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Increased fructose intake is an international issue. A maternal high-fructose diet during gestation and lactation could affect nervous system development in offspring. Long non-coding RNA (lncRNA) plays an important role in brain biology. However, the mechanism whereby maternal high-fructose diets influence offspring brain development by affecting lncRNAs is still unclear. Here, we administered 13% and 40% fructose water to establish a maternal high-fructose diet model during gestation and lactation. To determine lncRNAs and their target genes, full-length RNA sequencing was performed using the Oxford Nanopore Technologies platform, and 882 lncRNAs were identified. Moreover, the 13% fructose group and the 40% fructose group had differentially expressed lncRNA genes compared with the control group. Enrichment analyses and co-expression analyses were performed to investigate the changes in biological function. Furthermore, enrichment analyses, behavioral science experiments, and molecular biology experiments all indicated that the fructose group offspring showed anxiety-like behaviors. In summary, this study provides insight into the molecular mechanisms underlying maternal high-fructose diet-induced lncRNA expression and co-expression of lncRNA and mRNA. [ABSTRACT FROM AUTHOR]

Increased fructose over-intake is a global issue. Maternal fructose exposure during gestation and lactation can impair brain development in offspring. However, the effect on synapses is still unknown. For the diversification of RNA and biological functions, alternative splicing (AS) and alternative polyadenylation (APA) are essential. We constructed a maternal high-fructose diet model by administering 13% and 40% fructose water. The student's t-test analyzed the results of RT-qPCR. All other results were analyzed by one-way analysis of variance. The animal behavior experiment results revealed that conditioning and associative memory had been damaged. The proteins that form synapses were consistently low-expressed. In addition, compared with the control group, the Oxford Nanopore Technologies platform's full-length RNA-sequencing identified 298 different spliced genes (DSGs) and 51 differentially expressed alternative splicing (DEAS) genes in the 13% fructose group. 313 DSGs and 74 DEAS genes were in the 40% fructose group. Enrichment analysis based on these altered genes revealed some enlightening items and pathways. Our findings demonstrated the transcriptome mechanism underlying maternal fructose exposure during gestation and lactation and impaired synapse function during the transcripts' editing. • Maternal high-fructose diet impairs offspring's synapse development. • Maternal high-fructose diet changes offspring's alternative splicing events. • Maternal high-fructose diet changes offspring's alternative polyadenylation sites. • Synaptic proteins are significantly enriched and low-expressed. [ABSTRACT FROM AUTHOR]

Increased fructose intake is a global issue, especially in mothers. Maternal fructose exposure during gestation and lactation can affect learning and memory in offspring; however, the detailed mechanism is still unknown. The hippocampus is a mind locale liable for learning and memory. Here, we established a maternal high-fructose diet model by administering 13% and 40% fructose water, applied the Morris Water Maze test on postnatal day 60 offspring, and performed full-length RNA sequencing using the Oxford Nanopore Technologies platform to explore the changes in gene expression in the hippocampus. The results showed that learning and memory in offspring were negatively affected. Compared with the control group, 369 differentially expressed transcripts (DETs) were identified in the 13% fructose group, and 501 DETs were identified in the 40% fructose group. Gene Ontology enriched term and Kyoto Encyclopedia of Genes and Genomes enriched pathway analyses identified several terms and pathways related to brain development and cognitive function. Furthermore, we confirmed that the Wnt/β-catenin signaling pathway was down-regulated and neuron degeneration was enhanced. In summary, our results indicate that maternal fructose exposure during gestation and lactation can impair learning and memory in offspring and affect brain function at the transcriptome level. • Maternal high-fructose diet impairs offspring learning and memory. • Maternal high-fructose diet induces offspring's hippocampus neurons degeneration. • Maternal high-fructose diet affects differential expression in transcriptome-wide. • Wnt/β-catenin signaling pathway is significantly enriched and expression changed. [ABSTRACT FROM AUTHOR]

The influences of bran components and glucose oxidase on the gluten development and water distribution in bread dough were investigated. Two major bran components, such as cellulose and arabinoxylan (AX), were included in the dough formula, and exogenous ferulic acid (FA) was also added together with AX. GOX was included in both straight grade flour (SGF) dough and bran components containing dough. Bran components reduced the dough density and interfered protein polymerization in bread dough. AX caused more deterioration in gluten development than cellulose owing to its higher water competing ability with gluten. Inclusion of free FA induced a weaker gluten network probably because of its accelerating effect of dough breakdown. Moreover, GOX improved dough porosity and increased dough development time and stability. GOX stabilized protein secondary structure by increasing α-helix and β-sheet conformation and enhanced water availability to gluten by promoting the proportion of less-tightly bound water. Cellulose resulted in smaller enhancement of dough strength after GOX addition, for instance, half of the increase in dough stability compared to AX. Briefly, AX showed more interference with gluten formation than cellulose. Although the function was disturbed in bran component containing dough, GOX still improved the strength and structure of gluten. • Bran components and glucose oxidase (GOX) were added into bread dough formula. • Bran components resulted in decreased dough porosity and reduced protein aggregation. • Arabinoxylan caused more deterioration in gluten formation than cellulose. • Free ferulic acid induced an even weaker gluten probably by reducing dough tolerance. • GOX enhanced dough stability and structures by promoting disulfide bonds formation. [ABSTRACT FROM AUTHOR]