Effect of dietary supplementation with multinutrient soy flour on body composition and cognitive function in elderly individuals at the risk of low protein: a randomized, double-blind, placebo-controlled study.

Insufficient protein intake and cognitive decline are common in older adults; however, there have been few studies on low protein risk screening and complex nutrient interventions for elderly individuals in rural communities. This study aimed to evaluate the effect of dietary multinutrient soy flour (MNSF) on body composition and cognitive function in elderly individuals who are at risk of protein deficiency in a randomized, double-blind, placebo-controlled clinical trial. Nutritional interventions were given to those found to have low protein levels using bioelectrical impedance analysis (BIA). Among 733 older adults screened, 62 participants were included and randomly assigned into two groups, one taking soy flour and the other taking MNSF for 12 weeks. A previous cross-sectional survey found that 35.1% of the elderly people with an average age of 71.61 ± 5.94 years had an inadequate body protein mass proportion. After the intervention, the MNSF group demonstrated a significant improvement in protein mass, muscle mass, mineral levels, skeletal muscle mass, and fat-free mass compared with baseline (all P < 0.05), as well as a better upward trend compared with the soy flour group (P = 0.08; P = 0.07; P = 0.05; P = 0.08; P = 0.07). Regarding the mini-mental state examination (MMSE) scores, the MNSF group showed a significant decrease after 12 weeks (P < 0.05), which were significantly different compared with the soy flour group (P < 0.05). In the future, the application of MNSF as a food-based supplement to improve nutrition and delay cognitive decline in older adults at the risk of protein deficiency may be considered.

The Effects of n-3 PUFA Supplementation on Bone Metabolism Markers and Body Bone Mineral Density in Adults: A Systematic Review and Meta-Analysis of RCTs.

Supplemental n-3 polyunsaturated fatty acids (PUFA) on bone metabolism have yielded inconsistent results. This study aimed to examine the effects of n-3 PUFA supplementation on bone metabolism markers and bone mineral density through a meta-analysis of randomized controlled trials. A systematic literature search was conducted using the PubMed, Web of Science, and EBSCO databases, updated to 1 March 2023. The intervention effects were measured as standard mean differences (SMD) and mean differences (MD). Additionally, n-3 PUFA with the untreated control, placebo control, or lower-dose n-3 PUFA supplements were compared, respectively. Further, 19 randomized controlled trials (RCTs) (22 comparisons, n = 2546) showed that n-3 PUFA supplementation significantly increased blood n-3 PUFA (SMD: 2.612; 95% CI: 1.649 to 3.575). However, no significant effects were found on BMD, CTx-1, NTx-1, BAP, serum calcium, 25(OH)D, PTH, CRP, and IL-6. Subgroup analyses showed significant increases in femoral neck BMD in females (0.01, 95% CI: 0.01 to 0.02), people aged <60 years (0.01, 95% CI: 0.01 to 0.01), and those people in Eastern countries (0.02, 95% CI: 0.02 to 0.03), and for 25(OH)D in people aged ≥60 years (0.43, 95% CI: 0.11 to 0.74), treated with n-3 PUFA only (0.36, 95% CI: 0.06 to 0.66), and in studies lasting ≤6 months (0.29, 95% CI: 0.11 to 0.47). NTx-1 decreased in both genders (-9.66, 95% CI: -15.60 to -3.71), and serum calcium reduction was found in studies lasting >6 months (-0.19, 95% CI: -0.37 to -0.01). The present study demonstrated that n-3 PUFA supplementation might not have a significant effect on bone mineral density or bone metabolism markers, but have some potential benefits for younger postmenopausal subjects in the short term. Therefore, additional high-quality, long-term randomized controlled trials (RCTs) are warranted to fully elucidate the potential benefits of n-3 PUFA supplementation, as well as the combined supplementation of n-3 PUFA, on bone health.

Lipid extract from blue mussel (Mytilus edulis) improves glycemic traits in Chinese type 2 diabetic mellitus patients: a double-blind randomized controlled trial.

BACKGROUND: Studies have shown that blue mussel lipid extract (BMLE) has strong anti-inflammatory activity in both rheumatoid arthritis patients and animal arthritis models. Chronic inflammation was closely related to type 2 diabetes mellitus (T2DM). Though the beneficial effects cannot be completely attributed to n-3 polyunsaturated fatty acids, the aim of this study was to investigate whether BMLE can improve glycemic traits of T2DM patients. METHOD: In a double-blind randomized controlled trial, 133 Chinese T2DM participants were randomized to either fish oil (FO, n = 44), BMLE (n = 44), or corn oil (CO, n = 45) groups for 60 days. The participants were asked to take the corresponding oil capsules (two capsules per day, 0.8 g per capsule), which provided 1.6 g day-1 of FO (29.9% eicosapentaenoic acid + 20.4% docosahexaenoic acid), BMLE (20.7% eicosapentaenoic acid + 26.7% docosahexaenoic acid), or CO (53.5% linoleic acid). RESULTS: The fasting serum concentration of insulin (P = 0.005) and the homeostasis model of insulin resistance (P = 0.026) were significantly decreased in the BMLE group, whereas no significant change was found in the FO or CO groups. There was no significant difference between groups on serum glycosylated hemoglobin. Tumor necrosis factor-α was significantly decreased in the BMLE group (P = 0.003), but not in the FO or CO groups. A significant decrease of interleukin-1ß was observed in the BMLE and CO groups (P = 0.004 and P = 0.011 respectively), but not in the FO group. The total cholesterol was significantly decreased in the BMLE and CO groups (P < 0.001 and P < 0.001 respectively), but not in the FO group. Triacylglycerol was significantly decreased in the BMLE group (P = 0.007), but not in the FO or CO groups. High-density lipoprotein cholesterol was significantly lower in the BMLE and CO groups than in the FO group (P = 0.003). CONCLUSION: Blue mussel lipid supplements improved glycemic traits, inflammatory cytokines, and lipids profile in Chinese T2DM patients (Chinese Clinical Trial Registration number: ChiCTR1900025617). © 2022 Society of Chemical Industry.

Coffee peel extracts ameliorate non-alcoholic fatty liver disease via a fibroblast growth factor 21-adiponectin signaling pathway.

Coffee peel (CP) contains abundant phytochemicals which might prevent non-alcoholic fatty liver disease (NAFLD). The present study aimed to identify the main phytochemicals in CP extracts, and to investigate whether CP extracts could ameliorate NAFLD through a hepatic fibroblast growth factor (FGF) 21-adiponectin signaling pathway. Caffeine and seven monomers of flavonoids were identified from CP extracts by using high-performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS). After 8 weeks of intervention, the mice fed a high-fat and high-sugar diet showed the pathophysiological characteristics of NAFLD. Treatment with CP extracts significantly alleviated hepatic steatosis and insulin resistance and reduced the concentrations of serum alanine transaminase, FGF21, and triglyceride, and hepatic interleukin-6, interleukin-1ß, and tumor necrosis factor-α, while increasing serum adiponectin concentrations. Meanwhile, CP extract supplementation significantly decreased the gene and protein expression levels of FGF21, while enhancing adiponectin expression levels. The present study demonstrated that CP extracts contained caffeine and seven monomers of flavonoids, and protected against NAFLD through regulating the FGF21-adiponectin signaling pathway.

Lactobacillus casei Improve Anti-Tuberculosis Drugs-Induced Intestinal Adverse Reactions in Rat by Modulating Gut Microbiota and Short-Chain Fatty Acids.

The adverse effects of anti-tuberculosis (TB) drugs in the intestines were related to alteration of the intestinal microbiota. However, there was less information about microbial metabolism on the adverse reactions. This study aimed to explore whether Lactobacillus casei could regulate gut microbiota or short-chain fatty acids (SCFAs) disorders to protect intestinal adverse reactions induced by isoniazid (H) and rifampicin (R). Male Wistar rats were given low and high doses of Lactobacillus casei two hours before daily administration of anti-TB drugs. After 42 days, colon tissue and blood were collected for analysis. The feces at two-week and six-week were collected to analyze the microbial composition and the content of SCFAs in colon contents was determined. Supplementation of Lactobacillus casei increased the proportion of intestinal goblet cells induced by H and R (p < 0.05). In addition, HR also reduced the level of mucin-2 (p < 0.05), and supplementation of Lactobacillus casei restored. After two weeks of HR intervention, a decrease in OTUs, diversity index, the abundance of Bacteroides, Akkermansia, and Blautia, and an increase of the abundance of Lacetospiraceae NK4A136 group and Rumencoccus UCG-005, were observed compared with the control group (p all < 0.05). These indices in Lactobacillus casei intervention groups were similar to the HR group. Six-week intervention resulted in a dramatic reduction of Lacetospiraceae NK4A136 group, butyric acid, valeric acid and hexanoic acid, while an increase of Bacteroides and Blautia (p all < 0.05). Pretreatment with Lactobacillus casei significantly increased the content of hexanoic acid compared with HR group (p < 0.05). Lactobacillus casei might prevent intestinal injury induced by anti-tuberculosis drugs by regulating gut microbiota and SCFAs metabolism.

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.

Association between vitamin C intake and risk of hyperuricemia in US adults.

BACKGROUND AND OBJECTIVES: The relationship between vitamin C intake and hyperuricemia among the general US adult population has seldom been reported; thus, the present study examined the associations of total vitamin C (dietary vitamin C plus supplementary vitamin C) and dietary vitamin C intake with the risk of hyperuricemia. METHODS AND STUDY DESIGN: Pooled data from three 2-year cycles (2007-2012) of the cross-sectional National Health and Nutrition Examination Survey were used in the present study. Dietary intake data were extracted from two 24-hour dietary recall interviews. Logistic regression models were used to determine the associations between vitamin C intake and hyperuricemia risk. RESULTS: A total of 14885 adults aged 20 years or older (7269 men and 7616 women) were registered in the present study. The prevalence of hyperuricemia was 19.1%. Based on the lowest quartile of dietary vitamin C intake, multivariate adjusted odds ratios with 95% confidence intervals of hyperuricemia for quartiles 2-4 were 0.84 (0.74-0.95), 0.83 (0.73-0.94), and 0.72 (0.63-0.82), and those for total vitamin C intake were 0.87 (0.77-0.99), 0.85 (0.75-0.96), and 0.66 (0.58-0.76). Inverse associations between vitamin C intake and hyperuricemia were discovered in both men and women, even with or without covariate adjustments. CONCLUSIONS: Total vitamin C and dietary vitamin C intake are inversely associated with hyperuricemia in the general US adult population.

The protective effect of polyunsaturated fatty acid intake during pregnancy against embryotoxicity of sodium valproate in mice.

Sodium valproate (VPA) is an anti-epileptic drug, but has a strong embryotoxicity due to its induced disturbance of folate-homocysteine (Hcy) metabolism and fatty acid metabolism. The aim of the present study was to investigate whether polyunsaturated fatty acid (PUFA) intake during pregnancy can relieve the embryotoxicity of VPA. VPA (dose: 500 mg kg-1, concentration: 38.5 mg ml-1) was intraperitoneally injected into pregnant mice on day 8.5 of gestation (E8.5d). PUFA intake significantly decreased fetal mortality and NTD incidence induced by VPA: n-3 long chain PUFAs (n-3 LCPUFAs) in fish oil had the best decreasing effect, followed by C18:3n-3 in flaxseed oil and then C18:2n-6 in corn oil. VPA administration inhibited the mRNA and protein expressions of a series of enzymes involved in folate-Hcy metabolism in the liver of pregnant mice; however, it led to the mRNA and protein overexpression of these enzymes in embryos. An elevated Hcy level in embryos was observed 6 h after VPA injection. n-3 PUFA intake effectively relieved this disturbance of folate-Hcy metabolism in pregnant mice and embryos, and this relieving effect of n-3 LCPUFAs and C18:3n-3 is better than that of C18:2n-6. In addition, n-3 PUFA intake also relieved the growth retardation induced by VPA. In conclusion, PUFA intake during pregnancy can effectively decrease embryotoxicity of VPA by relieving VPA-induced disturbance of folate-Hcy metabolism in pregnant mice and embryos, and n-3 LCPUFA in fish oil had the optimal protection effect.

In Vivo MRI and X-Ray Bifunctional Imaging of Polymeric Composite Supplemented with GdPO4 ·H2 O Nanobundles for Tracing Bone Implant and Bone Regeneration.

Homogeneous and monodisperse GdPO4 ·H2 O nanobundles are successfully synthesized via a solvothermal method. Then, GdPO4 ·H2 O are incorporated into the composite of hydroxyapatite and poly(lactic-co-glycolic acid) to obtain a biodegradable and traceable bone implant. After implanted, the GdPO4 ·H2 O/HA/PLGA implant and the newly formed bone can be easily traced and observed through the combination of magnetic resonance imaging and X-ray imaging.

Selenium Inhibits Homocysteine-Induced Endothelial Dysfunction and Apoptosis via Activation of AKT.

BACKGROUND/AIMS: Endothelial cells are crucial in vascular homeostasis. Dysfunction of endothelial cells is involved in the development of cardiovascular diseases (CVD). High plasma homocysteine (Hcy) correlates with CVD while selenium supplementation counteracts development of CVD. However, the underlying mechanism remained unclear. Here, we investigated the effects of selenium on homocysteine-induced endothelial dysfunction. METHODS: An animal model of Hcy-induced endothelial dysfunction was established by intragastric administration of L-methionine. Plasma NO and von Willebrand factor (vWF) were quantified using NO assay and ELISA kit respectively. Relaxation was measured in thoracic aortic ring assays. Cell viability and migration were detected by Cell Counting Kit-8 and Bio-Coat cell migration chambers respectively. Cellular apoptosis was determined by Annexin V-FITC apoptosis kit. RESULTS: Selenium prevented homocysteine-induced endothelial injury and impairment of endothelium-dependent relaxation. Selenium reversed the impaired viability and migration of endothelial cells induced by homocysteine in a dose-dependent manner. Selenium inhibited the apoptosis of endothelial cells induced by homocysteine, through downregulating of Caspase-3 activity and expression of Caspase-3 and Bax, and by stimulating Bcl-2 expression. Selenium reversed the homocysteine-induced reduction of NO release, and increased the expression and phosphoylation of endothelial nitric oxide synthetase (eNOS) in a dose-dependent manner. Moreover, selenium enhanced AKT phosphorylation, and selenium-induced phosphorylation and expression of eNOS were inhibited by AKT inhibition. NO production, cell viability and migration rescued by selenium were inhibited, while cell apoptosis was reversed by AKT inhibition. CONCLUSION: Selenium protected against homocysteine-induced dysfunction and apoptosis of endothelial cells through AKT pathway. The observations may provide novel therapeutic opportunities in the treatment of CVD.