Beneficial Effects of Dietary Flaxseed Oil through Inflammation Pathways and Gut Microbiota in Streptozotocin-Induced Diabetic Mice.

Flaxseed oil (FO) has displayed potential anti-diabetes properties by providing a high content of α-linolenic acid. However, the effects and mechanisms of FO on type 1 diabetes are still unclear. The present study aims to explore the effects of different doses of FO feeding on hepatic inflammation and gut microbiota in streptozotocin-induced diabetic mice. Forty-eight six-week-old C57BL/6J male mice were divided into a control group (CON), a diabetic group (MOD), a diabetes with 7.0% w/w FO feeding group (FO-L), and a diabetes with 10.5% w/w FO feeding group (FO-H) for six weeks. The 7.0% w/w and 10.5% w/w FO feeding groups exhibited potential recovery of the number and size of pancreas tissues. The fasting blood glucose level was significantly decreased only after 4 weeks of feeding with 10.5% w/w FO in diabetic mice. The 10.5% w/w FO feeding group significantly decreased the postprandial blood glucose level of mice in the OGTT test. Hepatic glycogen levels were dramatically upregulated in the mice fed with both 7.0% w/w and 10.5% w/w FO. FO feeding significantly attenuated hepatic LPS, TNF-α, and IL-1ß levels. In addition, we observed that 7.0% w/w and 10.5% w/w FO feedings notably downregulated hepatic gene and protein expressions of TLR4, MyD88, and P65. Furthermore, only 10.5% FO regulated fecal microbiota by increasing the relative abundance of the Bacteroidetes phylum, Lactococcus family, and Muribaculaceae and Streptococcaceae family and genus in streptozotocin-induced diabetic mice. Therefore, we conclude that FO feeding plays a role in anti-inflammation via the regulation of hepatic LPS/TLR4/MyD88 pathways and gut microbiota. In addition, different doses of FO supplementation may exhibit varying mechanisms in streptozotocin-induced mice.

Reversible Macrocycle-to-Macrocycle Interconversion Driven by Solvent Selection.

Macrocycle-to-macrocycle interconversions are of interest because they can allow access to a variety of structures. However, reversible interconversion between different sized macrocycles remains challenging to control. Herein, we report a facile one-pot synthesis of a series of self-assembled macrocycles from readily prepared α,α'-linked oligopyrrolic dialdehydes and various alkyl diamines. The condensation of pyridine-bridged oligopyrrolic dialdehyde 3 and simple alkyl diamines proved independent of solvent, always yielding the [2 + 2] macrocyclic products. However, when 3 was condensed with 2,2'-oxybis(ethylamine) 14, either ([1 + 1] or [2 + 2]) products are obtained depending on the choice of solvent. Reaction of 3 and 14 in methanol, ethanol, or chloroform gave the [1 + 1] macrocycle as the sole product. In contrast, condensation of 3 and 14 in dimethyl sulfoxide (DMSO), N,N-dimethylformamide (DMF), or acetonitrile (MeCN) yielded the [2 + 2] macrocycle as the major product in the form of a precipitate. Reversible interconversion between the [1 + 1] and [2 + 2] macrocycles could be achieved by tuning the solvent, with the ratio driven by thermodynamic and solubility considerations.

[Effects of the mannose, the major component of Lycium barbarum polysaccharides, and its potential target metabolite inositol on mouse ß-TC6 cells].

OBJECTIVE: To investigate the effects of mannose, the major component of Lycium barbarum polysaccharide, and its potential target metabolite, inositol, on mouse islet ß-TC6 cells. METHODS: Different concentrations(0, 4. 6875, 9. 375, 18. 75, 37. 5, 75 and 150 µg/mL) of mannose or inositol were used to intervene ß-TC6 cells for 24 hours, and the proliferation activity of cells was determined by CCK-8 method. Enzyme-linked immunosorbent assay was used to detect insulin secretion after the intervention of the ß-TC6 cells from different concentration of the mannose or inositol(0, 18. 75, 75 and 150 µg/mL) combining with glucose stimulation(20 mmol/L) for 60 minutes. Pioglitazone(3. 92 mg/L) was set up as positive group, and after intervention of the mannose or inositol(0, 9. 375, 18. 75, 75 and 150 µg/mL) for 24 h, the expression levels of insulin, glucose kinase(GK), glucose transporter 4(GLUT4) and glycogen synthase(GS) mRNA were detected by real-time quantitative PCR. RESULTS: Compared with the control group, mannose and inositol promoted the proliferation of ß-TC6 cells in a concentration-dependent manner(18. 75-150 µg/mL)(P<0. 05). Although the inositol solution of 4. 6875 µg/mL and 9. 375 µg/mL had a tendency to promote cell proliferation, there was no statistical difference(P>0. 05). After stimulation with 20 mmol/L glucose combining with different intervention concentrations(18. 75, 75 and 150 µg/mL) of mannose or inositol, no significant difference was observed in the insulin secretion of each group(P>0. 05) comparing with the control group. RT-qPCR result showed that 150 µg/mL mannose increased the expression level of GLUT4(P<0. 01) and the expression levels of GK and GLUT4 genes in the 75 µg/mL inositol group were significantly increased(P<0. 01). The expression level of GLUT4 was improved only when the concentration was decreased to 18. 75 µg/mL in inositol group(P<0. 01). CONCLUSION: Mannose and inositol can improve the expression of GLUT4 mRNA, which may help to increase glucose uptake by peripheral cells. In addition, inositol can improve insulin sensitivity and glucose metabolism by increasing the expression level of GK mRNA.

The Evidence and Controversy Between Dietary Calcium Intake and Calcium Supplementation and the Risk of Cardiovascular Disease: A Systematic Review and Meta-Analysis of Cohort Studies and Randomized Controlled Trials.

Objective: Our objective was to synthesize both trial and observational studies and undertake a meta-analysis to explore the associations between calcium from dietary and supplemental intakes and cardiovascular disease (CVD) risks.Methods: Data sources were from PubMed, Cochrane Central, Scopus, and Web of Science, published from the inception dates up to March 2019. Randomized controlled trials (RCTs) and prospective cohort studies with data on dietary or supplemental intake of calcium, with or without vitamin D, and cardiovascular outcomes, were included.Results: Of the 1,212 identified studies, 26 prospective cohort studies and 16 RCTs were included. Results of cohort studies reveled that dietary calcium intakes (DCIs) ranging from 200 to 1500 mg/d did not affect the risk of CVD, coronary heart disease (CHD), and stroke (relative risk (RR) RR for CVD = 0.96, 95% CI, 0.87-1.05; RR for CHD = 0.98, 95% CI, 0.88-1.08; RR for stroke = 0.94, 95% CI, 0.85-1.04). Pooled RR of RCTs showed that the risk of CHD due to calcium supplements (CSs) increased 8% (RR = 1.08, 95% CI, 1.02-1.22; I2 = 0.0%) and increased 20% allocated to CSs alone (RR = 1.20, 95% CI, 1.08-1.33; I2 = 0.0%). CSs increased the risk of myocardial infarction (MI) by 14% (RR = 1.14, 95% CI, 1.05-1.25; I2 = 0.0%), and CSs alone increased the MI risk 21% (RR = 1.21, 95% CI, 1.08-1.35; I2 = 0.0%).Conclusions: We concluded that calcium intake from dietary sources do not adequately increase the risk of CVD including CHD and stroke, while calcium supplements might raise CHD risk, especially MI.