Toward nutrition improving outcome of critically ill patients: How to interpret recent feeding RCTs?

Critical Care, Journal Year: 2023, Volume and Issue: 27(1)

Published: Jan. 27, 2023

Abstract Although numerous observational studies associated underfeeding with poor outcome, recent randomized controlled trials (RCTs) have shown that early full nutritional support does not benefit critically ill patients and may induce dose-dependent harm. Some researchers suggested the absence of in RCTs be attributed to overrepresentation deemed at low risk, or a too amino acid versus non-protein energy dose formula. However, these hypotheses been confirmed by strong evidence. revealed any subgroup benefiting from support, nor increased doses indirect calorimetry-based dosing targeted 100% expenditure. Mechanistic feeding anabolic resistance futile catabolism extra provided acids, feeding-induced suppression recovery-enhancing pathways such as autophagy ketogenesis, which opened perspectives for fasting-mimicking diets ketone supplementation. Yet, presence an response cannot predicted monitored likely differs over time among patients. In monitor, value calorimetry seems obscure, especially acute phase illness. Until now, large focused on interventions were initiated first week critical There are no investigated impact different strategies after continued discharge intensive care unit recovering

Language: Английский

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Metabolism and epigenetics at the heart of T cell function

Trends in Immunology, Journal Year: 2023, Volume and Issue: 44(3), P. 231 - 244

Published: Feb. 9, 2023

T cell subsets adapt and rewire their metabolism according to functions surrounding microenvironment. Whereas naive cells rely on mitochondrial metabolic pathways characterized by low nutrient requirements, effector induce kinetically faster generate the biomass energy needed for proliferation cytokine production. Recent findings support concept that alterations in also affect epigenetics of cells. In this review we discuss connections between epigenetic changes such as histone post-translational modifications (PTMs) DNA methylation, well 'extra-metabolic' roles enzymes molecules. These collectively point a new group potential therapeutic targets treatment cell-dependent autoimmune diseases cancers.

Language: Английский

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Gut microbiome, short-chain fatty acids, alpha-synuclein, neuroinflammation, and ROS/RNS: Relevance to Parkinson's disease and therapeutic implications

Redox Biology, Journal Year: 2024, Volume and Issue: 71, P. 103092 - 103092

Published: Feb. 16, 2024

In this review, we explore how short-chain fatty acids (SCFAs) produced by the gut microbiome affect Parkinson's disease (PD) through their modulatory interactions with alpha-synuclein, neuroinflammation, and oxidative stress mediated reactive oxygen nitrogen species (ROS/RNS). particular, SCFAs-such as acetate, propionate, butyrate-are involved in gut-brain communication can modulate alpha-synuclein aggregation, a hallmark of PD. The patients PD has lower levels SCFAs than healthy individuals. Probiotics may be potential strategy to restore alleviate symptoms, but underlying mechanisms are not fully understood. Also discuss present guts brains PD, induce neuroinflammation via ROS/RNS. Alpha-synuclein is considered an early biomarker for link axis pathogenesis. Therefore, elucidating role impact on alpha-synuclein-induced microglia ROS/RNS crucial pathogenesis treatment.

Language: Английский

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The hormesis principle of neuroplasticity and neuroprotection

Cell Metabolism, Journal Year: 2024, Volume and Issue: 36(2), P. 315 - 337

Published: Jan. 10, 2024

Language: Английский

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Ketogenic diet and BHB rescue the fall of long-term potentiation in an Alzheimer’s mouse model and stimulates synaptic plasticity pathway enzymes

Communications Biology, Journal Year: 2024, Volume and Issue: 7(1)

Published: Feb. 16, 2024

Abstract The Ketogenic Diet (KD) improves memory and longevity in aged C57BL/6 mice. We tested 7 months KD vs. control diet (CD) the mouse Alzheimer’s Disease (AD) model APP/PS1. significantly rescued Long-Term-Potentiation (LTP) to wild-type levels, not by changing Amyloid-β (Aβ) levels. KD’s ‘main actor’ is thought be Beta-Hydroxy-butyrate (BHB) whose levels rose CD mice, BHB itself LTP APP/PS1 hippocampi. 6 most significant pathways induced brains RNAseq all related Synaptic Plasticity. increases synaptic plasticity enzymes p-ERK p-CREB both sexes, of brain-derived neurotrophic factor (BDNF) females. suggest rescues through BHB’s enhancement plasticity. falls Mild-Cognitive Impairment (MCI) human AD. BHB, because they are an approved supplement respectively, may therapeutically translationally relevant MCI phase Disease.

Language: Английский

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