Mitochondrial response to nutrient availability and its role in metabolic disease

Abstract

Metabolic inflexibility is defined as an impaired capacity to switch between different energy substrates and is a hallmark of insulin resistance and type 2 diabetes mellitus (T2DM). Hence, understanding the mechanisms underlying proper metabolic flexibility is key to prevent the development of metabolic disease and physiological deterioration. An important downstream player in the effects of metabolic flexibility is the mitochondrion. The objective of this review was to describe how mitochondrial metabolism adapts to limited nutrient situations or caloric excess by changes in mitochondrial function or biogenesis, as well as to define the mechanisms propelling these changes. Altogether, this should pinpoint key regulatory points by which metabolic flexibility might be ameliorated in situations of metabolic disease.

Effects of sea horse (Hippocampus abdominalis)-derived protein hydrolysate on skeletal muscle development

“…Nutrient depletion is said to increase the expression level of SIRT-1, a NAD + dependant deacetylase protein, thereby reducing muscle atrophy under energy expenditure/starvation (Gao et al 2014). In the present study, both the SHE administered mice groups -exercise and non-exercise-showed lower SIRT-1 expression level than their respective control groups, indicating that the protein supplement provides enough nutrients to the muscle tissue, thereby blocking them towards entering nutrition deprivation state (Data not provided in the figure).…”

Mitochondrial Dysfunction in Diabetic Neuropathy: a Series of Unfortunate Metabolic Events

“…[glucose] in diabetes leads to suppression of AMPK signaling via a fall in the AMP/ATP ratio [62,118,141,142]. Under these conditions, energy production is sufficient via glycolysis (the Crabtree effect) [139•, 140].…”

Metabolic signaling functions of ER–mitochondria contact sites: role in metabolic diseases

“…Mitochondria and endoplasmic reticulum (ER) play a crucial role in these processes, as their structure and function are dynamically regulated by nutritional and environmental cues, influencing energy metabolism. Particularly, both organelles are nutrient and energy sensors (Mandl et al 2009, Gao et al 2014, allowing the adaptation of cellular metabolism according to nutritional status. Moreover, both ER and mitochondria have recently emerged as crucial regulators of the innate immune response to both pathogens and cell stress (Martinon 2012, Lartigue & Faustin 2013, thus further controlling the metabolic adaptations in function of immune modifications.…”