Background
Obesity and diabetes are serious and growing public
health problems that result in reduced life expectancy
and increased morbidity due to disease-specific vascular
complications. Moreover, there is considerable evidence
linking obesity and diabetes with oxidative stress and
mitochondrial dysfunction in human and animal models.
For instance, serum thiobarbituric acid-reactive substances
(TBARS) were elevated, and serum total thiols and superoxide
dismutase (SOD) activity were decreased in patients
with metabolic syndrome compared with healthy subjects
[1]. Likely, systemic oxidative stress was increased in obese
children with and without metabolic syndrome [2], and reactive
oxygen species (ROS) and malondialdehyde (MDA)
were higher in diabetic subjects compared with control
subjects [3]. With respect to adenosine-5′-triphosphate
(ATP) synthesis, abdominal obesity was associated with
reduced mitochondrial ATP and ROS production rates in
skeletal muscle of men [4]. Moreover, diabetic patients
had reduced ATP synthesis and elevated lipid contents in
liver [5], as well as reduced ATP synthesis [6,7]; and
reduced expression of the α-subunit of ATP synthase [8]
in skeletal muscle as compared to control subjects.
Mitochondria isolated from the livers of mice