The prevalence of metabolic syndrome, a cluster of cardiovascular risk factors associated with obesity and insulin resistance,
is dramatically increasing in Western and developing countries. This disorder includes hypertriglyceridemia, altered lipoprotein levels, insulin resistance,
abnormal glucose tolerance, and hypertension, which—together with genetic susceptibility and abdominal obesity—are risk factors for
type 2 diabetes, vascular inflammation, atherosclerosis, and renal, liver, and heart diseases1.
A key defect in metabolic syndrome is mitochondrial dysfunction. Characteristics include changes in mitochondrial membrane potential,
reduced ATP levels, inhibition of mitochondrial oxygen consumption, and decreased mitochondrial biogenesis2,3.
The underlying mechanism of mitochondrial dysfunction is complex, influenced by genetic factors from both nuclear and mitochondrial genomes
and numerous environmental factors4. In addition, excessive reactive oxygen species (ROS) production in obesity and type 2 diabetes5
contributes to mitochondrial damage, whereas physiological ROS levels act as "redox messengers" in intracellular signaling. ROS from mitochondria
or other cellular sites can damage mitochondrial components and trigger degradative processes, contributing to aging.
When mitophagy is compromised, oxidized proteins accumulate, impairing cellular respiration and insulin secretion6.
Mitochondria remain a key target for the prevention and treatment of metabolic disorders7.
Quantitative mitochondrial profiling enables better understanding of metabolic disease progression and drug efficacy in patient-derived or hepatic cellular models.