Journal of Nutritional Biochemistry最新文献

Proper fetal development depends on maternal nutrition. We investigated the placental morphofunctional adaptations to a low-protein diet, and their impact on fetal and newborn outcomes. Swiss mice were fed either normal (NPD, 20% crude protein, n=29) or low protein (LPD, 8% crude protein, n=26) diets two weeks before and throughout pregnancy. Dams were euthanized at gestational days (GD) 7.5 and 17.5 for morphological and molecular evaluations. No biometrical or histological alterations were observed in embryonic sites in both GDs. However, LPD placentae exhibited 14.2% increase in maternal sinusoid and 8% reduction in fetal vessel proportions (P<0.05), without significant changes in cellular proliferation, or apoptosis. Placental gene expression analysis varied according to uterine location: LPD placentae near the ovary exhibited downregulation of Fatp4, Mtor, and Kiss1, while Stat3 was upregulated (P<0.05); in the middle third of the uterine horn, Snat1 and Kiss1 were upregulated, while Snat4 was downregulated (P<0.05); and close to the uterine body, Igf2r was downregulated, whereas Snat1 and Kiss1r were upregulated (P<0.05), suggesting region-specific compensatory mechanisms. LPD placentae and fetuses were lighter and exhibited higher brain-to-liver weight ratio in both genders (P<0.05). Maternal LPD intake disproportionately affected male fetuses, which presented higher placental efficiency (P<0.05), yet failed to reach their full growth potential. At birth, although newborn size was not affected by LPD, liver weights were lower and brain-to-liver weight ratios remained higher (P<0.05), particularly in males. Maternal LPD induces region-specific placental adaptations that partially compensate for nutrient restriction, yet still impair fetal growth, particularly in male offspring.

The aim of the study is to analyse the possible neuroprotective effect of two types of olive oils, one with a high content of alcoholic phenols (POO) and the other with a high content of alcoholic phenols and triterpenes (PTOO), in an experimental model of diabetes mellitus. We also aimed to assess the participation of triterpenes, alone or in association with hydroxytyrosol, in the neuroprotective effect of these olive oils. We administered 0.5 mL/kg/day of both oils to type 1 diabetic animals and performed a hypoxia-reoxygenation model in brain slices. Both oils reduced cell death in this experimental model: 38.3% with POO and 57.2% with PTOO. Both oils reduced brain oxidative stress in this model, with PTOO showing a greater effect than POO in increasing brain antioxidant variables. In in vitro experiments in the hypoxia-reoxygenation model, both hydroxytyrosol and triterpene compounds reduced cell death (IC₅₀ 17.7±0.5 µmol/L for triterpenes and 58.7±1.1 µmol/L for hydroxytyrosol. They also showed an antioxidant effect in the experimental model. When associating both types of compounds in proportion to their concentrations in POO and PTOO, a greater neuroprotective and antioxidant effect was quantified, mainly in the inhibition of lipid peroxidation and in the increase of antioxidant variables. It is concluded that the administration of PTOO exerts a greater neuroprotective effect, possibly due to a positive interaction between the content of triterpenes and alcoholic phenols present in olive oils.

Branched-chain α-amino acids (BCAAs) support protein synthesis and their oxidation is restrained by branched-chain α-keto acid dehydrogenase kinase (BCKDK). We previously observed that in the brains of Bckdk knockout (KO) mice, BCAAs fall while glutamate is preserved and other amino acids rise. We asked why this profile emerges and how it affects skeletal muscle versus brain during nutrient stress. Motor behavior, protein synthesis and nutrient signaling were compared in the skeletal muscle and brains of wildtype (WT) and Bckdk KO male mice. In addition, nitrogen delivery into brain from BCAAs was assessed using stable isotope tracing and mass spectrometry imaging. Bckdk KO showed normal grip strength but poor beam traversal and reduced wheel running during protein restriction. In skeletal muscle, leucine or protein-feeding stimulated and fasting suppressed mechanistic target of rapamycin complex 1 (mTORC1) signaling in both genotypes. Fasting reduced muscle protein synthesis in both strains without activating the integrated-stress response (ISR). In contrast, Bckdk KO brains exhibited ISR activation during fasting, and up-regulation of Atf4 and its target genes, including Slc7a5 mRNA. Tracer studies revealed lower serum [¹⁵N]-BCAA enrichment and diminished incorporation of BCAA-derived nitrogen into brain glutamate in Bckdk KO mice, despite unchanged total glutamate. Thus, in the nongrowing adult constitutive BCKDH activation limits BCAA-derived nitrogen delivery to brain and alters AA transporters as part of an adaptive ISR during nutrient scarcity. This creates a vulnerability in brain not observed in skeletal muscle. These data provide a metabolic basis for poor motor performance in Bckdk KO mice.

The aim of this study was to explore the association between copper intake from foods and mortality of respiratory disease among US adults. NHANES 1999-2018 data were linked to National Death Index Mortality Data. A multivariable Cox proportional hazard model and sensitivity analysis were adopted. Restricted cubic splines (RCS) were used to evaluate the potential non-linear relationship. During 500,324 person-years of follow-up (median 9.5 years [IQR 5.1-14.3 years]) between 1999 and 2018, we documented 580 respiratory disease deaths. Compared with individuals in the lowest tertile of dietary copper intake (<0.88 mg/d), those in the middle (≥0.88 and <1.34 mg/d) and highest tertile (>1.34 mg/d) had an adjusted hazard ratio (HR) of 0.68 (95% CI, 0.53, 0.88) and 0.62 (0.40, 0.95) for respiratory disease mortality, respectively. RCS analysis revealed an l-shaped association with a threshold at 1.07 mg/d of copper intake. When copper intake was <1.07 mg/d, each incremental increase in intake was associated with a reduced risk of respiratory disease mortality, with an adjusted HR of 0.48 (95% CI, 0.26-0.90, P=.022). However, when copper intake >1.07 mg/d, the risk of respiratory disease mortality showed no significant reduction, with an adjusted HR of 0.98 (95% CI, 0.76-1.27; P=.886) for each incremental increase in intake. In conclusion, in US adults from the NHANES, an l-shaped association between dietary copper intake and respiratory disease mortality was detected, suggesting that maintaining an optimal level of copper intake may be associated with decreased risk of respiratory disease mortality.