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Purpose: The aim of this study was to evaluate the effects of vitamin D and/or calcium supplementation on sleep quality in individuals with prediabetes., Methods: A 24-week randomized controlled trial (RCT) was conducted in a 212 Chinese population with prediabetes. Participants were randomly assigned to four groups: vitamin D + calcium group (1600 IU/day + 500 mg/day, n = 53), vitamin D group (1600 IU/day, n = 54), calcium group (500 mg/day, n = 51), and control group (placebo, n = 54). The Pittsburgh Sleep Quality Index (PSQI) was used as the primary outcome to assess sleep quality. Questionnaires and fasting blood samples were collected at baseline and post-intervention for demographic assessment and correlation index analysis., Results: After a 24-week intervention, a significant difference was observed in serum 25(OH)D concentration among the four groups (P < 0.05), and the total PSQI score in vitamin D + calcium group was lower compared to the preintervention levels. Subgroup analyses revealed improved sleep quality with calcium supplementation (P < 0.05) for specific groups, including women, individuals with a low baseline 25(OH)D level (< 30 ng/mL), and individuals in menopause. Moreover, correlation analysis revealed a negative correlation between the extent of change in sleep efficiency scores before and after the calcium intervention and the degree of change in insulin efficiency scores (r = - 0.264, P = 0.007), as well as the magnitude of change in islet beta cell function (r = - 0.304, P = 0.002)., Conclusions: The combined intervention of vitamin D and calcium, as well as calcium interventions alone, exhibits substantial potential for improving sleep quality in individuals with prediabetes., Clinical Trial Registration: The trial was registered in August 2019 as ChiCTR190002487., (© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany.)

Purpose: The burden of non-communicable diseases (NCDs) has increased in China. However, the contribution of dietary risks to the NCD burden has not been evaluated. This study aimed to estimate the burden of ischemic heart disease (IHD) and colorectal cancer (CRC) attributable to a diet low in fiber in China from 1990 to 2017. Methods: China data from the Global Burden of Disease Study (GBD) 2017 were used to assess the age-, sex-, and province-specific mortality and disability-adjusted life-years (DALYs) of IHD and CRC related to a diet low in fiber. Results: In 2017, a diet low in fiber contributed 170,143 [95% uncertainty interval (UI): 99,623–256,806] IHD deaths and 25,561 (95% UI: 13,726–39,215) CRC deaths, with the population attributable fractions (PAFs) were 9.7 and 13.7%, respectively. Males had higher risk-attributable mortality and DALY rates for IHD and CRC than females. An upward trend with age in rates of mortality and DALY was observed. All-age risk-attributable mortality and DALY rates increased significantly by 111.4 and 53.2% for IHD, and 94.4 and 59.6% for CRC from 1990 to 2017, respectively; however, the corresponding age-standardized rates for IHD and CRC showed relatively stable trends. Heilongjiang, Xinjiang, and Inner Mongolia were ranked as the top three provinces in terms of total risk-attributable NCD burden in 2017. Conclusions: China has a large and growing NCD burden attributable to a diet low in fiber. Greater priority in disease prevention and control should be given to male and older adults throughout China, particularly in some western provinces. [ABSTRACT FROM AUTHOR]

Purpose: This study was aimed to investigate the effects of a maternal low-protein diet on transcriptional regulation of the myostatin (MSTN) gene in skeletal muscle of weaning piglets. Methods: Sows were fed either a standard-protein (SP, 15 and 18 % crude protein) or a low-protein (LP, 50 % protein level of SP) diet throughout pregnancy and lactation. Longissimus dorsi muscle was sampled from male piglets at 28 days of age. The mRNA was determined by RT-PCR, and protein was measured by Western blot. Chromatin immunoprecipitation assay was used to determine the binding of transcription factors and histone H3 modifications on the MSTN gene promoter. Results: The maternal LP diet significantly decreased body weight and average daily gain ( P < 0.05), which was associated with significantly lower plasma concentration of urea nitrogen and total protein ( P < 0.05), as well as decreased muscle RNA content ( P < 0.05). MSTN mRNA ( P < 0.05) was significantly increased, together with enhanced ( P < 0.05) mRNA and protein expression of forkhead box class O family member protein 3 (FoxO3), and a tendency of an increase ( P = 0.10) in glucocorticoid receptor (GR) mRNA in the muscle of LP piglets. Furthermore, the binding of both FoxO3 and GR to the MSTN gene promoter was significantly higher ( P < 0.05) in muscle of LP piglets, together with significantly enriched ( P < 0.05) gene activation markers, H3K9Ac and H3K4me3. Conclusion: These results indicate that MSTN mediates maternal LP diet-induced growth retardation, through epigenetic regulation involving FoxO3 and GR binding to its promoter. [ABSTRACT FROM AUTHOR]

Purpose: We tested the hypothesis that maternal low-protein (LP) diet during gestation and lactation can program myostatin (MSTN) signaling and protein synthesis in skeletal muscle of offspring at weaning stage (35 days). Methods: Fourteen Meishan sows were fed either LP or standard-protein diets throughout gestation and lactation, male offspring piglets were killed at weaning stage and longissimus dorsi (LD) muscles were taken. The cross-sectional areas (CSA) of LD muscles were measured by hematoxylin and eosin staining. The levels of free amino acids in plasma were measured by amino acid auto-analyzer. Proteins and mRNA were determined by Western blot and RT-qPCR, respectively. Results: Body weight, LD muscle weight and the myofiber CSA were significantly decreased ( P < 0.05) in LP piglets; meanwhile, the concentration of branched-chain amino acids was also significantly decreased ( P < 0.001). MSTN protein content tended to be higher ( P = 0.098) in LP piglets, while the expression of MSTN receptors, activin type II receptor-beta and transforming growth factor type-beta type I receptor kinase, was significantly up-regulated ( P < 0.05). Furthermore, p38 mitogen-activated protein kinase, the downstream signaling factor of MSTN, was also enhanced significantly ( P < 0.05). In addition, key factors of translation initiation, phosphorylated eukaryotic initiation factor 4E and the 70 kDa ribosomal protein S6 kinase, were significantly decreased ( P < 0.05) in LP piglets. Conclusions: Our results suggest that maternal LP diet during gestation and lactation affects MSTN signaling and protein synthesis in skeletal muscle of offspring at weaning stage. [ABSTRACT FROM AUTHOR]

Purpose: Catch-up growth is always companied with later development of obesity and osteoporosis that are two interrelated clinical entities. However, the potential mechanism of the link between them during catch-up growth is unknown. Methods: Rats were divided into two groups. Rats of the normal control (NC) group were offered ad libitum access to food, while rats of CUGFR group were food restricted for 4 weeks, and then were allowed full access to food for 0, 2, 4 weeks, respectively. The fat percentage and distribution, bone mineral density, biochemical and histological indexes of bone were detected. Moreover, the expression of adipogenic or osteoblastic differentiation-related genes of mesenchymal stem cells (MSCs) was also determined. Results: Catch-up growth led to a rapid visceral fat accumulation. Although there was no difference in the histological indexes of bone between NC group and CUGFR group, the bone turnover marker, serum Bone Gla-protein (s-BGP), decreased in CUGFR group. The adipogenic differentiation-related gene of MSCs, PPAR-gamma, was significantly higher than that of NC group especially when catch-up growth for 4 weeks. Nevertheless, the osteoblastic differentiation-related gene of MSCs, Runx2, was increased but failed to reach the levels of the controls eventually. Both protein and mRNA of TAZ, a main transcriptional modulator of MSCs differentiation, failed to catch up even after being allowed full access to food for 4 weeks. Conclusion: CUGFR induces the differential differentiation of MSCs, potentially suppressing bone formation and favoring catch-up fat, which might be responsible for the increased risk of osteoporosis and obesity during CUGFR. [ABSTRACT FROM AUTHOR]