Hepatic glucokinase regulatory protein and carbohydrate response element binding protein attenuation reduce de novo lipogenesis but do not mitigate intrahepatic triglyceride accumulation in ALDOB deficiency.

OBJECTIVE: Stable isotope studies have shown that hepatic de novo lipogenesis (DNL) plays an important role in the pathogenesis of intrahepatic lipid (IHL) deposition. Furthermore, previous research has demonstrated that fructose 1-phosphate (F1P) not only serves as a substrate for DNL, but also acts as a signalling metabolite that stimulates DNL from glucose. The aim of this study was to elucidate the mediators of F1P-stimulated DNL, with special focus on two key regulators of intrahepatic glucose metabolism, i.e., glucokinase regulatory protein (GKRP) and carbohydrate response element binding protein (ChREBP). METHODS: Aldolase B deficient mice (Aldob-/-), characterized by hepatocellular F1P accumulation, enhanced DNL, and hepatic steatosis, were either crossed with GKRP deficient mice (Gckr-/-) or treated with short hairpin RNAs directed against hepatic ChREBP. RESULTS: Aldob-/- mice showed higher rates of de novo palmitate synthesis from glucose when compared to wildtype mice (p<0.001). Gckr knockout reduced de novo palmitate synthesis in Aldob-/- mice (p=0.017), without affecting the hepatic mRNA expression of enzymes involved in DNL. In contrast, hepatic ChREBP knockdown normalized the hepatic mRNA expression levels of enzymes involved in DNL and reduced fractional DNL in Aldob-/- mice (p<0.05). Of interest, despite downregulation of DNL in response to Gckr and ChREBP attenuation, no reduction in intrahepatic triglyceride levels was observed. CONCLUSIONS: Both GKRP and ChREBP mediate F1P-stimulated DNL in aldolase B deficient mice. Further studies are needed to unravel the role of GKRP and hepatic ChREBP in regulating IHL accumulation in aldolase B deficiency.

PoWRKY69-PoVQ11 module positively regulates drought tolerance by accumulating fructose in Paeonia ostii.

Drought is a detrimental environmental factor that restricts plant growth and threatens food security throughout the world. WRKY transcription factors play vital roles in abiotic stress response. However, the roles of IIe subgroup members from WRKY transcription factor family in soluble sugar mediated drought response are largely elusive. In this study, we identified a drought-responsive IIe subgroup WRKY transcription factor, PoWRKY69, from Paeonia ostii. PoWRKY69 functioned as a positive regulator in response to drought stress with nucleus expression and transcriptional activation activity. Silencing of PoWRKY69 increased plants sensitivity to drought stress, whereas conversely, overexpression of PoWRKY69 enhanced drought tolerance in plants. As revealed by yeast one-hybrid, electrophoretic mobility shift assay, and luciferase reporter assays, PoWRKY69 could directly bind to the W-box element of fructose-1,6-bisphosphate aldolase 5 (PoFBA5) promoter, contributing to a cascade regulatory network to activate PoFBA5 expression. Furthermore, virus-induced gene silencing and overexpression assays demonstrated that PoFBA5 functioned positively in response to drought stress by accumulating fructose to alleviate membrane lipid peroxidation and activate antioxidant defense system, these changes resulted in reactive oxygen species scavenging. According to yeast two-hybrid, bimolecular fluorescence complementation, and firefly luciferase complementation imaging assays, valine-glutamine 11 (PoVQ11) physically interacted with PoWRKY69 and led to an enhanced activation of PoWRKY69 on PoFBA5 promoter activity. This study broadens our understanding of WRKY69-VQ11 module regulated fructose accumulation in response to drought stress and provides feasible molecular measures to create novel drought-tolerant germplasm of P. ostii.

Lipoprotein(a) and Diet: Consuming Sugar-Sweetened Beverages Lowers Lipoprotein(a) Levels in Obese and Overweight Adults.

Lipoprotein(a) [Lp(a)] is a risk factor for cardiovascular disease. A size polymorphism in the apolipoprotein(a) [apo(a)] gene, determined by the number of Kringle (K) repeats, inversely regulates Lp(a) levels. Non-genetic factors including dietary saturated fat influence Lp(a) levels. However, less is known about the effects of carbohydrates including dietary sugars. In this double-blind, parallel-arm study among 32 overweight/obese adults, we investigated the effect of consuming glucose- or fructose-sweetened beverages providing 25% of energy requirements for 10 weeks on Lp(a) level and assessed the role of the apo(a) size polymorphism. The mean (± SD) age of participants was 54 ± 8 years, 50% were women, and 75% were of European descent. At the end of the 10-week intervention, Lp(a) level was reduced by an average (± SEM) of -13.2% ± 4.3% in all participants (p=0.005); by -15.3% ± 7.8% in the 15 participants who consumed glucose (p=0.07); and by -11.3% ± 4.5% in the 17 participants who consumed fructose (p=0.02), without any significant difference in the effect between the two sugar groups. The relative changes in Lp(a) levels were similar across subgroups of lower vs higher baseline Lp(a) level or carrier vs non-carrier of an atherogenic small (≤22K) apo(a) size. In contrast, LDL-C increased. In conclusion, in older, overweight/obese adults, consuming sugar-sweetened beverages reduced Lp(a) levels by ∼13% independently of apo(a) size variability and the type of sugar consumed. The Lp(a) response was opposite to that of LDL-C and triglyceride concentrations. These findings suggest that metabolic pathways might impact Lp(a) levels.

Assessing the impact of concurrent high-fructose and high-saturated fat diets on pediatric metabolic syndrome: A review.

High-saturated fat (HF) or high-fructose (HFr) consumption in children predispose them to metabolic syndrome (MetS). In rodent models of MetS, diets containing individually HF or HFr lead to a variable degree of MetS. Nevertheless, simultaneous intake of HF plus HFr have synergistic effects, worsening MetS outcomes. In children, the effects of HF or HFr intake usually have been addressed individually. Therefore, we have reviewed the outcomes of HF or HFr diets in children, and we compare them with the effects reported in rodents. In humans, HFr intake causes increased lipogenesis, hypertriglyceridemia, obesity and insulin resistance. On the other hand, HF diets promote low grade-inflammation, obesity, insulin resistance. Despite the deleterious effects of simultaneous HF plus HFr intake on MetS development in rodents, there is little information about the combined effects of HF plus HFr intake in children. The aim of this review is to warn about this issue, as individually addressing the effects produced by HF or HFr may underestimate the severity of the outcomes of Western diet intake in the pediatric population. We consider that this is an alarming issue that needs to be assessed, as the simultaneous intake of HF plus HFr is common on fast food menus.

Molecular insight into the potential functional role of pseudoenzyme GFOD1 via interaction with NKIRAS2.

The glucose-fructose oxidoreductase/inositol dehydrogenase/rhizopine catabolism protein (Gfo/Idh/MocA) family includes a variety of oxidoreductases with a wide range of substrates that utilize NAD or NADP as redox cofactor. Human contains two members of this family, namely glucose-fructose oxidoreductase domain-containing protein 1 and 2 (GFOD1 and GFOD2). While GFOD1 exhibits low tissue specificity, it is notably expressed in the brain, potentially linked to psychiatric disorders and severe diseases. Nevertheless, the specific function, cofactor preference, and enzymatic activity of GFOD1 remain largely unknown. In this work, we find that GFOD1 does not bind to either NAD or NADP. Crystal structure analysis unveils that GFOD1 exists as a typical homodimer resembling other family members, but lacks essential residues required for cofactor binding, suggesting that it may function as a pseudoenzyme. Exploration of GFOD1-interacting partners in proteomic database identifies NK-κB inhibitor-interacting Ras-like 2 (NKIRAS2) as one potential candidate. Co-immunoprecipitation (co-IP) analysis indicates that GFOD1 interacts with both GTP- and GDP-bound forms of NKIRAS2. The predicted structural model of the GFOD1-NKIRAS2 complex is validated in cells using point mutants and shows that GFOD1 selectively recognizes the interswitch region of NKIRAS2. These findings reveal the distinct structural properties of GFOD1 and shed light on its potential functional role in cellular processes.

Inducible biosynthesis of bacterial cellulose in recombinant Enterobacter sp. FY-07.

Bacterial cellulose (BC) is an extracellular polysaccharide with myriad unique properties, such as high purity, water-holding capacity and biocompatibility, making it attractive in materials science. However, genetic engineering techniques for BC-producing microorganisms are rare. Herein, the electroporation-based gene transformation and the λ Red-mediated gene knockout method with a nearly 100 % recombination efficiency were established in the fast-growing and BC hyperproducer Enterobacter sp. FY-07. This genetic manipulation toolkit was validated by inactivating the protein subunit BcsA in the cellulose synthase complex. Subsequently, the inducible BC-producing strains from glycerol were constructed through inducible expression of the key gene fbp in the gluconeogenesis pathway, which recovered >80 % of the BC production. Finally, the BC properties analysis results indicated that the induced-synthesized BC pellicles were looser, more porous and reduced crystallinity, which could further broaden the application prospects of BC. To our best knowledge, this is the first attempt to construct the completely inducible BC-producing strains. Our work paves the way for increasing BC productivity by metabolic engineering and broadens the available fabrication methods for BC-based advanced functional materials.

High dietary Fructose Drives Metabolic Dysfunction-Associated Steatotic Liver Disease via Activating ubiquitin-specific peptidase 2/11ß-hydroxysteroid dehydrogenase type 1 Pathway in Mice.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most common cause of chronic liver-related morbidity and mortality. Though high fructose intake is acknowledged as a metabolic hazard, its role in the etiology of MASLD requires further clarification. Here, we demonstrated that high dietary fructose drives MASLD development and promotes MASLD progression in mice, and identified Usp2 as a fructose-responsive gene in the liver. Elevated USP2 levels were detected in the hepatocytes of MASLD mice; a similar increase was observed following fructose exposure in primary hepatocytes and mouse AML12 cells. Notably, hepatocytes overexpressing USP2 presented with exaggerated lipid accumulation and metabolic inflammation when exposed to fructose. Conversely, USP2 knockdown mitigated these fructose-induced changes. Furthermore, USP2 was found to activate the C/EBPα/11ß-HSD1 signaling, which further impacted the equilibrium of cortisol and cortisone in the circulation of mice. Collectively, our findings revealed the role of dietary fructose in MASLD pathogenesis and identified the USP2-mediated C/EBPα/ 11ß-HSD1 signaling as a potential target for the management of MASLD.

Investigation of the relationship between inflammation and microbiota in the intestinal tissue of female and male rats fed with fructose: Modulatory role of metformin.

BACKGROUND: It has been reported that High-Fructose (HF) consumption, considered one of the etiological factors of Metabolic Syndrome (MetS), causes changes in the gut microbiota and metabolic disorders. There is limited knowledge on the effects of metformin in HF-induced intestinal irregularities in male and female rats with MetS. OBJECTIVES: In this study, we investigated the sex-dependent effects of metformin treatment on the gut microbiota, intestinal Tight Junction (TJ) proteins, and inflammation parameters in HF-induced MetS. METHODS: Fructose was given to the male and female rats as a 20% solution in drinking water for 15 weeks. Metformin (200 mg/kg) was administered by gastric tube once a day during the final seven weeks. Biochemical, histopathological, immunohistochemical, and bioinformatics analyses were performed. Differences were considered statistically significant at p < 0.05. RESULTS: The metformin treatment in fructose-fed rats promoted glucose, insulin, Homeostasis Model Assessment of Insulin Resistance Index (HOMA-IR), and Triglyceride (TG) values in both sexes. The inflammation score was significantly decreased with metformin treatment in fructose-fed male and female rats (p < 0.05). Moreover, metformin treatment significantly decreased Interleukin-1 Beta (IL-1ß) and Tumor Necrosis Factor-Alpha (TNF-α) in ileum tissue from fructose-fed males (p < 0.05). Intestinal immunoreactivity of Occludin and Claudin-1 was increased with metformin treatment in fructose-fed female rats. HF and metformin treatment changed the gut microbial composition. Firmicutes/Bacteroidetes (F/B) ratio increased with HF in females. In the disease group, Bifidobacterium pseudolongum; in the treatment group, Lactobacillus helveticus and Lactobacillus reuteri are the prominent species in both sexes. When the male and female groups were compared, Akkermansia muciniphila was prominent in the male treatment group. CONCLUSION: In conclusion, metformin treatment promoted biochemical parameters in both sexes of fructose-fed rats. Metformin showed a sex-dependent effect on inflammation parameters, permeability factors, and gut microbiota. Metformin has partly modulatory effects on fructose-induced intestinal changes.

Inhibitory effect of organogermanium compound 3-(trihydroxygermyl)propanoic acid on fructose-induced glycation of amino compounds.

3-(Trihydroxygermyl)propanoic acid (THGP), a hydrolysate of poly-trans-[(2-carboxyethyl)germasesquioxane] (Ge-132, also known as repagermanium), can inhibit glycation between glucose/ribose and amino compounds. In addition, THGP may inhibit glycation by inhibiting reactions that occur after Amadori rearrangement and inducing the reversible solubilization of AGEs. In this study, we first investigated the effects and mechanisms on the glycation of fructose and amino compounds by THGP, as a greater reactivity was obtained with fructose than with glucose. Unlike other anti-glycation materials, THGP can form a complex with fructose, the initial compound of glycation. THGP also inhibited the production of AGEs and suppressed the reduction of fructose in a reaction between fructose and arginine. These results indicate that THGP forms a complex with cyclic fructose possessing a cis-diol structure at a reducing end, and that it suppresses the ring-opening of fructose and the progress of the initial glycation reaction. We next tried to evaluate the suppressive effect of glucosyl hesperidin (GHes) and THGP on the reaction of glycation between fructose and collagen. Both compounds effectively reduced the production of AGEs individually, and the combination of them led to a synergistic suppression. Therefore, through combination with other antiglycation materials, THGP may cooperatively exhibit glycation-inhibitory effects and be able to suppress the AGE production.

Fructose vs. glucose: modulating stem cell growth and function through sugar supplementation.

In multicellular organisms, stem cells are impacted by microenvironmental resources such as nutrient availability and oxygen tension for their survival, growth, and differentiation. However, the accessibility of these resources in the pericellular environment greatly varies from organ to organ. This divergence in resource availability leads to variations in the potency and differentiation potential of stem cells. This study aimed to explore the distinct effects of glucose and fructose, as well as different oxygen tensions, on the growth dynamics, cytokine production, and differentiation of stem cells. We showed that replacing glucose with fructose subjected stem cells to stress, resulting in increased Hif1α expression and stability, which in turn led to a reduction in cell proliferation, and alterations in cytokine production. However, fructose failed to induce differentiation of human mesenchymal stem cells (hMSCs) as well as mouse fibroblasts into mature adipocytes compared to glucose, despite the upregulation of key markers of adipogenesis, including C/EBPß, and PPARγ. Conversely, we showed that fructose induced undifferentiated mouse fibroblasts to release cytokines associated with senescence, including IL1α1, IL6, IL8, MCP1, and TNF1α, suggesting that these cells were undergoing lipolysis. Taken together, our results suggest that altering the culture conditions through changes in hexose levels and oxygen tension places considerable stress on stem cells. Additional research is required to further characterize the mechanisms governing stem cell response to their microenvironments.

A High-Fat and High-Fructose Diet Exacerbates Liver Dysfunction by Regulating Sirtuins in a Murine Model.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is rapidly emerging as the most prevalent chronic liver disease, closely linked to the escalating rates of diabesity. The Western diet's abundance of fat and fructose significantly contributes to MASLD, disrupting hepatic glucose metabolism. We previously demonstrated that a high-fat and high-fructose diet (HFHFD) led to increased body and liver weight compared to the low-fat diet (LFD) group, accompanied by glucose intolerance and liver abnormalities, indicating an intermediate state between fatty liver and liver fibrosis in the HFHFD group. Sirtuins are crucial epigenetic regulators associated with energy homeostasis and play a pivotal role in these hepatic dysregulations. Our investigation revealed that HFHFD significantly decreased Sirt1 and Sirt7 gene and protein expression levels, while other sirtuins remained unchanged. Additionally, glucose 6-phosphatase (G6Pase) gene expression was reduced in the HFHFD group, suggesting a potential pathway contributing to fibrosis progression. Chromatin immunoprecipitation analysis demonstrated a significant increase in histone H3 lysine 18 acetylation within the G6Pase promoter in HFHFD livers, potentially inhibiting G6Pase transcription. In summary, HFHFD may inhibit liver gluconeogenesis, potentially promoting liver fibrosis by regulating Sirt7 expression. This study offers an epigenetic perspective on the detrimental impact of fructose on MASLD progression.

A Case Study of a Rare Disease (Fructosemia) Diagnosed in a Patient with Abdominal Pain.

Hereditary fructose intolerance is a rare genetic disorder that is inherited in an autosomal recessive manner, with mutations sometimes occurring spontaneously. Consuming fructose triggers biochemical abnormalities, disrupting liver processes like glycogenolysis and gluconeogenesis. Recent studies have revealed elevated intrahepatic fat levels in affected individuals. Symptoms include aversion to fructose-containing foods, hypoglycemia, liver and kidney dysfunction, and growth delays, with severe cases leading to liver enlargement, fatty liver disease, kidney failure, and life-threatening hypoglycemia. In this case study, we present a 20-month-old child with symptoms including difficulty passing stool, abdominal rigidity, abdominal pain with bloating and hypoglycemia. Initial clinical findings revealed elevated liver enzymes, a mildly enlarged hyperechoic liver, hypercholesterolemia, and borderline alpha-fetoprotein values. Diagnostic assessments identified hereditary fructose intolerance (HFI) with pathogenic variants in the ALDOB gene, along with a diagnosis of celiac disease. Genetic testing of the parents revealed carrier status for pathological aldolase B genes. This case underscores the importance of comprehensive clinical evaluation and genetic testing in pediatric patients with complex metabolic presentations.

Effects of Liquid Fructose Supplementation and Chronic Unpredictable Stress on Uterine Contractile Activity in Nonpregnant Rats.

Increased fructose consumption and chronic stress, the major characteristics of modern lifestyle, impact human health; however, the consequences of their combination on the uterus remain understudied. In this study, we investigated contractile activity, morphology, and intracellular activity of antioxidant enzymes in uteri from virgin Wistar rats subjected to liquid fructose supplementation and/or unpredictable stress over 9 weeks. Contractile activity and uterine response to oxytocin or adrenaline were examined ex vivo using isolated bath chambers. Fructose supplementation, irrespective of stress, affected uterine morphology by increasing endometrium while decreasing myometrium volume density, attenuated uterine response to increasing doses of oxytocin, and increased glutathione peroxidase activity. Stress, irrespective of fructose, attenuated dose-dependent adrenaline-induced uterine relaxation. Stress, when applied solely, decreased mitochondrial superoxide dismutase activity. In the combined treatment, irregular estrous cycles and both reduced response to oxytocin and to adrenaline (as a consequence of fructose consumption and exposure to stress), along with fructose-related alteration of uterine morphology, were detected. In conclusion, fructose and stress affect uterine contractile activity, irrespective of each other, by inducing completely distinct responses in isolated uteri. In the combined treatment, the effects of both factors were evident, suggesting that the combination exerts more detrimental effects on the uterus than each factor individually.

Nutrient Composition and Quality Assessment of Royal Jelly Samples Relative to Feed Supplements.

Royal jelly is a substance secreted by the hypopharyngeal and mandibular glands of nurse honey bees, serving as crucial nutritional source for young larvae, queen honey bees, and also valuable product for humans. In this study, the effect of the feed supplements on the nutritional composition and qualities of royal jelly was investigated. Two types of royal jelly samples were acquired: one from honey bees fed with sugar syrup as a feed supplement and the other from honey bees fed with honey. The production, harvesting, and storage of all royal jelly samples followed standard procedures. Parameters for quality assessment and nutritional value, including stable carbon isotopic ratio, moisture content, 10-hydroxy-2-decenoic acid (10-HDA) level, carbohydrate composition, amino acid composition, and mineral contents, were analyzed. The results revealed that despite variability in moisture content and carbohydrate composition, fructose was lower (2.6 and 4.1 g/100 g as is for sugar-fed and honey-fed royal jelly, respectively) and sucrose was higher (7.5 and 2.7 g/100 g as is for sugar-fed and honey-fed royal jelly, respectively) in the sugar-fed group. The stable isotope ratio (-16.4608‱ for sugar-fed and -21.9304‱ for honey-fed royal jelly) clearly distinguished the two groups. 10-HDA, amino acid composition, and total protein levels were not significantly different. Certain minerals, such as potassium, iron, magnesium, manganese, and phosphorus were higher in the honey-fed group. Hierarchical analysis based on moisture, sugar composition, 10-HDA, and stable carbon isotopes categorized the samples into two distinct groups. This study demonstrated that the feed source could affect the nutritional quality of royal jelly.

GFPT2 expression is induced by gemcitabine administration and enhances invasion by activating the hexosamine biosynthetic pathway in pancreatic cancer.

Our previous studies revealed a novel link between gemcitabine (GEM) chemotherapy and elevated glutamine-fructose-6-phosphate transaminase 2 (GFPT2) expression in pancreatic cancer (PaCa) cells. GFPT2 is a rate-limiting enzyme in the hexosamine biosynthesis pathway (HBP). HBP can enhance metastatic potential by regulating epithelial-mesenchymal transition (EMT). The aim of this study was to further evaluate the effect of chemotherapy-induced GFPT2 expression on metastatic potential. GFPT2 expression was evaluated in a mouse xenograft model following GEM exposure and in clinical specimens of patients after chemotherapy using immunohistochemical analysis. The roles of GFPT2 in HBP activation, downstream pathways, and cellular functions in PaCa cells with regulated GFPT2 expression were investigated. GEM exposure increased GFPT2 expression in tumors resected from a mouse xenograft model and in patients treated with neoadjuvant chemotherapy (NAC). GFPT2 expression was correlated with post-operative liver metastasis after NAC. Its expression activated the HBP, promoting migration and invasion. Treatment with HBP inhibitors reversed these effects. Additionally, GFPT2 upregulated ZEB1 and vimentin expression and downregulated E-cadherin expression. GEM induction upregulated GFPT2 expression. Elevated GFPT2 levels promoted invasion by activating the HBP, suggesting the potential role of this mechanism in promoting chemotherapy-induced metastasis.

Spirulina (Arthrospira platensis) Improved Nonalcoholic Fatty Liver Disease Characteristics and Microbiota and Did Not Affect Organ Fibrosis Induced by a Fructose-Enriched Diet in Wistar Male Rats.

Spirulina (Arthrospira platensis) is reported to play a role in improving nonalcoholic fatty liver disease (NAFLD) and intestinal microbiota (IM). To study spirulina's effects in the improvement of NAFLD characteristics, IM, and pancreatic-renal lesions induced by a fructose-enriched diet, 40 Wistar healthy male rats, weighing 200-250 g, were randomly divided into four groups of 10, and each rat per group was assigned a diet of equal quantities (20 g/day) for 18 weeks. The first control group (CT) was fed a standardized diet, the second group received a 40% fructose-enriched diet (HFr), and the third (HFr-S5) and fourth groups (HFr-S10) were assigned the same diet composition as the second group but enriched with 5% and 10% spirulina, respectively. At week 18, the HFr-S10 group maintained its level of serum triglycerides and had the lowest liver fat between the groups. At the phylae and family level, and for the same period, the HFr-S10 group had the lowest increase in the Firmicutes/Bacteroidetes ratio and the Ruminococcaceae and the highest fecal alpha diversity compared to all other groups (p < 0.05). These findings suggest that at a 10% concentration, spirulina could be used in nutritional intervention to improve IM, fatty liver, metabolic, and inflammatory parameters associated with NAFLD.

Muscle-specific lack of GFPT1 in knock-in mice triggers ER stress to alleviate misfolded proteins.

Pathogenic variants in GFPT1, encoding a key enzyme to synthesize UDP-N-acetylglucosamine (UDP-GlcNAc), cause congenital myasthenic syndrome (CMS). We made a knock-in (KI) mouse model carrying a frameshift variant in Gfpt1 exon 9 simulating a CMS patient. As Gfpt1 exon 9 is exclusively included in striated muscles, Gfpt1-KI mice were deficient for Gfpt1 only in skeletal muscles. In Gfpt1-KI mice, (i) UDP-HexNAc, CMP-NeuAc, and protein O-GlcNAcylations were reduced in skeletal muscles; (ii) aged Gfpt1-KI mice showed poor exercise performance and abnormal neuromuscular junction structures; and (iii) markers for unfolded protein response (UPR) were elevated in skeletal muscles. Denervation-mediated enhancement of ER stress in Gfpt1-KI mice facilitated protein folding, ubiquitin-proteasome degradation, and apoptosis, whereas autophagy was not induced and protein aggregates were markedly increased. Lack of autophagy was accounted for by enhanced degradation of FoxO1 by increased Xbp1-s/u proteins. Similarly, in Gfpt1-silenced C2C12 myotubes, ER stress exacerbated protein aggregates and activated apoptosis, but autophagy was attenuated. In both skeletal muscles in Gfpt1-KI mice and Gfpt1-silenced C2C12 myotubes, maladaptive UPR failed to eliminate protein aggregates and provoked apoptosis.

Gongronella sp. w5 hydrolyzes plant sucrose and releases fructose to recruit phosphate-solubilizing bacteria to provide plants with phosphorus.

The mechanisms of how plant-beneficial rhizospheric fungi interact with the soil microbial community to promote plant growth by facilitating their phosphorus acquisition are poorly understood. This work supported that a Mucoromycotina fungus, Gongronella sp. w5 (w5), could promote phosphorus uptake of Medicago truncatula by increasing the available phosphorus (P) in the soil. The abundance of phosphate-solubilizing bacteria (PSB) and the activity of alkaline phosphatase (ALP) in alfalfa rhizosphere soil increased after w5 inoculation. Further analysis showed that w5 donated a portion of ALP activity and also stimulated the PSB to secrete ALP during plant-w5-PSB interaction to help release more available P in the rhizosphere of M. truncatula. Unlike most plant-beneficial rhizospheric fungi that mainly acquire hexoses from plants, w5 gained sucrose directly from the host plant and then recruited PSB to aid P acquisition by hydrolyzing sucrose and releasing mainly fructose to induce PSB to secrete ALP. IMPORTANCE: This work supported that after absorbing plant sucrose, Gongronella sp. w5 mainly releases sucrose hydrolysis product fructose into the environment. Fructose was used as a carbon source and signaling molecules to induce PSB to co-produce higher alkaline phosphatase activity, releasing soil-available phosphorus and promoting M. truncatula growth. This is the first report that plant-beneficial fungi could directly metabolize sucrose from plants and then recruit PSB to aid P acquisition by providing fructose. Our findings revealed the diversity in pathways of plant-fungi-PSB interactions on soil P acquisition and deepened our understanding of the cooperation of growth-promoting microorganisms in plant rhizosphere.

Tapioca-starch-based bionanocomposites with fructose and titanium dioxide for food packaging and fertilization applications.

Bionanocomposites offer a promising solution to the plastic waste crisis. Although tapioca starch shows potential as a bioplastic material, it is characterized by low mechanical properties, poor thermal stability, and high water absorption owing to its hydrophilic nature. To increase the flexibility of the material and reduce the transmission rate of oxygen and water vapor, additives such as fructose and titanium dioxide (TiO2) can be incorporated into the material. TiO2 nanoparticles are commonly utilized in agriculture to enhance nutrient release and promote plant growth. In this study, X-ray diffraction analysis revealed that TiO2 reduced crystal size while increasing the crystallinity of bionanocomposites. Fourier-transform infrared spectroscopy analysis revealed an absorption peak at 3397 cm-1, indicating hydrogen bonding between TiO2 and starch-OH groups, and a peak at 773 cm-1, indicating an increase in the intensity of Ti-O-Ti stretching vibrations with the incorporation of TiO2. Water absorption rate results confirmed that TiO2 addition enhanced bionanocomposite resistance to water vapor and moisture, evidenced by increased tensile strength from 0.11 to 0.49 MPa and Young's modulus from 2.48 to 5.26 MPa, as well as decreased elongation at break from 21.46 % to 2.36 % in bionanocomposites with TiO2. Furthermore, with TiO2 addition, the biodegradation rate of the bionanocomposites decreased, which is beneficial for enhancing plant nutrient content.

A fluorescent NBD "turn-on" probe for the rapid and on-site analysis of fructose in food.

High fructose intake is an important cause of metabolic disease. Due to the increasing prevalence of metabolic diseases worldwide, the development of an accurate and efficient tool for monitoring fructose in food is urgently needed to control the intake of fructose. Herein, a new fluorescent probe NBD-PQ-B with 7-nitrobenz-2-oxa-1, 3-diazole (NBD) as the fluorophore, piperazine (PQ) as the bridging group and phenylboronic acid (B) as the recognition receptor, was synthesized to detect fructose. The fluorescence of NBD-PQ-B increased linearly at 550 nm at an excitation wavelength of 497 nm with increasing fructose concentration from 0.1 to 20 mM. The limit of detection (LOD) of fructose was 40 µM. The pKa values of NBD-PQ-B and its fructose complexes were 4.1 and 10.0, respectively. In addition, NBD-PQ-B bound to fructose in a few seconds. The present technique was applied to determine the fructose content in beverages, honey, and watermelon with satisfactory results. Finally, the system could not only be applied in an aqueous solution with a spectrophotometer, but also be fabricated as a NBD-PQ-B/polyvinyl oxide (PEO) film by electrospinning for on-site food analysis simply with the assistance of a smartphone.