Journal of Nutritional Biochemistry最新文献

Deciduous teeth are a unique medium that record exposure to various elements over time, as they are formed during fetal and infantile periods. We aimed to evaluate the association between infant feeding methods and changes in the distribution of Barium (Ba) and Strontium (Sr) in deciduous teeth of children. The current analysis included 216 children around 6-7 years of age whose deciduous central incisor teeth were provided between March 2018 and February 2020, as an adjunct study of the Japan Environment and Children's study. Ba, Sr, and Calcium (Ca) levels in the deciduous teeth of these children were measured using laser ablation-inductively coupled plasma-mass spectrometry. We estimated the association between feeding methods or season of birth and the Ba to Ca (Ba:Ca) and Sr to Ca (Sr:Ca) ratios using multivariable linear mixed effects models. The Ba:Ca and Sr:Ca ratios were higher in the formula feeding group than in the breastfeeding group during the postnatal period (Ba:Ca: β=0.242 [95% CI: 0.149-0.335], Sr:Ca: β=0.223 [95% CI: 0.160-0.287] for formula group) and prenatal period (Ba:Ca: β=0.145 [95% CI: 0.062-0.227], Sr:Ca: β=0.152 [95% CI: 0.093-0.210] for formula group). Furthermore, the Sr:Ca ratio tended to be higher for summer-born children than for winter-born ones. The Ba:Ca and Sr:Ca ratios in deciduous teeth can serve as useful biomarkers for estimating feeding methods. Deciduous central incisors may serve as useful indicators of longitudinal elemental exposure and nutritional status from the prenatal to postnatal periods.

Type 2 diabetes is characterized by chronic low-grade inflammation and insulin resistance resulting from activation and infiltration of immune cells into adipose tissue. Vitamin D reportedly exerts an anti-inflammatory effect by regulating immune cell activity and inflammatory cytokine production. This study aimed to investigate the effects of vitamin D supplementation on lymphoid and myeloid immune cell distribution in the adipose tissue and explore the mechanisms by which vitamin D modulates adipose tissue inflammation in diabetes. Five-week-old, male C57BLKS/J-m⁺/m⁺ (CON) and C57BLKS/J-db/db (DB) mice were fed diets containing either 1,000 or 10,000 IU vitamin D/kg diet for 8 weeks. Vitamin D supplementation resulted in a smaller weight gain (33.8% lower), less adipocyte hypertrophy (16.9% lower), and a lower fasting blood glucose concentration (7.4% lower) in DB group. Vitamin D supplementation did not inhibit macrophage and dendritic cell infiltration into adipose tissue; nonetheless, it reduced the percentage of CD8⁺ T cells (18% lower). In DB group, vitamin D supplementation downregulated the gene expression of interleukin 6 (Il6) and CC motif chemokine ligand 2 (Ccl2) in stromal vascular cells (28.2% and 17.3% lower, respectively) as well as that of Il6, Ccl2, sterol regulatory element-binding transcription factor 1 (Srebf1), and advanced glycosylation end product-specific receptor (Ager) in adipose tissue (42.8%, 24.9%, 33.1%, and 58.2% lower, respectively). In conclusion, vitamin D supplementation attenuated the inflammatory response and adipocyte hypertrophy in adipose tissue from diabetic mice. The inhibition of Ager and Srebf1 by vitamin D supplementation potentially contributes to vitamin D's anti-inflammatory and anti-adiposity effects in diabetic mice.

Dietary intervention is crucial for the clinical management of alcoholic liver injury. As the primary bioactive component in fermented tea, theaflavin-3,3'-digallate (TF3) possesses potent antioxidative and anti-inflammatory capacities, but its protective mechanisms against alcoholic liver injury via the gut-liver axis require systematic elucidation. This study evaluated the protective effects and underlying mechanisms of high-purity TF3 (2.5/5/10 mg/kg, 12-week oral gavage) against alcoholic liver injury in C57BL/6 J mice. TF3 administration significantly reduced serum lipids, attenuated hepatic steatosis, and suppressed oxidative stress and pro-inflammatory cytokine production in alcohol-fed mice. Mechanistically, TF3 enhanced intestinal barrier integrity by upregulating tight junction proteins in the colon and ileum, increased beneficial microbiota like Lactobacillus and Bifidobacterium, and modulated microbial metabolites including short-chain fatty acids (SCFAs) and tryptophan. These changes reduced circulating lipopolysaccharide (LPS), suppressed hepatic toll-like receptor 4 (TLR4)/nuclear factor kappa-B (NF-κB) pathway activation, and ultimately ameliorated hepatic inflammation while enhancing oxidative stress regulation. This work reveals novel mechanisms of TF3 in preventing alcoholic liver injury, providing a theoretical foundation for dietary applications.

Excessive dietary fat intake was associated with intestinal inflammation and lipotoxicity, but the underlying mechanism remained elusive. In this study, we investigated the effects and mechanisms of dietary fat addition on intestinal inflammation and lipid metabolism by using yellow catfish Pelteobagrus fulvidraco, a freshwater teleost fish of ecological and economic importance. Here, we found that high fat diet (HFD) and fatty acid (FA) incubation induced intestinal lipotoxicity and barrier damage, activated oxidative stress and induced intestinal inflammation by activating cysteinyl aspartate specific proteinase 3 (caspase 3)/ gasdermin E (Gsdme) -dependent pyroptosis; oxidative stress mediated FA-induced pyroptosis, lipogenic metabolism and lipid accumulation; high dietary fat induced full-length sterol regulatory element binding protein 1 (Srebp1) cleavage by caspase 3, which in turn produced the active cleaved forms of Srebp1, and accordingly contributed to lipogenic metabolism and lipid accumulation; D444 was identified as the cleavage site of Srebp1 by caspase 3. Mechanistically, overexpression of the cleaved Srebp1 (Flag-N-Srebp1) by caspase 3 increased the activities of the promoters of lipogenic genes (fatty acid synthase [fas], acetyl CoA carboxylase [acca] and stearoyl-CoA desaturase 1 [scd1]), thereby up-regulating lipogenic metabolism and inducing lipid accumulation. Thus, our study elucidated the novel mechanism of high fat diet (HFD) inducing inflammation and lipotoxicity, and found that oxidative stress and caspase 3/ GsdmE-dependent pyroptosis played important roles in these processes.

Cadmium (Cd) exposure is well-known to be hazardous to renal function. Although animal experiments suggest that selenium (Se) supplementation has beneficial effects on Cd-induced organ damage, epidemiological evidence on the mitigation of Se on Cd-induced renal damage is still insufficient. We used data from the National Health and Nutrition Examination Survey (NHANES) cycles from 2011 to 2018, and performed survey-weighted linear regression, logistic regression, and restricted cubic spline analyses to evaluate the associations of urine Cd (UCd), blood Cd (BCd), daily Se intake (DSe), and blood Se (BSe) with estimated glomerular filtration rate (eGFR), urine albumin creatinine ratio (UACR), and CKD risk, including the effects of DSe and BSe on the associations of UCd and BCd with renal health. In our study, UCd and BSe were positively associated with eGFR, but negatively associated with CKD risk. UCd and BCd were positively associated with UACR, and BCd was positively associated with CKD risk. No independent associations of DSe with eGFR, UACR, and CKD risk were observed. Additionally, we observed that the associations of Cd exposure with renal injury indicators and CKD risk were attenuated in participants with adequate DSe levels and/or higher BSe levels. Our findings suggested that Cd exposure was associated with renal impairment and CKD risk, and maintaining adequate DSe and good Se status attenuated the associations of Cd exposure with renal health. Further research is needed to evaluate the health effects of interactions between Se and Cd.