Quantifying the Effect of Supplementation with Algae and Its Extracts on Glycolipid Metabolism: A Meta-Analysis of Randomized Controlled Trials.

AIMS: The effect of algae and its extract supplementation on glycolipid metabolism has not been finalized. Therefore, the purpose of the meta-analyses was to assess the effects of its supplementation on glycolipid metabolism concentration. METHODS: We have systematically searched PubMed, Web of Science, the Cochrane Library and Embase to identify randomized controlled trials (RCTs) that investigated the impact of algae and its extracts supplementation on glycolipid metabolism. Effect size analysis was performed using weighted mean difference (WMD) and 95% CI between the methods of the experiment group and the control group. Subgroup analyses were performed to explore the possible influences of study characteristics. Publication bias and sensitivity analysis were also performed. RESULTS: A total of 27 RCTs (31 trials) with 1221 participants were finally selected for the meta-analysis. The algae and its extract intervention significantly decreased glycosylated hemoglobin (HbA1c, WMD = -0.18%; 95% CI: -0.27 to -0.10; p < 0.001), high-density lipoprotein cholesterol (HDL-C, WMD = -0.22 mmol/L; 95% CI: -0.38 to -0.06; p = 0.008), and triglycerides (TC, WMD = -0.31 mmol/L; 95% CI: -0.37 to -0.25; p < 0.001) levels and increased insulin (WMD = 6.05 pmol/mL; 95% CI: 4.01 to 8.09; p < 0.001) levels. It did not significantly change the blood glucose, homeostasis model assessment-insulin resistance index (HOMA-IR), 2-h post-meal blood glucose (2hPBG) and other lipid profiles. Subgroup analyses based on the duration of intervention and subjects demonstrated that the intervention of algae and its extracts for 10 weeks or fewer and more than 40 subjects decreased TC levels (p < 0.05). Moreover, the intervention reduced TC and 2hPBG concentrations for East Asians (p < 0.05). CONCLUSIONS: Our findings provided evidence that algae and its extract interventions were beneficial for the regulation of human glycolipid metabolism. More precise RCTs on subjects are recommended to further clarify the effect of algae, seaweed polysaccharide, seaweed polypeptide, algae polyphenol and its products intervention on glycolipid metabolism.

[Changes in the antioxidant level, cell cycle progression and apoptosis of testicular cells in rats with diet-induced impaired glucose regulation].

OBJECTIVE: To detect the changes of the antioxidant level, cell cycle progression, necrosis and apoptosis, calcium ion concentration ([Ca2+] i) and mitochondrial membrane potential (deltapsim) in the model rats of impaired glucose regulation (IGR) induced by long-range high-fat diet, and to explore IGR-induced male reproductive injury and its mechanisms. METHODS: Forty male Wistar rats were randomly divided into a normal control (n = 10) and an IGR model group (n = 30), and the IGR model was established by 20 weeks of long-range high-fat diet. Pathological changes in the rat spermatogenic cells were detected by HE staining; the content of malondialdehyde (MDA) and activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) were measured with biochemical methods; changes in the cell cycle progression, necrosis and apoptosis were determined using flow cytometry with propidium iodide (PI) dyeing and the Annexin V-FITC kit, respectively, and [Ca2+]i and deltapsim were detected by flow cytometry with Fluo-3 and Rhodamine probe labeling, respectively. RESULTS: After 20 weeks of continuous high-fat diet, fasting blood glucose was kept at 6.1 - 7.0 mmol/L and blood glucose at 7.8 - 11.1 mmol/L after 2 h glucose load in 12 rats, with a 40% success rate of modeling. Lots of dividing spermatocytes and spermatids were seen in the tissue sections of the normal control rats under the microscope, but few or none in the IGR models. Compared with the normal controls, the IGR model rats showed remarkably increased MDA content and decreased SOD, CAT and GSH-Px activities in the testis tissue (P < 0.05 or P < 0.01) , reduced G0/G1 cells and increased G2/M cells (P < 0.05 or P < 0.01), decreased necrotic cells and increased apoptotic cells (P < 0.05 or P < 0.01), increased [Ca2+]i and decreased deltapsim (P < 0.01), but no significant changes in the percentages of S cells and normal cells. CONCLUSION: IGR can cause spermatogenic cell division disorder in rats, which may be attributed to increased oxidative damage, decreased antioxidant enzyme activities, G2/M phase arrest, [Ca2+]i elevation, deltapsim reduction, and apoptosis of testicular cells.