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Glucose homeostasis of adipocytes could be regulated by immune-adipose crosstalk. In order to investigate the effects of Lymphotoxin-like inducible protein that competes with glycoprotein D for herpesvirus entry on T cells (LIGHT) on glucose metabolism, we performed the present study. Our results showed that LIGHT deficiency improved glucose tolerance and enhanced glucose consumption of inguinal white adipose tissue (iWAT) under high fat diet. Consistently, Light overexpression could inhibit glucose uptake during the process of white adipogenesis. Mechanistically, LIGHT interacted with lymphotoxin-β receptor (LTβR) to attenuate AKT pathway leading to downregulation of glucose transporter-4 (GLUT4) expression, which resulted in glucose uptake inhibition. In summary, our findings revealed LIGHT-LTβR-AKT-GLUT4 axis as a regulator of glucose uptake in adipose tissue, which suggested the pivotal role of LIGHT in maintaining glucose homeostasis.

In this work, a new N-halamine precursor with two epoxy groups, 1,3-bis(2,3-epoxypropyl)-s-triazine-2,4,6-trione (BETT), was synthesized and used to enhance the compatibility between poly(lactic acid) (PLA) and poly (butylene adipate-co-terephthalate) (PBAT). The rheological analysis and GPC indicated that chain extension between PLA and PBAT occurred during the melt-blending in the presence of BETT. The PLA/PBAT chain extensions improved the compatibility between PLA and PBAT and hindered the crystallization of PLA. SEM images showed that PLA/PBAT blend gradually changed from the typical sea-island phase without BETT to a co-continuous structure with increase in amount of BETT. This showed that the interfacial compatibility between PLA and PBAT improved significantly on addition of BETT. Moreover, compared to PLA/PBAT blend, the mechanical properties of PLA/PBAT/BETT blends showed great improvement. Furthermore, the chlorinated PLA/PBAT/BETT sheets displayed excellent antibacterial activities against E. coli (CMCC 44103) and S. aureus (ATCC 6538) cultures, wherein the sheets with 17.5 ± 0.8 μg/cm2 of the active chlorine could kill all inoculated bacteria within 30 min.

It is considered that intestinal barrier dysfunction and systemic endotoxemia drive obesity and its related complications. However, what causes barrier dysfunction remains to be elucidated. Here, we showed that the gut microbiota from high-fat diet (HFD)-fed mice had impaired ability to degrade dietary flavonoids, and in correspondence, the microbial-derived flavonoid metabolite desaminotyrosine (DAT) was reduced. Supplementation of DAT in the drinking water was able to counter the HFD-induced body fat mass accumulation and body weight increment. This is correlated with the role of DAT in maintaining mucosal immune homeostasis to protect barrier integrity. DAT could attenuate dextran sodium sulfate (DSS)-induced mucosal inflammation in a type I interferon signal-dependent manner. Furthermore, intraperitoneal injection of DAT-protected mice from bacterial endotoxin-induced septic shock. Together, we identified DAT as a gut microbiota-derived anti-inflammatory metabolite that functions to modulate local and systemic immune homeostasis. Our data support the notion of dysbiosis being an important driving force of mucosal barrier dysfunction and systemic metabolic complications.

FTL10 is an early-flowering mutant of rice (Oryza sativa L.) with a premature senescent phenotype. Early leaf senescence can cause negative effects on rice yield. Moreover, rice leaves are damaged under high-light conditions, which promote rice senescence. Artificial shading can reduce the amount of light absorbed by rice leaves. The aim of this study was to investigate the effects of shading at noon (11:30–14:00) on the senescence and yield of FTL10. The results showed that shading improved the total antioxidant capacity of rice leaves, reduced the accumulation of reactive oxygen species (ROS) and reduced the expression of genes related to senescence. In the shaded group, the degradation rate of chlorophyll and Rubisco proteins, which are related to photosynthesis, was relatively slow, and the photosynthetic rate was relatively high. Compared with those under the natural growth conditions, the proportion of photosynthetic electron allocated to photorespiration in the shaded group rice leaves was lower, and the proportion allocated to carbon fixation was higher. The yield data showed that the single-spike weight and yield per plant of rice significantly increased after shading. Therefore, our research shows that shading at noon could delay FTL10 senescence and increase yields.

Efficient capture of radioactive iodine (129I, 131I) is of great significance in spent fuel treatment. In this paper, a new adsorbent named Catechin@ACF was successfully prepared through interface assembly of specific recognition gripper with plant polyphenols (catechin) on activated collagen fiber (ACF), and the catechin membrane with specific grip on iodine was successfully constructed on the surface of ACF. The results showed that the adsorbent assembled catechin membrane was rich in aromatic rings, hydroxyl groups and imine adsorption sites, and possessed specific recognition and capture characteristics of iodine. Moreover, the as-prepared Catechin@ACF showed excellent capture capacity for iodine vapor and iodine in organic solution with the maximum capture capacity of 2122.68 mg/g and 258.29 mg/g, respectively. In iodine-cyclohexane solution, the adsorption process was in according with the Pseudo first order kinetic and Langmuir isothermal model. In addition, the specific recognition and capture mechanism analysis indicated that the aromatic rings, phenolic hydroxyl groups and imine groups in the catechin membrane were the specific and effective grippers for iodine, and finally iodine formed a stable conjugated system with the adsorbent in the form of I- and I3-. Therefore, the as-prepared specific iodine capturer Catechin@ACF was expected to play a vital role in the capture of radioactive iodine in spent fuel off-gas because of its specific recognition, high capture capacity, large-scale preparation, and environment-friendly.

Immune and nervous system sensing are two important ways of detecting inner and outer environmental changes. Immune cell activation in the gut can promote metabolic disorders. However, whether enteric nervous system sensing and activities are also important in metabolic syndromes is not clear. Enteric glial cells (EGCs) are thought to have sensing ability, but little is known about the potential connections between EGC and metabolic disorders. Consuming a modern Western-type high-fat low-fiber diet increases the risk of obesity. Here, we reported that dietary shift from a normal chow diet to a high-fat diet in wild-type (WT) C57BL/6 mice induced a transient emergence of glial fibrillary acidic protein (GFAP)-positive EGC network in the ileal lamina propria, accompanied by an increase of glial-derived neurotrophic factors production. Inhibition of EGC metabolic activity via gliotoxin fluorocitrate or glial-intrinsic deletion of myeloid differentiation factor 88 (Myd88) in mice blocked this dietary change-induced activity. Furthermore, we found a different role of MYD88 in glial cells versus adipocyte in diet-induced obesity. The glial Myd88 knockout mice gained less body weight after HFD feeding compared to the littermate controls. In contrast, adipocyte deletion of Myd88 in mice had no impact on the weight gain but had exacerbated glucose metabolic disorders. Pharmacological interventions of glial activities by fluorocitrate prevented body weight gain in a dietary type- and glial MYD88-independent manner. Collectively, our data reveal a previously unappreciated function of EGC in sensing a dietary shift-induced perturbation and glial activities as a whole may play roles in diet-induced obesity.New & NoteworthyIt is known that obesity and its related metabolic syndrome can damage the neuronal system. However, whether the neuronal system also participates in the development of obesity is unclear. Diet is an important contributing factor to obesity. Our study reveals that consuming a high-fat diet can induce a transient enteric glial cell response via its intrinsic sensing molecule(s). Inhibiting overall glial cell activities may have an impact on the development of the metabolic syndrome.

The physiologic signals that regulate beige adipogenesis remain incompletely understood, especially those that limit browning and prevent overexpenditure of energy. In this study, the TNF family member cytokine lymphotoxin-like inducible protein that competes with glycoprotein D for herpesvirus entry on T cells (LIGHT), also known as TNF super family protein 14 (TNFSF14), can inhibit adipose precursor differentiation into beige adipocytes. In acute cold stress, LIGHT deficiency in mice accelerated browning in the subcutaneous white adipose tissue (scWAT). Further experiments showed that LIGHT interacting with lymphotoxin-β receptor (LTβR) on adipose precursors blocked beige fat biogenesis. LTβR signals attenuated the JNK pathway, which contributed to their antibeiging effect. Blocking JNK activation using a small molecular inhibitor prevented cold-induced scWAT beiging. Furthermore, LIGHT/LTβR signals acted as an attenuator of white adipogenesis. LIGHT deficiency in mice promoted obesity during high-fat diet feeding. These findings identify the LIGHT axis as a regulator of adipose tissue homeostasis and suggest that LIGHT signaling functions as a mechanism to divert energy in favor of immune activation.-Kou, Y., Liu, Q., Liu, W., Sun, H., Liang, M., Kong, F., Zhang, B., Wei, Y., Liu, Z., Wang, Y. LIGHT/TNFSF14 signaling attenuates beige fat biogenesis.

The efficient capture of radioactive iodine (I-129, I-131) and radon (Rn-222) is crucial to the development of nuclear energy in spent fuel treatment. Herein, we successfully synthesized a new type of three-dimensional hydrolyzed collagen aerogel immobilized with catechin (Catechin@3DCF aerogel) as an effective adsorbent to remove iodine and radon through enzymatic hydrolysis, dialysis, freeze-drying, immobilization, and cross-linking. The as-prepared adsorbent was systematically characterized by FE-SEM, EDX, FT–IR, and XPS, showing that the adsorbent possesses ultra-high porosity, high content flake structure, and abundant adsorption sites on the surface of adsorbent. The results show that Catechin@3DCF aerogel exhibited excellent capture capacity for iodine and radon, with the maximum capture capacity of 222.67 wt% (88.5 wt% for 3DCF aerogel) and 44,877.9 Bq/Kg, respectively. Through the active group-shielding experiment analysis, the phenolic hydroxyl groups on the surface of adsorbent played a major role in iodine capture, followed by the -NHR group. In addition, mechanism studies have shown that the capture of iodine is mainly by chemical adsorption, while the capture of radon is mainly through physical adsorption, which is related to the numerous mesopores and flake structure of the adsorbent. Furthermore, Catechin@3DCF aerogel still maintains excellent adsorption capacity for iodine and radon under 60Co γ-ray irradiation at a total dose ranging from 10 to 350 kGy, indicating that it has excellent radiation resistance stability. Advantages such as novelty, ultra-high porosity, high-radiation stability, ultra-high capture capacity, environment-friendly, and low-cost indicate that biomass-derived Catechin@3DCF aerogel plays a role in the capture of radioactive iodine and radon from airborne effluents.

The conformation and stability of zein in solution are closely associated with its solvation process and influence the mechanical properties of the related zein-based materials. In this work, a common solvent dimethyl sulfoxide (DMSO) was used to dissolve zein, rather than solvents frequently used such as aqueous ethanol and acetic acid. It was found that DMSO could dissolve zein readily and the solution was stable for at least 2 weeks. Rheological analysis and small-angle X-ray scattering (SAXS) were employed to characterize the zein DMSO solution. Results of rheological analysis suggested a Huggins coefficient of 0.24, indicating DMSO to be a good solvent for zein. SAXS results revealed that zein adopted an elongated conformation and had dimensions of 2.8 nm × 2.8 nm × 14.8 nm in DMSO solution. Moreover, robust zein films were fabricated from zein DMSO solutions. The content of residual DMSO in the films was determined to be approximately 15 wt % by thermogravimetric analysis, in consistence with the value obtained by other two methods. The film showed a large breaking strain of 320.6% with a considerable breaking stress of 1.9 MPa, yielding a breaking energy of 376.2 MJ/m3. Therefore, the ease of dissolution and good mechanical performance of the final zein-based material make DMSO a potential solvent for fabrication of zein materials, thereby improving the scope of practical applications of zein.

Injury to the biliary epithelium triggers cholangiopathies. However, factors involved in regulating the pathogenesis remains incompletely understood. Here, we report that the gut microbiota is important in regulating hepatobiliary fibroproliferative regenerative process. In helminth Clonorchis sinensis-induced bile duct injury model, wild-type mice showed more extensive peribiliary fibroproliferative responses than non-littermate IL-33-deficient mice. However, these reactions could be attenuated by co-housing of the animals together. In the meantime, the relatively fibroproliferative-resistant IL-33-deficient mice could become fibroproliferative-responsive especially in large intrahepatic bile duct by antibiotics treatment. Furthermore, microbiota-derived metabolite butyrate was able to inhibit biliary organoid expansion in vitro and temper 3,5-diethoxycarbonyl-1,4-dihydrocollidine-induced biliary fibrosis in vivo. Together, our data implies a potential way of management of hepatobiliary diseases by modulating gut microbiota.

In this study, the structural characterization of Sphallerocarpus gracilis polysaccharide (SGP) and its hypoglycaemic activities are reported for the first time. SGP, which has a weight average molar mass (Mw) of 7.413×105, was isolated from Sphallerocarpus gracilis and purified by ion-exchange chromatography. The polysaccharide is composed of rhamnose, arabinose, mannose, glucose and galactose, with the molar ratio of 4.12: 8.99: 5.45: 65.94: 15.50. The mechanism underlying the hypoglycaemic effect of SGP was evaluated. Experimental results showed that SGP protected pancreatic β-cells from alloxan damage by several possible mechanisms, including: (1) repairing free radical damage; (2) reducing the apoptosis of pancreatic β-cells by inhibiting the activities of caspase-3 and bax, and enhancing the activity of bcl-2; (3) stimulating insulin secretion and upregulating the pancreatic and duodenal homeobox 1 gene and the insulin gene and the pancreatic in pancreatic β-cells. The results obtained in this study suggest that SGP may be a promising therapeutic agent in the treatment of diabetes mellitus.

The pH-sensitive hydrogels composed of sodium caseinate (SC) and N,O-carboxymethyl chitosan (NOCC) were prepared and a new method to characterize the gelation process was presented in this work. Reological tests suggested that RSC/NOCC=3/7 (the weight ratio of SC and NOCC) was the best ratio of hydrogel. The well-developed three-dimensional network structures in the hydrogel were confirmed by AFM. Two structural parameters, tIS and tCS, denoted as the initial and critical structure formation time, respectively, were used to provide an exact determination of the start of structure formation and description of gelation process. The gelation process strongly depended on temperature changes, a high temperature resulted in an early start of gelation. The non-kinetic model suggested the higher activation energy in the higher temperatures was disadvantageous to structure formation, and vice versa. Due to the smart gel reported here was very stable at room temperature, we believed that the gel is required for applications in drug delivery or could be exploited in the development of potential application as molecular switches in the future.

Sphallerocarpus gracilis (S. gracilis) is a little-investigated edible plant and used as traditional Chinese medicine. In this study, polysaccharide extracted from S. gracilis,deproteined and purified. The polysaccharide (SGP) was chemically modified to obtain its sulfated derivatives (S-SGP) using the method of chlorosulfonic acid/pyridine (CSA/Pyr). In order to acquire the derivative with the highest degree of substitution (DS), the optimum conditions of the sulfation were obtained based on response surface design (RSD), and the structural characterizations and antioxidant properties of the S-SGP were comparatively investigated by Fourier transform infrared spectrometry (FT-IR), GC-MS analysis, size exclusion chromatography (SEC), and DPPH radical assay, hydroxyl radical assay, superoxide radical assay, and reducing power assay, respectively. Results showed that the modification was successful, and obtained the optimum combination of conditions. Compared with SGP, the sulfated polysaccharide with relatively the decreased degree of molecular weight (Mw) but the same composition of monosaccharides exhibited better antioxidant activities in DPPH, hydroxyl, superoxide radical and reducing power assay. These results indicated that the antioxidant activities in vitro of the S-SGP from S. gracilis may be related to combined effects of Mw, monosaccharide composition, and sulfate content.

The heterotrimeric G protein subunit Gsα couples receptors to activate adenylyl cyclase and is required for the intracellular cAMP response and protein kinase A (PKA) activation. Gsα is ubiquitously expressed in many cell types; however, the role of Gsα in neural crest cells (NCCs) remains unclear. Here we report that NCCs-specific Gsα knockout mice die within hours after birth and exhibit dramatic craniofacial malformations, including hypoplastic maxilla and mandible, cleft palate and craniofacial skeleton defects. Histological and anatomical analysis reveal that the cleft palate in Gsα knockout mice is a secondary defect resulting from craniofacial skeleton deficiencies. In Gsα knockout mice, the morphologies of NCCs-derived cranial nerves are normal, but the development of dorsal root and sympathetic ganglia are impaired. Furthermore, loss of Gsα in NCCs does not affect cranial NCCs migration or cell proliferation, but significantly accelerate osteochondrogenic differentiation. Taken together, our study suggests that Gsα is required for neural crest cells-derived craniofacial development.