Ferritin and iron supplements in gestational diabetes mellitus: less or more?

Iron metabolism has been found to be closely related to gestational diabetes mellitus (GDM). Excessive ferritin levels were shown to be related to an increased risk of GDM because of iron overload which may lead to insulin resistance and ß-cell injury by enhancing oxidative stress and inflammatory responses. On the contrary, insufficient ferritin levels can cause a number of obstetric complications, such as high incidence rates of anaemia and gestational hypertension. Therefore, high or low ferritin levels may have adverse effects on the mother and the foetus, putting clinicians in a dilemma when giving pregnant women iron supplements. This also explains why there have been more conflicting findings in the studies on dietary or oral iron supplementation during pregnancy. Hence, there is an urgent need for more evidence and strategies for appropriate recommendations for ferritin levels and iron supplementation during pregnancy to prevent iron insufficiency without causing iron overload and increasing the risk of GDM. Therefore, we gave an updated review on the association of GDM with ferritin metabolism, ferritin levels and iron supplementation based on the summary of the latest research.

Negatively charged nano-hydroxyapatite can be used as a phosphorus fertilizer to increase the efficacy of wollastonite for soil cadmium immobilization.

Improper application of phosphorus (P) fertilizer during soil cadmium (Cd) immobilization reduces the efficiency of fertilizer and Cd remediation. In this study, we synthesized three types of nano-hydroxyapatite (NHAP) with different surface charges as slow-release P fertilizers during Cd immobilization. We also evaluated the effects of wollastonite application with or without NHAP addition, in comparison with triple superphosphate (TSP) or bulk hydroxyapatite, on Cd accumulation in Amaranthus tricolor L. The results showed that adding wollastonite significantly reduced P availability (23.5%) in the soil, but it did not inhibit plant P uptake. In wollastonite-amended soil, the application of negatively/positively charged NHAP significantly increased plant biomass by 643-865% and decreased Cd uptake by 74.8-75.1% compared to the unamended soil as well as showed greater efficiency than those with TSP. This was ascribed to the increased soil pH (from 3.94 to 6.52-6.63) and increased abundance of organic acids (including citric acid, malic acid, lactic acid, and acetic acid) secreted by plants. In addition, the P-preferring bacterial class Bacteroidia was specific to soils amended with both wollastonite and NHAP-. These results suggest that NHAP- may be an appropriate P fertilizer for soil Cd immobilization using wollastonite.

Nitrogen and phosphorus addition exerted different influences on litter and soil carbon release in a tropical forest.

Terrestrial soils release large amount of carbon dioxide (CO2) each year, which are mainly derived from litter and soil carbon (C) decomposition. Nutrient availability, especially nitrogen (N) and phosphorus (P), plays an important role in both litter and soil C decomposition. Therefore, understanding the underlying mechanism is crucial for mitigating CO2 emission and climate changes. Here, we assessed patterns of litter and soil C decomposition after 11 yrs. in-situ N and P addition in a tropical forest where corn leaves or corn roots were added as litter C. The total CO2 efflux was quantified and partitioned using 13C isotope signatures to determine the sources (litter or soil C) every three months. In addition, Changes in C-degrading enzyme activities: ß-1,4-glucosidase (BG), phenol oxidase (PHO) and peroxidase (PER), and microbial biomarkers were assessed to interpret the underlying mechanism. Total C-release was enhanced up to17% by the long-term N addition but inhibited up to 15% by P addition. Precisely, N addition only accelerated the litter decomposition and increased about 42% and 6% of the litter C release at 0-5 cm and 5-10 cm soil depths, respectively; while P addition only impeded the soil C decomposition and decreased about 9% and 11% of the soil C release at 0-5 cm and 5-10 cm, respectively. The enhanced C release under N addition might be attributed to the enhanced microbial biomass, the ratio of fungi to bacteria and C-degrading enzyme activities. However, P addition resulted in the reverse result in microbial properties and C-degrading enzyme activities, associated with a decreased C release. Our study suggests that the long-term N and P addition selectively affected the litter and soil C decomposition because of their different physiochemical properties and this tendency might be more pronounced in tropical forests exposed to increasing atmospheric N deposition in the future. The study indicates that the different patterns of litter and soil C decomposition under climate change should be taken account in the future C management strategies.

N1­methylnicotinamide ameliorates insulin resistance in skeletal muscle of type 2 diabetic mice by activating the SIRT1/PGC­1α signaling pathway.

Insulin resistance is one of important factors causing type 2 diabetes; therefore, regulating insulin sensitivity is considered a beneficial therapeutic approach against type 2 diabetes. The present study aimed to determine the effects of N1­methylnicotinamide (MNAM) on insulin resistance (IR) in skeletal muscle from a mouse model of type 2 diabetes mellitus (T2DM), and to investigate the regulatory mechanisms of the sirtuin 1 (SIRT1)/peroxisome proliferator­activated receptor γ coactivator­1α (PGC­1α) signaling pathway. C57BL/6 mice were fed a normal diet with or without 1% MNAM and ob/ob mice were also fed a normal diet with or without 0.3 or 1% MNAM. Blood glucose, insulin levels, insulin resistance (IR), sensitivity indices and triglyceride (TG) content were detected using ELISAs. The expression of gluconeogenesis­related, insulin signaling­related and SIRT1/PGC­1α pathway­related proteins was analyzed using reverse transcription­quantitative PCR (RT­qPCR) and western blotting. In vitro, C2C12 cells were used to establish an IR muscle cell model by 0.75 mM palmitic acid (PA) treatment (PA group). The IR cell model was subsequently supplemented with 1 mM MNAM (PM group) or 1 mM MNAM + 30 µM SIRT1 inhibitor, EX527 (PME group). After treatment the glucose levels and insulin signaling­related proteins were detected by ELISAs and western blotting, respectively. Furthermore, the expression levels of SIRT1/PGC­1α signaling pathway­related mRNA and proteins under MNAM treatment were detected by RT­qPCR and western blotting. MNAM reduced body weight gain in T2DM mice, decreased fasting blood glucose and fasting insulin levels, and inhibited IR. MNAM also regulated insulin signal transduction and promoted glucose utilization in skeletal muscle, and reduced lipid deposition. Thus, MNAM improved IR in the skeletal muscle of T2DM mice. Following application of a SIRT1 inhibitor, the effects of MNAM on the increased glucose utilization in insulin­resistant myocytes and the insulin signaling pathway were suppressed. The mechanism of action was associated with activation of the SIRT1/PGC­1α signaling pathway, which promoted the activation of the insulin receptor substrate IRS1/PI3K/AKT pathway.

Changes in Bone Metabolism in Morbidly Obese Patients After Bariatric Surgery: A Meta-Analysis.

BACKGROUND: The aim is to evaluate via meta-analysis bone metabolism and bone mineral density (BMD) in morbidly obese patients before and after bariatric surgery. METHODS: We searched Medline, EMBASE, and the Cochrane Library for relevant studies published before January 2014. The following outcomes were evaluated: serum calcium, serum parathyroid hormone (PTH), serum 25-hydroxyvitamin D [25(OH)D], serum or urinary N-telopeptide (NTX), bone-specific alkaline phosphatase (BSAP), and bone mineral density (BMD). RESULTS: Ten studies, including 344 patients, met our inclusion criteria. Results showed a significant decrease in serum calcium (MD = -0.10, 95 %CI -0.14 to -0.07, P < 0.00001) and increase in serum PTH (MD = 12.41, 95 %CI 6.51 to 18.31, P < 0.00001) but no significant difference in serum 25(OH)D (MD = 1.35, 95 %CI -1.12 to 3.83, P = 0.28) following bariatric surgery. There were significant increases in serum or urinary NTX (MD = 18.49, 95 %CI 3.33 to 33.66, P = 0.02) and BSAP (MD = 7.47, 95 %CI 0.21 to 14.72, P = 0.04) but a significant decrease in BMD (MD = -0.08, 95 %CI -0.13 to -0.04, P < 0.00001) after bariatric surgery. CONCLUSION: BMD was significantly decreased, while bone turnover was elevated, and bone remodeling was accelerated following bariatric surgery. Basal bone metabolism should be evaluated preoperatively. To prevent secondary hyperparathyroidism and bone loss, calcium and vitamin D should be monitored closely and supplemented accordingly after the surgery.