Sarcopenia, highly linked with fall, frailty, and disease burden, is an emerging problem in aging society. Higher protein intake has been suggested to maintain nitrogen balance. Our objective was to investigate whether pre-sarcopenia status was associated with lower protein intake. A total of 327 community-dwelling elderly people were recruited for a cross-sectional study. We adopted the multivariate nutrient density model to identify associations between low muscle mass and dietary protein intake. The general linear regression models were applied to estimate skeletal muscle mass index across the quartiles of total protein and vegetable protein density. Participants with diets in the lowest quartile of total protein density (<13.2%) were at a higher risk for low muscle mass (odds ratio (OR) 3.03, 95% confidence interval (CI) 1.37–6.72) than those with diets in the highest quartile (≥17.2%). Similarly, participants with diets in the lowest quartile of vegetable protein density (<5.8%) were at a higher risk for low muscle mass (OR 2.34, 95% CI 1.14–4.83) than those with diets in the highest quartile (≥9.4%). Furthermore, the estimated skeletal muscle mass index increased significantly across the quartiles of total protein density (p = 0.023) and vegetable protein density (p = 0.025). Increasing daily intakes of total protein and vegetable protein densities appears to confer protection against pre-sarcopenia status.

The association between serum concentrations of zinc, copper, or iron and the risk of metabolic syndrome are inconclusive. Therefore, we conduct a case-control study to explore the relationship between serum levels of zinc, copper, or iron and metabolic syndrome as well as each metabolic factor and insulin resistance. We enrolled 1165 adults, aged ≥ 40 (65.8 ± 10) years in a hospital-based population to compare the serum levels of zinc, copper, and iron between subjects with and without metabolic syndrome by using multivariate logistic regression analyses. The least square means were computed by general linear models to compare serum concentrations of zinc, copper, and iron in relation to the number of metabolic factors. The mean serum concentrations of zinc, copper, and iron were 941.91 ± 333.63 μg/L, 1043.45 ± 306.36 μg/L, and 1246.83 ± 538.13 μg/L, respectively. The odds ratios (ORs) of metabolic syndrome for the highest versus the lowest quartile were 5.83 (95% CI: 3.35–10.12; p for trend < 0.001) for zinc, 2.02 (95% CI: 1.25–3.25; p for trend: 0.013) for copper, and 2.11 (95% CI: 1.24–3.62; p for trend: 0.021) for iron after adjusting for age, sex, personal habits, body mass index, and homeostatic model assessment insulin resistance. Additionally, the serum zinc, copper, and iron concentrations increased as the number of metabolic factors rose (p for trend < 0.001). This was the first study to clearly demonstrate that higher serum levels of zinc, copper, and iron were associated with the risk of metabolic syndrome and the number of metabolic factors independent of BMI and insulin resistance.

To confer further therapeutic potential and prevent some adverse effects by the mesenchymal stem cells (MSCs) transplantation, we explored the effects of locally intrarenal arterial administration of hypoxic preconditioned MSCs in the anti-Thy1.1 induced rat glomerulonephritis. Proteinuria, histochemical staining, and western blotting were used to explore the therapeutic effects and mechanisms. Locally intrarenal arterial MSCs transplantation successfully implanted the fluorescent or CD44 labeled MSCs in the nephritic glomeruli, ameliorated proteinuria, and glomerulosclerosis in nephritic rats. Hypoxic preconditioning significantly upregulated hypoxic inducible factor-1α/VEGF (HIF-1α/VEGF) in the MSCs and was more efficient than normoxic MSCs in reducing the degree of urinary protein, glomerulosclerosis, fibrosis, macrophage/monocyte infiltration, GRP78 mediated endoplasmic reticulum stress, Beclin-1/LC3-II mediated autophagy, and Bax/Bcl-2/caspase 3 mediated apoptosis. Hypoxic MSCs could further promote intranuclear nuclear factor (erythroid-derived 2, Nrf2) and reduce nuclear factor kappa B expression in nephritic kidneys. As compared to normoxic MSCs, hypoxic MSCs transplantation significantly upregulated the renal expression of anti-oxidative response elements/enzymes including glutamate-cysteine ligase catalytic subunit, glutamate-cysteine ligase modifier subunit, glutathione peroxidase, catalase, Mn, and Cu/Zn superoxide dismutase. In summary, intrarenal hypoxic preconditioning MSCs transplantation was more effective to activate hypoxic inducible factor-1α/VEGF/Nrf2 (HIF-1α/VEGF/Nrf2) signaling, preserve anti-oxidant proteins and anti-oxidative responsive element proteins, and subsequently reduce glomerular apoptosis, autophagy, and inflammation.

Background: Bariatric surgery is associated with a significant improvement in depressive mood in the initial postoperative years, but the maintenance of the improvement is under debate. Aim: To explore the association between bariatric surgery and major depressive disorder (MDD) in a 12-year nationwide cohort study. Method: Using the National Health Insurance Research Database of Taiwan, we identified 2302 patients who underwent bariatric surgery in 2001–2009. These patients were matched by propensity score to 6493 obese patients who did not receive bariatric surgery. We followed the surgical and control cohorts until death, any diagnosis of MDD or 31 December 2012. We used Cox proportional hazard regression models to calculate the relative risk of MDD in those who received bariatric surgery. Results: Overall, there was a 1.70-fold (95% CI: 1.27–2.27) higher risk of MDD in the surgical group. Subjects receiving malabsorptive procedures showed a higher risk of MDD (3.01, 95% CI: 1.78–5.09) than those receiving restrictive procedures (1.51, 95% CI: 1.10–2.07). Stratified by follow-up period, there was a higher risk of MDD in the surgical group (2.92, 95% CI: 1.75–4.88) than in the restrictive group four years after bariatric surgery. Conclusions: Bariatric surgery was significantly associated with an elevated risk of MDD.

Few studies have investigated the association between selenium and metabolic syndrome. This study aimed to explore the associations between the serum selenium level and metabolic syndrome as well as examining each metabolic factor. In this case-control study, the participants were 1165 adults aged ≥40 (65.8 ± 10.0) years. Serum selenium was measured by inductively coupled plasma-mass spectrometry. The associations between serum selenium and metabolic syndrome were examined by multivariate logistic regression analyses. The least square means were computed by general linear models to compare the serum selenium levels in relation to the number of metabolic factors. The mean serum selenium concentration was 96.34 ± 25.90 μg/L, and it was positively correlated with waist circumference, systolic blood pressure, triglycerides, fasting glucose, and homeostatic model assessment insulin resistance (HOMA-IR) in women, but it was only correlated with fasting glucose and HOMA-IR in men. After adjustment, the odds ratios (ORs) of having metabolic syndrome increased with the selenium quartile groups (p for trend: <0.05), especially in women. The study demonstrated that the serum selenium levels were positively associated with metabolic syndrome following a non-linear dose–response trend. Selenium concentration was positively associated with insulin resistance in men and women, but it was associated with adiposity and lipid metabolism in women. The mechanism behind this warrants further confirmation.