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The cereal formula powder, Zhengda Jingshan (ZDJS), comprises dietary fiber, multivitamins, fine protein, and various cereal ingredients. The present study evaluated the effects of ZDJS on glucose metabolism and explored the corresponding mechanisms in terms of modulating gut microbiota and the fecal metabolome. Type 2 diabetic db/db mice were given ZDJS (1 g/kg) orally twice daily for 55 days, after which glucose metabolism, inflammation, gut microbiota, and fecal metabolomics were assayed. Repeated administration of ZDJS was associated with a trend toward decreasing fasting blood glucose and a 0.12% decrease in hemoglobin A1c (HbA1c), as well as statistically significant increases in the insulin sensitivity index and decreases in serum levels of tumor necrosis factor (TNF‐α) and ileum expression of mucin‐2. ZDJS also ameliorated the compensatory enlargement of islets and decreased the ratio of the α‐cell area to total islet area; however, this amelioration of impaired oral glucose tolerance became less pronounced as treatment continued. In addition, ZDJS remarkably decreased the abundance of phylum Proteobacteria and the phylum ratio of Firmicutes to Bacteroidetes, as well as altered the fecal metabolic profile. Taken together, our findings demonstrate that ZDJS improved glucose metabolism and reduced inflammation in type 2 diabetic db/db mice, which may be associated with a reshaping of the gut microbiome and fecal metabolome in db/db mice. Thus, our study suggests that ZDJS may represent a complementary therapy for patients with type 2 diabetes. [ABSTRACT FROM AUTHOR]

Prior research has documented a relationship between narcissism and aggression but has focused only on dispositional narcissism without considering situational factors that may increase narcissism temporarily. This study explored the possibility that an increase in state narcissism would foster aggressive responding by increasing anger and hostile attributional bias following unexpected provocation among 162 college students from China. We created a guided-imagination manipulation to heighten narcissism and investigated its effects on anger, aroused hostile attribution bias, and aggressive responses following a provocation with a 2 (narcissism/neutral manipulation) × 2 (unexpected provocation/positive evaluation condition) between-subjects design. We found that the manipulation did increase self-reported state narcissism. The increase in state narcissism in turn heightened aggression, and this relation was mediated by increased anger. Regardless of the level of state narcissism, individuals were more aggressive after being provoked and this effect of provocation was mediated by hostile attributional bias. The findings indicate that narcissism can be temporarily heightened in a nonclinical sample of individuals, and that the effect of state narcissism on aggression is mediated by anger. Differences between state and trait narcissism and possible influences of culture are discussed. Aggr. Behav. 42:333-345, 2016. © 2015 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Aim: Non‐alcoholic fatty liver is the most common cause of chronic liver disease. GPR40 is a potential therapeutic target for energy metabolic disorders. GPR40 is a potential therapeutic target for energy metabolic disorders. SZZ15‐11 is a newly synthesized GPR40 agonist. In this study, we estimate the potency of SZZ15‐11 in fatty liver treatment. Methods: In vivo, diet‐induced obese (DIO) mice received SZZ15‐11 (50 mg/kg) and TAK875 (50 mg/kg) for 6 weeks. Blood glucose and lipid, hepatocyte lipid and liver morphology were analysed. In vitro, HepG2 cells and GPR40‐knockdown HepG2 cells induced with 0.3 mM oleic acid were treated with SZZ15‐11. Triglyceride and total cholesterol of cells were measured. At the same time, the AMPK pathway regulating triglycerides and cholesterol esters synthesis was investigated via western blot and quantitative polymerase chain reaction in both liver tissue and HepG2 cells. Results: SZZ15‐11 was found to not only attenuate hyperglycaemia and hyperlipidaemia but also ameliorate fatty liver disease in DIO mice. At the same time, SZZ15‐11 decreased triglyceride and total cholesterol content in HepG2 cells. Whether examined in the liver of DIO mice or in HepG2 cells, SZZ15‐11 upregulated AMPKα phosphorylation and then downregulated the expression of the cholesterogenic key enzyme 3‐hydroxy‐3‐methylglutaryl coenzyme A reductase and inhibited acetyl‐CoA carboxylase activity. Furthermore, SZZ15‐11 promotes AMPK activity via [cAMP]i accumulation. Conclusion: This study confirmed that SZZ15‐11, a novel GPR40 agonist, improves hyperlipidaemia and fatty liver, partially via Gs signalling and the AMPK pathway in hepatocytes. [ABSTRACT FROM AUTHOR]

Reciprocal self‐disclosure has reportedly been associated with increased interpersonal trust. However, existing research mainly focuses on online disclosure between acquaintances and overlooks the types of reciprocal disclosure, especially in the initial interactions between strangers communicating online. This study aimed to investigate how three types of reciprocal self‐disclosure (turn‐taking reciprocity, extended reciprocity and non‐reciprocity) contribute to trust and the mechanism of positive interpersonal liking, and whether any effect was instant and stable or increased across two interactions during computer‐mediated communication (CMC). Participants were assigned to one of the three reciprocal disclosure conditions and engaged in online interactions. Self‐reported and behavioural results demonstrated higher levels of interpersonal trust and liking in the second interaction phase than in the first across all conditions. The turn‐taking reciprocity condition showed higher interpersonal trust than did the extended condition, and higher interpersonal liking than did the extended and non‐reciprocity conditions; this effect was apparent in both interactions. These findings help us understand the relationship between online self‐disclosure and interpersonal trust, suggesting that certain patterns of communication with strangers (e.g., turn‐taking reciprocity) may foster more positive social outcomes during CMC over time, while demonstrating the importance of immediacy in synchronous conversations. [ABSTRACT FROM AUTHOR]

The effects of the combination of bis (α‐furancarboxylato) oxovanadium (IV) (BFOV) and metformin (Met) on hepatic steatosis were investigated in high‐fat diet‐induced obese C57BL/6J mice (HFC57 mice) for 6 weeks. Oral glucose tolerance test was performed to evaluate glucose metabolism. Moreover, blood and hepatic biochemical and histological indices were detected. Besides, Affymetrix‐GeneChip analysis and Western blot of the liver were performed. Comparing to the monotherapy group, BFOV + Met showed more effective improvement in glucose metabolism, which decreased the fasting blood glucose, insulin levels and improved insulin sensitivity in HFC57 mice. BFOV + Met significantly decreased serum ALT and AST activities and reduced hepatic triglyceride content and iNOS activities, accompanied by ameliorating intrahepatic fat accumulation and hepatocellular vacuolation. Enhanced hepatic insulin signalling transduction and attenuated inflammation pathway were identified as the major pathways in the BFOV + Met group. BFOV + Met significantly down‐regulated the protein expression levels of MMPs, NF‐κB, iNOS and up‐regulated phosphorylation of AKT and AMPK levels. We concluded that a combination of BFOV and metformin ameliorates hepatic steatosis in HFC57 mice via alleviating hepatic inflammation and enhancing insulin signalling pathway, suggesting that the combination of BFOV and metformin is a potential treatment for hepatic steatosis. [ABSTRACT FROM AUTHOR]

Aims: To evaluate a novel tetrahydroisoquinoline derivative YR4‐42 as a selective peroxisome proliferator‐activated receptor γ (PPARγ) modulator (SPPARM) and explore its anti‐diabetic effects in vitro and in vivo. Materials and methods: Using two standard full PPARγ agonists rosiglitazone and pioglitazone as controls, the PPARγ binding affinity and transactivation action of YR4‐42 were evaluated using biochemical and cell‐based reporter gene assays. The capacity of YR4‐42 to recruit coactivators of PPARγ was also assessed. The effects of YR4‐42 on adipogenesis and glucose consumption and PPARγ Ser273 phosphorylation were investigated in 3T3‐L1 adipocytes. The effects of YR4‐42 and pioglitazone, serving as positive control, on glucose and lipids metabolism were investigated in high‐fat diet‐induced obese (DIO) C57BL/6J mice. The expression of PPARγ target genes involved in glucose and lipid metabolism was also assessed in vitro and in vivo. Results: In vitro biochemical and cell‐based functional assays showed that YR4‐42 has much weaker binding affinity, transactivation, and recruitment to PPARγ of the coactivators thyroid hormone receptor‐associated protein complex 220 kDa component (TRAP220) and PPARγ coactivator 1‐α (PGC1α) compared to full agonists. In 3 T3‐L1 adipocytes, YR4‐42 significantly improved glucose consumption without a lipogenesis effect, while blocking tumour necrosis factor α‐mediated phosphorylation of PPARγ at Ser273, thereby upregulating the expression of the PPARγ Ser273 phosphorylation‐dependent genes. Furthermore, in DIO mice, oral administration of YR4‐42 ameliorated the hyperglycaemia, with a similar insulin sensitization effect to that of pioglitazone. Importantly, YR4‐42 also improved hyperlipidaemia‐associated hepatic steatosis without weight gain, which avoids a major side effect of pioglitazone. Thus, YR4‐42 appeared to selectively modulate PPARγ responses. This finding was supported by the gene expression analysis, which showed that YR4‐42 selectively targets PPARγ‐regulated genes mapped to glucose and lipid metabolism in DIO mice. Conclusions: We conclude that YR4‐42 is a novel anti‐diabetic drug candidate with significant advantages compared to standard PPARγ agonists. YR4‐42 should be further investigated in preclinical and clinical studies. [ABSTRACT FROM AUTHOR]