Journal of Nutrition最新文献

Background: Ethanolamine (Etn), a precursor of phosphatidylethanolamine (PE), may alter hepatic lipid homeostasis and gut health; its dietary effects remain undefined.

Objective: The objective of this study was to determine the effects of dietary Etn on lipid and glucose metabolism and liver/gut health in high-fat diet (HFD)-fed mice, complemented by in vitro hepatocyte assays.

Methods: Ten-wk-old C57BL/6 mice (20 male, 18 female) were fed ad libitum HFD (45% energy from fat) with [Ethanolamine supplementation (ES-group)] or without (CON-group) Etn (8 g/kg diet) for 10 wk. Outcomes included body/liver weight, glucose tolerance test (GTT) results, plasma phosphatidylcholine (PC)/cholesteryl ester (CE)/triacylglycerol (TG) concentrations, hepatic TG/PC/PE concentrations, hepatic endoplasmic reticulum (ER)-stress, and inflammation markers, jejunal morphology/barrier/inflammation genes, and fecal microbiota (α/β diversity). HuH7 cells received 20 μM or 5 mM Etn to assess TG/PC/PE synthesis.

Statistics: repeated-measures analysis of variance (ANOVA) (GTT), t-test or Wilcoxon (other endpoints), permutational multivariate analysis of variance (PERMANOVA) (β diversity); α=0.05.

Results: ES increased hepatic TG in females by 230% compared with CON (P = 0.001), and trended higher in males (P = 0.054); hepatic PC and PE masses were unchanged. In ES males, GTT area under the curve decreased by 22.6% (P = 0.037), and plasma PC, CE, and TG were reduced by: PC -16.6%, CE -24.5%, TG -25.9%, respectively (all P < 0.05). ES males showed higher hepatic Tnf and Cd68 and increased C/EBP homologous protein (CHOP) (all P < 0.05). In vitro, Etn did not alter hepatocellular TG, PC, or PE synthesis (all P > 0.05). Female ES mice exhibited altered fecal β-diversity (PERMANOVA P = 0.006) with early jejunal inflammatory signals (Tnf ↑; P = 0.055).

Conclusions: Dietary Etn modifies hepatic lipid storage and gut microbiota in a sex-dependent manner and improves glucose tolerance in males, whereas in vitro data indicate no direct effect on hepatocyte lipid synthesis.

Background: Although several studies have examined the relationship between omega-3 (ω-3) fatty acids and pulmonary function and clinical outcomes in critically ill patients, their findings remain mixed and inconclusive, and additional research is warranted.

Objectives: This study aimed to evaluate the effects of ω-3 fatty acids on pulmonary function and clinical outcomes in critically ill patients.

Methods: We searched 5 databases (PubMed, Web of Science, Embase, EBSCO, and Cochrane Central Register of Controlled Trials) to identify randomized controlled trials involving critically ill adults who received ω-3 fatty acids. Both enteral and parenteral routes of administration were included. Effect estimates were pooled using fixed- or random-effects models, and heterogeneity among studies was assessed using the I² statistic.

Results: The analysis included 29 studies involving 2551 critically ill patients. The ω-3 fatty acids intervention significantly increased EPA and DHA levels. For inflammatory and immune markers, it increased CD4⁺ T lymphocytes, the CD4⁺/CD8⁺ ratio, and decreased C-reactive protein (CRP) levels. For pulmonary function, it increased PaO₂, SaO₂, and PaO₂/FiO₂, and decreased airway resistance, positive end expiratory pressure, and lactate levels. For clinical outcomes, it significantly shortened mechanical ventilation days [mean difference: -1.31; 95% confidence interval (CI): -2.54, -0.09; P = 0.04] and length of hospitalization (mean difference: -3.96; 95% CI: -7.83, -0.09; P = 0.04). Both enteral and parenteral supplementation with ω-3 could reduce CRP levels, shorten hospital stay, and improve the oxygenation index. Besides, ω-3 via enteral nutrition also increases PaO₂ and shortens mechanical ventilation days.

Conclusions: In critically ill patients, ω-3 fatty acids may improve fatty acid concentrations, modulate immune regulation, enhance pulmonary function, and be associated with improved clinical outcomes.

Background: Supplementation with recombinant bovine β-lactoglobulin (rBLG), a precision-engineered mimetic of dairy-derived whey, supports similar resistance exercise (RE) training-induced muscle remodeling to whey protein (WHEY). However, the influence of rBLG on recovery indices and muscle protein synthesis rates after damaging exercise is unknown.

Objectives: To determine the influence of rBLG supplementation on indices of muscle recovery and integrated myofibrillar protein synthesis (iMyoPS) over 72 h following damaging RE, compared with WHEY and a carbohydrate placebo.

Methods: In a randomized double-blind, placebo-controlled, parallel-group design, 27 healthy adults consuming a controlled diet (∼0.9 g/kg body mass/d of protein) were supplemented thrice daily with 0.3 g/kg body mass of rBLG, WHEY, or isocaloric carbohydrate placebo for 3 d following an acute bout of damaging lower-body RE (8 × 10 maximal, unilateral, eccentric knee extensions). Consumption of deuterated water combined with serial vastus lateralis muscle biopsies permitted the measurement of iMyoPS 72 h before (habitual) and after RE. Knee extensor maximum voluntary contraction (MVC), muscle soreness, and plasma concentrations of creatine kinase and lactate dehydrogenase (LDH) were also assessed post-RE to characterize muscle recovery.

Results: iMyoPS fractional synthetic rate (%/d) increased following damaging RE (P < 0.001), with no significant differences between groups. Knee extensor MVC decreased, and subjective muscle soreness and plasma LDH concentrations increased following strenuous exercise (P < 0.05 for all) with no significant differences between groups.

Conclusions: At habitual dietary protein intakes ∼0.9 g/kg body mass/d, further rBLG or WHEY supplementation did not influence muscle recovery or iMyoPS rates, suggesting that protein supplementation, at the intakes studied, may have limited efficacy as a tool to enhance muscle recovery and remodeling from damaging exercise.

Background: Extended exposure to hypobaric hypoxia at high altitude induces negative energy balance through elevations in resting metabolic rate (RMR) and decreases in energy intake. It is unknown if an overnight bout of normobaric hypoxic (NH) exposure at sea level induces similar changes in energy balance and associated mechanisms.

Objectives: The aim of this study is to determine the effects of a single overnight exposure to NH on RMR, heart rate (HR) variability (HRV), appetite, and energy intake compared with an overnight exposure to normobaric normoxia (NN) in normal-weight adults.

Methods: In this randomized, single-blind, sham-controlled, crossover study, 20 adults (22.7 ± 1.7 kg/m², 24.5 ± 3.9 y) slept 8 h in a tent maintained at either ∼15% (∼2640 m elevation) or ∼20% oxygen (∼305m elevation). The following morning, HRV was measured inside the tent using electrocardiography; RMR was measured outside the tent using indirect calorimetry; and energy intake and subjective appetite were assessed outside the tent with an ad libitum breakfast buffet and visual analog scales, respectively.

Results: Overnight peripheral oxygen saturation was lower in NH (mean ± SD: 88.2% ± 2.3%) compared with NN (96.2% ± 0.9%; P-condition < 0.0001). Root mean square of successive RR interval difference and high frequency activity, markers of parasympathetic nervous system (PNS) activity, were lower after NH (47.7 ± 19.5 ms and 524 ± 335 ms², respectively) compared with NN (58.3 ± 22.6 ms, P-condition = 0.034 and 748 ± 476 ms², P-condition = 0.052, respectively). HR was greater in NH (61.3 ± 7.4 bpm) compared with NN (56.2 ± 7.6 bpm; P-condition < 0.0001). RMR was elevated in NH (1.07 ± 0.18 kcal/min) compared with NN (1.04 ± 0.13 kcal/min; P-condition = 0.018). Appetite and energy intake did not differ between conditions (P-condition > 0.05).

Conclusions: One-night exposure to NH reduced PNS activity, increased HR and RMR, and had no impact on energy intake or appetite when compared with NN exposure. This trial is registered at https://clinicaltrials.gov/ as NCT04151927.