Abstract
Mitochondrial DNA (mtDNA) encodes core subunits of oxidative phosphorylation complexes and, as a result of intricate regulatory crosstalk between nuclear and mitochondrial genomes, the total number of mtDNA copies fits the requirements of each cell type. Deviations from the physiological number of mtDNA copies are expected to be deleterious and might cause some inherited diseases and normal ageing. We studied 46 obese patients with type 2 diabetes (T2DM) one year after a laparoscopic sleeve gastrectomy (LSG) and Roux-en-Y gastric bypass (RYGB). The results were compared with normal-weight patients without T2DM (control group 1) (body mass index (BMI) = 22.5 ± 3.01 kg/m2) and patients with obesity without T2DM (control group 2) (BMI = 36 ± 3.45 kg/m2). We detected an increase of mtDNA copy number in the cells of the buffy coat obtained from peripheral blood, sampled one year after bariatric surgery. We also found that average mtDNA copy number as well as its dynamics (before and after the surgery) are gender-specific. To the best of our knowledge, this is the first evidence for the restoration of mtDNA copy number in obese patients after LSG and RYGB.
Highlights
Human mitochondria contain double-stranded circular DNA that encodes 13 proteins of oxidative phosphorylation complexes and RNA elements of Mitochondrial DNA (mtDNA) gene translation machinery [1,2].it is becoming more evident that mtDNA has more informational capacity than previously imagined
We investigated the relationship of mtDNA copies with the concentrations of carbohydrate metabolism components in the blood plasma of operated patients, depending on the type of bariatric surgery
We found here that plasma ghrelin level was decreased in patients with T2DM after laparoscopic sleeve gastrectomy (LSG) compared to the pre-operating conditions (p < 0.05, Wilcoxon test) and correlated positively with glucose level (r = 0.45) and body mass index (BMI) (r = 0.36) in all observed patients with
Summary
It is becoming more evident that mtDNA has more informational capacity than previously imagined. In addition to the universally recognized genes [3], mtDNA may encode some functional peptides [4,5], long noncoding RNAs [6,7], and even microRNAs [8]. This implies that the functional capacity of mtDNA may be much broader than previously assumed and deviations in the normal crosstalk between nuclear and mitochondrial genome may be the cause of predisposition to numerous diseases.
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