From mitochondrial disturbances to energy requirements

Pierre Singer*

*Corresponding author for this work

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review


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.

Original languageEnglish
Title of host publicationNutrition in Intensive Care Medicine
Subtitle of host publicationBeyond Physiology
EditorsPierre Singer
Number of pages11
StatePublished - 2013
Externally publishedYes

Publication series

NameWorld Review of Nutrition and Dietetics
ISSN (Print)0084-2230
ISSN (Electronic)1662-3975


Dive into the research topics of 'From mitochondrial disturbances to energy requirements'. Together they form a unique fingerprint.

Cite this