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Lycium chinense is acknowledged for its substantial nutritional benefits, particularly attributed to the high levels of ascorbic acid (AsA) found in its fruits. The "Mengqi No.1" variety of L. chinense, which is cultivated in Qinghai, is known for its high yield and exceptional quality. We utilized the "Mengqi No.1" variety as experimental materials and combined metabolomic, transcriptomic, and physiological analyses to investigate the metabolites, genes, and enzymes related to AsA metabolism in L. chinense fruits. The results revealed nine differential metabolites associated with AsA metabolism in L. chinense fruits across three stages, including 1D-Myo-Inositol-1,4-Bisphosphate, D-Fructose, L-(+)-Arabinose, I-Inositol, L-Arabinitol, D-Galactose-1-P, lactose, α-D-Glucose, and D-Glucose-6-P. Notably, the contents of D-Glucose-6-P, D-Galactose-1-P, and D-Fructose were increased as the fruit developed. Additionally, fresh weight, longitudinal length, and radial width were increased, while the contents of AsA and DHA were decreased. GalDH and DHAR are critical enzymes for the accumulation of AsA and DHA, exhibiting positive correlation coefficient. Furthermore, PMM1, PMM5, GME2, and GME3 were identified as key regulatory genes in the L-Galactose pathway of AsA synthesis, influencing D-Galactose-1-P, D-Glucose-6-P, α-D-Glucose, and D-Fructose. DHAR1 and DHAR2 are considered key positive regulator genes of AsA and DHA in the AsA-GSH cycle. However, the majority of genes (nine) act as negative regulators of AsA and DHA. These findings provide a foundation for the understanding of the regulatory mechanism of AsA metabolism in L. chinense fruits and offer insights into the utilization of AsA from L. chinense. [ABSTRACT FROM AUTHOR]

The fecal microbiota was studied in patients with inflammatory bowel disease (IBD), and the characteristics of gut microbiota were compared among patients with different subtypes and stages of IBD, aiming to identify the gut microbiota associated with IBD. Methods: Fecal samples were collected from 41 IBD patients (18 patients with ulcerative colitis [UC] and 23 patients with Crohn's disease [CD]) in the Department of Gastroenterology of East China Hospital, Fudan University between January 2021 and January 2022. In addition, fecal samples were collected from 20 healthy volunteers. The fecal microbiota was subjected to 16S rRNA gene sequencing, followed by bioinformatics analysis. Results: There was significant difference in the fecal microbiota between IBD patients and controls. The abundance and diversity of fecal microbiota in the IBD patients were significantly lower than in controls. The relative abundance of Subdoligranulum, Ruminococcus, Anaerostipes and Lachnospira was reduced markedly in the IBD patients. As compared to controls, the relative abundance of Streptococcus increased dramatically in the UC patients. The relative abundance of Lachnoclostridium, Fusobacterium, Cloacibacillus and Erysipelatoclostridium significantly increased in the CD patients. As compared to CD patients, the relative abundance of Alistipes was reduced markedly in the UC patients; the relative abundance of Faecalibacterium, Roseburia and Haemophilus was reduced dramatically in the CD patients. In addition, significant difference was also noted in the fecal microflora between patients with active IBD and those with IBD in remission period. In active IBD patients, the relative abundance of Roseburia, Coprococcus and Ruminiclostridium was reduced significantly. Conclusion: There is intestinal microbiota imbalance in IBD patients, and the abundance of Roseburia, Coprococcus and Ruminiclostridium is reduced significantly in the active period of IBD, which may be related to the active IBD. [ABSTRACT FROM AUTHOR]

Purpose: This study was aimed to study the hypothesis that forkhead box O1 (FOXO1) gene rs17446614 and rs17592236 single nucleotide polymorphisms (SNPs) influenced the development of diabetic nephropathy (DN). Methods: This study included 138 DN patients and 149 healthy controls. Controls were matched with the patients in age and gender. The method of polymerase chain reaction-restriction fragment length polymorphisms (PCR-RFLP) was used to detect FOXO1 gene polymorphisms. Haploview software was conducted to analyze the linkage disequilibrium and haplotypes of FOXO1 gene polymorphisms. Relative risk of DN was expressed by odds ratios (ORs) and 95% confidence intervals (95% CIs), then the results were adjusted by clinical characteristics of the study subjects using logistic regression analysis. Subgroup analysis was performed according to gender. Results: AA genotype of rs17446614 SNPs was significantly associated with the risk of DN (P =.037, adjusted OR = 5.412, 95% CI = 1.103–26.559), especially in female (OR = 8.700, 95% CI = 1.008–75.062, P =.021). FOXO1 rs17446614 A allele positively associated with the development of DN (P =.027, adjusted OR = 1.680, 95% CI = 1.060–2.662), particularly in women (OR = 2.003, 95% CI = 1.070–3.749, P =.028). A-C haplotype formed by FOXO1 gene rs17446614 and rs17592236 SNPs was significantly associated with the increased risk of DN (P =.011, OR = 1.850, 95% CI = 1.146–2.986). Conclusion:FOXO1 gene rs17446614 SNP, and the A-C haplotype of rs17446614 and rs17592236 polymorphisms were risk factors for the development of DN. [ABSTRACT FROM AUTHOR]

Purpose: This study aimed to investigate the role of sclerostin and dkk1 in the bone metabolism of type 2 diabetic patients.Methods: This cross-sectional study included 95 inpatients with type 2 diabetes mellitus. We divided the patients into three groups (i.e., the normal bone mineral density (BMD) group, osteopenia group and osteoporosis group) based on their different BMD levels and measured the serum levels of sclerostin, dkk1, 25-hydroxyvitamin D3(25OHD3), bone turnover markers and other biochemical data in each group.Results: Significantly increased levels of serum sclerostin and dkk1 were found in the osteoporosis group, even when the male and female cohorts were considered separately. Ordinal logistic regression analysis suggested that the levels of serum sclerostin were independently associated with the presence of osteopenia and osteoporosis after adjusting for age, gender and 25OHD3(sclerostin: OR = 1.02,p = 0.001). The areal BMDs were negatively correlated with the levels of serum sclerostin and dkk1 and positively correlated with 25OHD3. In addition, age, glycosylated hemoglobin and serum sclerostin levels were predictors for N-terminal propeptide of type 1 procollagen and serum dkk1 levels were the only predictors for crosslinked carboxyterminal telopeptide in type 1 collagen.Conclusions: The sclerostin and dkk1 levels increased in conjunction with the reduction of BMD, confirming that the Wnts, inhibited by sclerostin and dkk1, were potentially responsible for bone fragility in type 2 diabetes patients with osteoporosis. Note that the serum sclerostin levels were predictors for bone formation, while the DKK1 levels predicted bone resorption. [ABSTRACT FROM AUTHOR]

Secreted protein acidic and rich in cysteines-like protein 1 (SPARCL1) has been implicated in tumor initiation, formation, and progression of various cancers, yet its role in hilar cholangiocarcinoma remains largely uncharacterized. In the present study, tissue microarrays containing resected hilar cholangiocarcinoma specimens from 92 patients were used to evaluate the expression of SPARCL1 protein by immunohistochemistry (IHC). In vitro assays were used to determine the effect of SPARCL1 overexpression on cell growth and migration. Loss of SPARCL1 expression was observed in 46 (50.0 %) of the 92 primary tumors. SPARCL1 expression is inversely associated with poorly or undifferentiation specimens ( P = 0.030) in addition to lymph node metastasis ( P = 0.047). Survival analysis demonstrated that SPARCL1 is an independent factor in predicting the outcome of patients with hilar cholangiocarcinoma. SPARCL1 overexpression suppressed tumor cell migration in vitro by inhibiting MMP-9, MMP-2, Vimentin, and Fibronectin expression, whereas did not inhibit cell proliferation in vitro. Our results suggest that loss of SPARCL1 is involved in the tumorigenesis of hilar cholangiocarcinoma and may serve as a novel molecular biomarker for patients' outcome. [ABSTRACT FROM AUTHOR]

Purpose: This study aimed to investigate the role of sclerostin and dkk1 in the bone metabolism of type 2 diabetic patients. Methods: This cross-sectional study included 95 inpatients with type 2 diabetes mellitus. We divided the patients into three groups (i.e., the normal bone mineral density (BMD) group, osteopenia group and osteoporosis group) based on their different BMD levels and measured the serum levels of sclerostin, dkk1, 25-hydroxyvitamin D3 (25OHD3), bone turnover markers and other biochemical data in each group. Results: Significantly increased levels of serum sclerostin and dkk1 were found in the osteoporosis group, even when the male and female cohorts were considered separately. Ordinal logistic regression analysis suggested that the levels of serum sclerostin were independently associated with the presence of osteopenia and osteoporosis after adjusting for age, gender and 25OHD3 (sclerostin: OR = 1.02, p = 0.001). The areal BMDs were negatively correlated with the levels of serum sclerostin and dkk1 and positively correlated with 25OHD3. In addition, age, glycosylated hemoglobin and serum sclerostin levels were predictors for N-terminal propeptide of type 1 procollagen and serum dkk1 levels were the only predictors for crosslinked carboxyterminal telopeptide in type 1 collagen. Conclusions: The sclerostin and dkk1 levels increased in conjunction with the reduction of BMD, confirming that the Wnts, inhibited by sclerostin and dkk1, were potentially responsible for bone fragility in type 2 diabetes patients with osteoporosis. Note that the serum sclerostin levels were predictors for bone formation, while the DKK1 levels predicted bone resorption. [ABSTRACT FROM AUTHOR]