The associations between sarcopenia and metabolic syndrome (MetS) in non-obese middle-aged and older adults remain controversial. Thus, this meta-analysis aimed to evaluate the overall prevalence of MetS and the correlations between sarcopenia and MetS in middle-aged and older non-obese adults. We performed a systematic searched strategy using PUBMED, EMBASE and Web of Science databases for relevant observational studies investigating sarcopenia and MetS up to 11 May 2017. The polled prevalence of MetS and odds ratios with 95% confidence intervals (CI), as well as subgroup analyses were calculated using a random effects model. Twelve articles with a total of 35,581 participants were included. The overall prevalence of MetS was 36.45% (95% CI, 28.28–45.48%) in middle-aged and older non-obese adults with sarcopenia. Our analysis demonstrated a positive association between sarcopenia and MetS (OR = 2.01, 95% CI, 1.63–2.47). The subgroup analysis showed that both larger cohort size and the use of dual-energy X-ray absorptiometry to measure body composition can enhance the relationship. Our study revealed that a higher proportion of MetS in middle-aged and older non-obese people with sarcopenia. Moreover, sarcopenia was positively associated with MetS in this population. Further large-scale prospective cohort studies are needed to investigate the causality between sarcopenia and MetS.

Epidemiological studies on the impact of fish consumption on coronary heart disease (CHD) incidence have shown inconsistent results. In addition, in terms of CHD mortality, although previous meta-analyses showed that fish consumption reduces the risk of CHD, six newly incorporated studies show that fish consumption has no impact on CHD. Therefore, the results still need to be verified. The purpose of this study is to quantitatively evaluate the impact of fish consumption on CHD incidence and mortality. Relevant studies were identified from PubMed, Web of Science, and Embase databases up to October 2019. The multivariate-adjusted relative risks (RRs) for the highest versus the lowest fish consumption categories and the 95% confidence intervals were computed with a random-effect model. A restricted cubic spline regression model was used to assess the dose–response relationship between fish consumption and CHD incidence and mortality. Forty prospective cohort studies were incorporated into research. Among them, 22 studies investigated the association between fish consumption and CHD incidence (28,261 cases and 918,783 participants), and the summary estimate showed that higher fish consumption was significantly associated with a lower CHD incidence [RR: 0.91, 95% CI: (0.84, 0.97); I² = 47.4%]. Twenty-seven studies investigated the association between fish consumption and CHD mortality (10,568 events and 1,139,553 participants), and the summary estimate showed that higher fish intake was significantly associated with a lower CHD mortality [RR: 0.85, 95% CI: (0.77, 0.94); I² = 51.3%]. The dose–response analysis showed that the CHD incidence and mortality were reduced by 4%, respectively, with a 20 g/day increment in fish consumption. This meta-analysis indicates that fish consumption is associated with a lower CHD incidence and mortality.

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.

Malnutrition is associated with an increased risk of pulmonary tuberculosis (PTB) treatment failure. Currently, there is no effective adjunctive nutritional therapy. The current objective is to investigate the association of dietary micronutrient intake with PTB treatment outcome.A cohort study including 1834 PTB patients was conducted in Linyi, China. The dietary micronutrient intake was assessed through a three-day 24 h dietary recall questionnaire. The treatment outcome was assessed by combinations of sputum smear and computerized tomography results. A multivariate binary regression model was used to assess the associations. The final model was adjusted for potential confounding factors. A low intake of vitamin C (adjusted OR (95% CI): 1.80 (1.07, 3.04), P_trend = 0.02) and Zn (adjusted OR (95% CI): 2.52 (1.25, 5.08), P_trend = 0.02) was associated with a high treatment failure rate. In addition, a low intake of vitamin C and Mn was associated with a severe tuberculosis symptom, as indicated by a high TB score. A supplementation of vitamin C and Zn may be beneficial in PTB treatment. Previous meta-analysis of randomized controlled trials (RCTs) reported a null effect of Zn supplementation on PTB treatment. The effect of vitamin C supplementation should be investigated by RCTs.

Type 2 diabetes mellitus (T2DM) results in compromised bone microstructure and quality, and subsequently increased risks of fractures. However, it still lacks safe and effective approaches resisting T2DM bone fragility. Pulsed electromagnetic fields (PEMFs) exposure has proven to be effective in accelerating fracture healing and attenuating osteopenia/osteoporosis induced by estrogen deficiency. Nevertheless, whether and how PEMFs resist T2DM-associated bone deterioration remain not fully identified. The KK-Ay mouse was used as the T2DM model. We found that PEMF stimulation with 2 h/day for 8 wk remarkably improved trabecular bone microarchitecture, decreased cortical bone porosity, and promoted trabecular and cortical bone material properties in KK-Ay mice. PEMF stimulated bone formation in KK-Ay mice, as evidenced by increased serum levels of bone formation (osteocalcin and P1NP), enhanced bone formation rate, and increased osteoblast number. PEMF significantly suppressed osteocytic apoptosis and sclerostin expression in KK-Ay mice. PEMF exerted beneficial effects on osteoblast- and osteocyte-related gene expression in the skeleton of KK-Ay mice. Nevertheless, PEMF exerted no effect on serum biomarkers of bone resorption (TRAcP5b and CTX-1), osteoclast number, or osteoclast-specific gene expression (TRAP and cathepsin K). PEMF upregulated gene expression of canonical Wnt ligands (including Wnt1, Wnt3a, and Wnt10b), but not noncanonical Wnt5a. PEMF also upregulated skeletal protein expression of downstream p-GSK-3β and β-catenin in KK-Ay mice. Moreover, PEMF-induced improvement in bone microstructure, mechanical strength, and bone formation in KK-Ay mice was abolished after intragastric administration with the Wnt antagonist ETC-159. Together, our results suggest that PEMF can improve bone microarchitecture and quality by enhancing the biological activities of osteoblasts and osteocytes, which are associated with the activation of the Wnt/β-catenin signaling pathway. PEMF might become an effective countermeasure against T2DM-induced bone deterioration. NEW & NOTEWORTHY PEMF improved trabecular bone microarchitecture and suppressed cortical bone porosity in T2DM KK-Ay mice. It attenuated T2DM-induced detrimental consequence on trabecular and cortical bone material properties. PEMF resisted bone deterioration in KK-Ay mice by enhancing osteoblast-mediated bone formation. PEMF also significantly suppressed osteocytic apoptosis and sclerostin expression in KK-Ay mice. The therapeutic potential of PEMF on T2DM-induced bone deterioration was associated with the activation of Wnt/ß-catenin signaling.

The gut–liver axis may provide a new perspective for treating anti-tuberculosis drug-induced liver injury (ATDILI). Herein, the protective effect of Lactobacillus casei (Lc) was investigated by modulating gut microflora (GM) and the toll like receptor 4 (TLR4)–nuclear factor (NF)-κB–myeloiddifferentiationfactor 88 (MyD88) pathway. C57BL/6J mice were given three levels of Lc intragastrically for 2 h before administering isoniazid and rifampicin for 8 weeks. Blood, liver, and colon tissues, as well as cecal contents, were collected for biochemical and histological examination, as well as Western blot, quantitative real time polymerase chain reaction (qRT-PCR), and 16S rRNA analyses. Lc intervention decreased alkaline phosphatase (ALP), superoxide dismutase (SOD), glutathione (GSH), malondialdehyde (MDA), and tumor necrosis factor (TNF)-α levels (p < 0.05), recovered hepatic lobules, and reduced hepatocyte necrosis to alleviate liver injury induced by anti-tuberculosis drugs. Moreover, Lc also increased the abundance of Lactobacillus and Desulfovibrio and decreased Bilophila abundance, while enhancing zona occludens (ZO)-1 and claudin-1 protein expression compared with the model group (p < 0.05). Furthermore, Lc pretreatment reduced the lipopolysaccharide (LPS) level and downregulated NF-κB and MyD88 protein expression (p < 0.05), thus restraining pathway activation. Spearman correlation analysis indicated that Lactobacillus and Desulfovibrio were positively correlated with ZO-1 or occludin protein expression and negatively correlated with pathway protein expression. Desulfovibrio had significant negative relationships with alanine aminotransferase (ALT) and LPS levels. In contrast, Bilophila had negative associations with ZO-1, occludin, and claudin-1 protein expressions and positive correlations with LPS and pathway proteins. The results prove that Lactobacillus casei can enhance the intestinal barrier and change the composition of the gut microflora. Moreover, Lactobacillus casei may also inhibit TLR4–NF-κB–MyD88 pathway activation and alleviate ATDILI.