Mitochondrial Dysfunction and Bioenergetic Deficits in Peripheral Blood Mononuclear Cells of Type 2 Diabetes Patients in Kogi State

Mitochondrial dysfunction is increasingly recognized as both a cause and consequence of insulin resistance and hyperglycaemia in type 2 diabetes, and its characterisation in peripheral blood mononuclear cells provides an accessible clinical window into metabolic bioenergetics in affected patients. This study characterises mitochondrial function and bioenergetic profiles in peripheral blood mononuclear cells from type 2 diabetes patients compared to healthy controls in Kogi State. Forty type 2 diabetes patients attending Kogi State General Hospital Lokoja and forty age- and sex-matched healthy controls were enrolled. Peripheral blood mononuclear cells were isolated by density gradient centrifugation and assessed for mitochondrial function using the Seahorse XF Mito Stress Test, measuring basal respiration, ATP-linked respiration, proton leak, maximal respiratory capacity, and spare respiratory capacity. Mitochondrial membrane potential was assessed by JC-1 fluorescent dye flow cytometry. Mitochondrial DNA copy number was determined by quantitative PCR. Complex I and III activities of the electron transport chain were measured spectrophotometrically in isolated mitochondria. Reactive oxygen species production from isolated mitochondria was quantified by MitoSOX fluorescence. Results show significantly reduced basal respiration, ATP-linked respiration, maximal respiratory capacity, and spare respiratory capacity in type 2 diabetes patients compared to controls. Mitochondrial membrane potential was significantly reduced. Complex I activity was significantly impaired in the diabetes group. Mitochondrial DNA copy number was reduced by 38 percent compared to controls. Mitochondrial ROS production was significantly elevated, indicating electron transport chain uncoupling. These findings establish mitochondrial bioenergetic deficits as a measurable feature of systemic metabolic dysfunction in Kogi State type 2 diabetes patients. Keywords: mitochondrial dysfunction, type 2 diabetes, bioenergetics, peripheral blood mononuclear cells, Kogi State.