Background: Previous studies have yielded inconsistent results on the association between maternal dietary protein intake and birth weight. Moreover, little is known about the effects of dietary protein intake from different sources on fetal growth. This study aimed to investigate the associations of different dietary protein sources (total protein, animal protein, plant protein, and major dietary protein sources) during pregnancy with birth weight and the related adverse birth outcomes. Methods: 7310 women were recruited using a stratified multistage random sampling method at 0–12 months (median: 3; 10–90th percentile: 0–7) after delivery in Shaanxi, China. Maternal diets were gathered by a validated FFQ and other characteristics were collected by a standard questionnaire. Multilevel linear or logistic regression models were used to estimate birth weight changes or ORs (95% CIs) for adverse birth outcomes associated with different dietary protein sources during pregnancy. Results: The mean percentage of energy from total protein was 11.4% (SD 2.2), with only 27.4% of total protein derived from animal protein. Per 3% increase in energy from total protein, animal protein, and dairy protein was associated with birth weight increases of 19.4 g (95% CI 6.0–32.9), 20.6 g (4.8–36.5), and 18.2 g (4.7–31.7), respectively. Per 3% increase in energy from total protein, animal protein, and dairy protein was also associated with lower risks of low birth weight (LBW) (total protein: OR = 0.78, 95% CI 0.64–0.94; animal protein: 0.79, 0.65–0.96; dairy protein: 0.71, 0.56–0.91), small for gestational age (SGA) (total protein: 0.88, 0.79–0.98; animal protein: 0.87, 0.78–0.97; dairy protein: 0.81, 0.68–0.96), and intrauterine growth retardation (IUGR) (total protein: 0.84, 0.72–0.98; animal protein: 0.86, 0.75–0.98; dairy protein: 0.78, 0.66–0.92). We observed no associations of plant protein and other major dietary protein sources with birth weight and the above birth outcomes. The results did not change when maternal protein was substituted for fat or carbohydrate. Conclusions: Among Chinese pregnant women with low intake of protein, higher intake of dietary protein, in particular animal protein and dairy protein, is associated with higher birth weight and lower risks of LBW, SGA, and IUGR.

The relationship between maternal oxidative balance score (OBS) in pregnancy, representing overall oxidative balance status by integrating dietary and lifestyle factors, and congenital heart defects (CHD) remains unclear; therefore, this study attempted to explore their associations among the Chinese population. We conducted a case-control study including 474 cases and 948 controls in Northwest China. Pregnant women were interviewed to report diets and lifestyles in pregnancy by structured questionnaires. Logistic regression models were used to estimate the adjusted ORs (95%CIs). Maternal OBS ranged from 6 to 34 among cases, and 5 to 37 among controls. Comparing the highest with the lowest tertile group, the adjusted OR for CHD was 0.31 (0.19–0.50). The CHD risk was reduced by 7% (OR = 0.93, 95%CI = 0.90–0.95) in association with per 1 higher score of OBS during pregnancy. The inverse relationship between maternal OBS and CHD risk appeared to be more pronounced among participants in urban areas (OR = 0.89, 95%CI = 0.86–0.93). Maternal OBS during pregnancy showed good predictive values for fetal CHD, with the areas under the receiver operating characteristic curve 0.78 (0.76–0.81). These findings highlighted the importance of reducing oxidative stress through antioxidant-rich diets and healthy lifestyles among pregnant women to prevent fetal CHD.

Background and Aims: Macrophages play plastic roles during fibrogenesis and fibrosis regression. Phagocytosis is considered a trigger for shifting macrophages from a profibrotic phenotype to a restorative phenotype. However, the underlying mechanism by which macrophages enhance phagocytosis remains unclear. Our present study investigated the role of reactive oxygen species (ROS)‐modulated TRPM2 activation in this process. Methods: The changes of TRPM2 expression, ROS intensity, and macrophage phagocytosis were assessed in fibrogenesis and fibrosis regression models. RNA sequencing was utilised to reveal pathway enrichment caused by TRPM2, and the role of TRPM2 in enhancing phagocytosis was verified. The coordinate regulation of ROS‐TRPM2 in different functions of macrophages was demonstrated by modulating ROS intensity and TRPM2 expression. Mitochondrial dynamics changes induced by ROS‐stimulated TRPM2 activation were evaluated by analysing the expression of dynamics‐related molecules and mitochondrial imaging, and intervention in mitochondrial dynamics confirmed their impact on macrophage phagocytosis. Results: Low‐intensity ROS stimulation up‐regulated the expression of TRPM2 and coordinately enhanced macrophage phagocytosis and the expression of matrix degradation‐related proteins (MMPs), a process akin to fibrosis regression. However, high‐intensity ROS inclined macrophages to produce more profibrotic cytokines, associating with oxidative stress caused by liver injury. ROS‐mediated TRPM2 activation mobilised Ca ²⁺ and promoted mitochondrial fission; either inhibiting mitochondrial fission or chelating Ca ²⁺ counteracted phagocytosis, as well as decreasing MMPs. Conclusions: ROS‐TRPM2 coordinately regulate macrophage functions. During the liver fibrosis regression period, ROS‐induced activation of TRPM2 helps enhance macrophage phagocytosis and switches them to a restorative phenotype. Modulating this process may provide means for developing effective therapeutic strategies.

Background/Objectives: The impact of choline on congenital heart defects (CHDs) in humans remains unclear. This study aimed to investigate the associations between maternal dietary intakes of choline and choline derivatives during pregnancy and CHD. Methods: This case–control study included 474 cases and 948 controls from hospitals in Northwest China. Pregnant women admitted for delivery were enrolled and completed a validated food frequency questionnaire to assess their dietary intake during pregnancy. A standardized questionnaire was also administered to collect additional pregnancy-related information. Mixed logistic regression models were used to estimate ORs (95%CIs) for CHD in association with choline intake. Results: Higher intakes of total choline, phosphatidylcholine, sphingomyelin, glycerophosphocholine, and phosphocholine in pregnancy were associated with reduced risks of total CHD, ventricular septal defects, and atrial septal defects, with all trend tests showing statistical significance (all p < 0.05). The ORs (95%CIs) of total CHD, comparing the highest with the lowest tertiles of intake, were 0.38 (0.24–0.61) for total choline, 0.51 (0.38–0.70) for phosphatidylcholine, 0.37 (0.26–0.51) for sphingomyelin, 0.34 (0.21–0.53) for glycerophosphocholine, and 0.53 (0.34–0.82) for phosphocholine. The inverse associations remained unchanged according to maternal age, work, education, parity, passive smoking, anemia, medication use, or folate/iron supplements use in pregnancy; however, these associations appeared to be more pronounced among pregnant women in urban areas. Conclusions: Higher maternal intake of dietary choline during pregnancy may be associated with a lower risk of CHD. Promoting choline intake in pregnant women could serve as a potential strategy for the primary prevention of fetal CHD in China.