Effect of Sea Buckthorn on Plasma Glucose in Individuals with Impaired Glucose Regulation: A Two-Stage Randomized Crossover Intervention Study.

Sea buckthorn (SB) has been indicated to have hypoglycemic potential, but its effects on glucose in people with impaired glucose regulation (IGR) are still unclear. This work presents a randomized, double-blinded, two-way crossover study. A total of 38 subjects with IGR completed the intervention of consuming sea buckthorn fruit puree (SBFP, 90 mL/day, five weeks), washing out (four weeks), and then consuming placebo (90 mL/day, five weeks) or in reverse order. In our methodology, a unified questionnaire was used to gather information on physical activity and dietary intakes, and physical examinations were performed to measure blood pressure, height, and weight. Fasting blood samples were collected to detect the fasting plasma glucose (FPG) and glycated serum protein (GSP). To calculate the area under the curve of 2 h postprandial plasma glucose (2 h PG-AUC), blood samples at t = 30, 60, and 120 min were also collected and analyzed. Effects of the intervention were evaluated by paired-sample Wilcoxon test and mixed model analyses. Our results show that the FPG in subjects with IGR decreased by a median reduction of 0.14 mmol/L after five weeks' consumption of SBFP, but increased by a median of 0.07 mmol/L after placebo intervention, and the comparison of these two interventions was statistically significant (p = 0.045). During the wash-out period, a similar difference was observed as the FPG decreased in the group that received SBFP intervention first, but increased in another group (p = 0.043). Both SBFP and placebo significantly raised GSP during the intervention period, but lowered it in the wash-out period (p < 0.05), while no significant difference was found between the two interventions. The 2 h PG-AUC remained relatively stable throughout the study. Our results indicated that consumption of SBFP for five weeks showed a slight downward trend on FPG in subjects with IGR.

Association between Dietary Inflammatory Index, C-Reactive Protein and Metabolic Syndrome: A Cross-Sectional Study.

Increased prevalence of metabolic syndrome (MetS) has become a global major public health problem. Chronic low-grade inflammation associated with diet was found to play an import role in the development of MetS, although further studies are needed. The main purpose of this study was to explore the association between the dietary inflammatory index (DII), C-reactive protein (CRP) as a sign of inflammation status, and MetS. A total of 1712 participants from eight cities in China were included. Sociodemographic and health-related information was collected by a self-administrated questionnaire. Anthropometric information and fasting blood samples were collected for identification of MetS. DII scores were computed based on one time 24-h dietary recall. No significant association between MetS and DII was observed except for the blood pressure component of MetS (OR T3 versus T1 = 1.40; 95% CI: 1.03 to 1.89). A significant increased prevalence for MetS was observed for higher CRP (OR = 1.66; 95% CI: 1.26 to 2.18), as well as four out of five of MetS components. In stratified analyses by sex, the associations between DII/CRP and MetS among women, but not men, are comparable to the whole sample. In addition, Both the 2nd and 3rd tertile of the DII had a higher CRP level (β-Coefficients T2 versus T1 = 0.086, 95% CI: 0.004 to 0.167; β-Coefficients T3 versus T1 = 0.145, 95% CI: 0.045 to 0.245) among subjects with MetS. Participants with higher DII scores reported a higher degree of “Shanghuo” (p = 0.007), which is a traditional concept characterized by “redness, swelling, fever and pain” in Chinese Medicine. This study suggested a close association between CRP and MetS, while the association between the DII and MetS was limited. DII was only specifically associated with CRP at a higher level among participants with MetS.

[Expression and purification of mucin 16 and preparation and characterization of anti-mucin 16 monoclonal antibody].

AIM: To generate monoclonal antibodies (mAbs) against mucin 16 using purified recombinant protein of human mucin 16 N terminus with His tag (His-mucin 16N) as the antigen. METHODS: Mucin 16 N terminus was cloned into a prokaryotic expression vector pET-32. His-mucin 16N was then expressed in E.coli and purified by the affinity chromotography. Cell fusion was performed after the BALB/c mice were immunized with the purified His-mucin 16N protein. We screened hybridoma cell strains producing mAbs against mucin 16. The specificity and titer of the antibodies were characterized with ELISA, Western blotting, immunofluorescent and immunohistochemical staining. RESULTS: The recombinant protein of His-mucin 16N was expressed and purified. A few hybridoma cell strains which could secrete specific mAbs against mucin 16 were obtained, and one anti-mucin 16 mAb with good specificity and high titer was selected and purified. The isotype of this anti-mucin 16 mAb was determined as IgG1, which indicated that this anti-mucin 16 mAb could be used for ELISA, Western blotting, immunofluorescent and immunohistochemical staining. The endogenous expression of mucin 16 in various cancer cell lines or tissues was also examined with this anti-mucin 16 antibody by Western blotting and other immunoassays. CONCLUSION: The recombinant protein of His-mucin 16N was expressed and purified successfully, with which we prepared anti-mucin 16 mAb with good specificity and high titer.