Peripheral and central glucose utilizations modulated by mitochondrial DNA 10398A in bipolar disorder

Psychoneuroendocrinology
Cheng-Ta LiTung-Ping Su

Abstract

Bipolar disorder (BD) is highly heritable and associated with dysregulation of brain glucose utilizations (GU). The mitochondrial DNA (mtDNA) 10398A polymorphism, as a reported BD risk factor, leads to deficient glycolytic energy production by affecting mitochondrial matrix pH and intracellular calcium levels. However, whether mtDNA-10398A has functional effects on the brain and how our body responds remain elusive. We compared peripheral and central glucose-utilizing patterns between mtDNA A10398G polymorphisms in BD and their unaffected siblings (BDsib). Since siblings carry identical mtDNA, we hypothesized that certain characteristics co-segregate in BD families. We recruited twenty-seven pairs of non-diabetic BD patients and their BDsib and 30 well-matched healthy control subjects (HC). The following were investigated: mtDNA, fasting plasma glucose/insulin, cognitive functions including Montreal Cognitive Assessment (MoCA), and brain GU at rest. Insulin resistance was rechecked in sixty-one subjects (19-BD, 18-BDsibib, and 24-HC) six months later. We found that BD-pairs (BD+BDsib) carried more mtDNA-10398A and had higher fasting glucose, even after controlling for many covariates. BD-pairs had abnormally lower dorso-prefron...Continue Reading

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Citations

Feb 13, 2016·Journal of Affective Disorders·Rodrigo B MansurElisa Brietzke
Aug 21, 2015·International Journal of Legal Medicine·Monika StoljarovaBruce Budowle
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Mar 30, 2018·Molecular Neuropsychiatry·Euijung RyuJoanna M Biernacka

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