Abstract
Obesity, a major risk factor for metabolic disorders, is highly prevalent in Qatari population. Maternal transmission of obesity traits can be significant; for example, X haplogroup is known to be associated with lower BMI and body fat mass in Northern Europeans and T haplogroup which is a sister haplogroup of J is known to be associated with obesity in Caucasian subjects from Austria and Southern Italy. We aimed to delineate the mitochondrial haplogroups and variants associated with obesity in Qatari population. Mitochondrial genomes of 864 Qatari individuals were extracted from whole exome sequencing data with an average coverage of 77X. We distributed the participants into 2 sub-cohorts: obese (BMI ≥ 30) and non-obese (BMI < 30); the mean value of BMI from these two groups were 36.5 ± 5.7 and 26.5 ± 2.6, respectively. Mitochondrial haplogroup profiling followed by uni- and multivariant association tests adjusted for covariates were performed. Qatari individuals with mitochondrial haplogroup J had an increased (twofold) risk of obesity (odds ratio [OR] 1.925; 95% CI 1.234–3.002; P = 0.0038; the Bonferroni adjusted P value threshold is 0.0041), whereas the individuals with haplogroup X were at low risk of obesity (OR 0.387; 95% CI 0.175–0.857; P = 0.019). Further, a set of 38 mitochondrial variants were found to be associated (at P ≤ 0.05) with obesity in models adjusted for age, sex and haplogroup.
Highlights
Obesity occurs when an individual’s energy balance is positive; i.e., energy intake exceeding energy expenditure leads to weight gain
The mitochondria genome is a double-stranded circular molecule of 16.6 kilo base pairs carrying 37 genes that encode for 13 proteins, 22 transfer RNAs, and 2 ribosomal RNAs6; the majority of the proteins functioning in the mitochondria are, encoded in nuclear DNA
These mitochondrial DNA (mtDNA) mismatches lead to accumulated variants, such as single nucleotide polymorphisms (SNPs) and insertions/deletions (INDELs); such variants enable the tracing of maternal lineages
Summary
Obesity occurs when an individual’s energy balance is positive; i.e., energy intake exceeding energy expenditure leads to weight gain. The susceptibility rate is increased at the non-coding region of the mitochondria, called the D-loop region, especially under oxidative stress These mtDNA mismatches lead to accumulated variants, such as single nucleotide polymorphisms (SNPs) and insertions/deletions (INDELs); such variants enable the tracing of maternal lineages. It is worth noting that these studies on maternal haplogroups were performed using variants that were extracted either from genome-wide genotype data generated using BeadChips in genome-wide association studies or from sequencing partial sections of the mitochondria genome using Sanger sequencing. Both genotyping strategies limit the number of analyzed SNPs and subsequently impact the resolution of maternal haplogroup prediction and the overall results. We extracted mtDNA from whole exome data on 864 Qatari individuals and evaluated the mitochondrial variants and haplogroups for associations with obesity
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