mice fed a HF diet. C57Bl/6J male mice were fed with either a control, HF, or HF with curdlan supplementation diets for 7 days (acute) or 15 weeks (chronic). We found that acute curdlan supplementation prevented the gut microbial composition shift induced by HF diet. Chronic curdlan supplementation prevented cognitive declines induced by HF diet. In addition, curdlan protected against the HF diet-induced abnormities in colonic permeability, hyperendotoxemia, and colonic inflammation. Furthermore, in the prefrontal cortex (PFC) and hippocampus, curdlan mitigated microgliosis, neuroinflammation, and synaptic impairments induced by a HF diet. Thus, curdlan-as a food additive and prebiotic-can prevent cognitive deficits induced by HF diet via the colon-brain axis.

Background: “Western” style dietary patterns are characterised by a high proportion of highly processed foods rich in fat and low in fibre. This diet-pattern is associated with myriad metabolic dysfunctions including neuroinflammation and cognitive impairment. β-glucan, the major soluble fibre in oat and barley grains, are fermented in the lower gastrointestinal tract, potentially impacting the microbial ecosystem and thus may improve elements of the gut-brain axis. The present study aimed to evaluate the effect of β-glucan on the microbiota-gut-brain axis and cognitive function in an obese mouse model induced by a high-fat and fibre deficient diet (HFFD). Results: After chronic supplementation for 15 weeks, β-glucan prevented HFFD diet-induced cognitive impairment assessed behaviourally by object location and nesting building tests. In the hippocampus, β-glucan countered the HFFD-induced microglia activation and its engulfment of synaptic puncta, and up-regulation of proinflammatory cytokine (TNF-α, IL-1β and IL-6) mRNA expression. Also in the hippocampus, β-glucan significantly promoted PTP1B-IRS-pAKT-pGSK3β-pTau signalling for synaptogenesis; improved the synaptic ultrastructure examined by transmission electron microscopy and increased both pre- and post-synaptic protein levels compared to the HFFD-treated group. In the colon, β-glucan reversed HFFD-induced gut barrier dysfunction: increased the thickness of colonic mucus (Alcian blue and mucin-2 glycoprotein immunofluorescence staining); increased the levels of tight junction proteins occludin and zonula occludens-1; and attenuated bacterial endotoxin translocation. The HFFD diet resulted in widespread microbiota dysbiosis, effects abrogated by chronic β-glucan supplementation, with the β-glucan effects on bacteroidetes and its lower taxa particularly striking. Importantly, acute study of β-glucan supplementation for 7 days demonstrated pronounced, rapid differentiating microbiota changes before the cognitive improvement, suggesting the possible causality of gut microbiota profile on cognition. In support, broad-spectrum antibiotic intervention to severely deplete gut microbiota colonisation, eliminated β-glucan’s effects on improving cognition, highlighting the role of gut microbiota to mediate cognitive behavior. Conclusion: This study provides the first evidence that β-glucan improves indices of cognition and brain function with major beneficial effects all along the gut microbiota-brain axis. Our data suggest that elevating consumption of β-glucan-rich foods is an easily implementable nutritional strategy to alleviate detrimental features of gut-brain dysregulation and prevent neurodegenerative diseases associated with Westernized dietary patterns.

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Maturity-onset diabetes mellitus of the young (MODY) is a monogenic diabetes characterized by autosomal dominant inheritance. Its atypical clinical features make diagnosis difficult and it can be misdiagnosed as type 1 or type 2 diabetes. Fourteen subtypes of MODY have been diagnosed so far, of which MODY12 is caused by mutation of the ABCC8 (ATP Binding Cassette Subfamily C Member 8) gene, which is rarely reported in China. This paper reports a Chinese family of MODY12 caused by a rare missense mutation on the ABCC8 gene, which has not been reported to be associated with MODY in China or in other countries, with the aim of increasing clinicians' awareness and attention to the disease.

Background Premature ovarian failure is characterized by amenorrhea, hypoestrogenism, and hypergonadotropinism, and occurs in women under 40 years of age. The prevalence of premature ovarian failure in women younger than 20 years of age is only 0.01%. Immune disorders are one of the causes of premature ovarian failure. Graves’ disease and chronic urticaria are also associated with immune disorders. Case presentation We report a case of a 15-year-old Han Chinese girl with premature ovarian failure complicated by Graves’ disease and chronic urticaria. She experienced menarche at 13 years of age and presented with amenorrhea after 7 months of irregular menstruation. Laboratory examinations indicated hypoestrogenism and hypergonadotropinism. Ultrasound imaging revealed that her uterus and ovaries were small in size. Gene and antibody tests related to premature ovarian failure returned negative results. Both thyroid peroxidase autoantibody and thyrotropin receptor antibody were positive. After reviewing the literature on the relationship between these three diseases and immune disorders, our patient was diagnosed as having atypical autoimmune polyglandular syndrome. After taking small doses of estrogen for 6 months, the size of her uterus increased, and her psychological anxiety was relieved. Conclusions We report a case of an unusual association of premature ovarian failure, Graves’ disease, and chronic urticaria. This case presents an atypical combination of adolescent autoimmune polyglandular syndrome, which is worthy of the attention of clinicians and presents an important lesson for them. Our case highlights that premature ovarian failure in adolescents requires long-term follow-up and medical treatment as well as psychological counselling.

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to misdiagnose, which is worthy of clinicians' attention. Typical clinical symptoms include intrauterine growth retardation, microcephaly, a low auricle, heart defects, seizures, intellectual disability, mental and language disorders, and dysplasia of the corpus callosum (2). While most 21q deletions are associated with other chromosomal abnormalities, the patient in the present study has a rare pure 21q22.3 deletion. At present, the most comprehensive studies about 21q deletion are from Roberson et al. (3) and Lyle et al. (4), who discussed 11 and 10 cases of partial 21q