From mitochondrial disturbances to energy requirements.
An organism requires nutrients to produce ATP, but the substrate oxidative process increases oxidative stress. This fine-tuning is centralized in the mitochondria, which is able to react to any excess or deprivation in nutrients. In normal subjects, these regulations can induce inflammatory effect and obesity in energy excess and a decrease in oxidative stress in a hypocaloric diet. In the critically ill patient, the mitochondrial capacity to cope with severe illness not only includes oxygen supply and nutrient and substrate supply with adequate coupling efficiency of oxidative phosphorylation, but also limitation of hormonal disturbances, maintenance of mitochondrial gene transcription, and limitation of the activity of mitochondrial proteases that lead to autophagy. In the macroscopic perspective, overfeeding increases glycemia, infection rate, length of ventilation, and length of stay. Many observational studies correlate hypocaloric regimens with increased complications and mortality. This chapter integrates the mitochondrial mechanism's modeling nutrient administration with acute illness.
Critical Care Medicine, Institute for Nutrition Research, Rabin Medical Center, Beilison Hospital, Petah Tikva, Israel.
Pierre
P
Singer
D002153:Calorimetry, Indirect; D016638:Critical Illness / Q000628:therapy; D002149:Energy Intake; D004734:Energy Metabolism; D006801:Humans; D007413:Intestinal Mucosa / Q000378:metabolism; D008928:Mitochondria / Q000378:metabolism*; D009751:Nutritional Requirements