Smaller genetic risk in catabolic process explains lower energy expenditure, more athletic capability and higher prevalence of obesity in Africans

Abstract

Lower energy expenditure (EE) for physical activity was observed in Africans than in Europeans, which might contribute to the higher prevalence of obesity and more athletic capability in Africans. But it is still unclear why EE is lower among African populations. In this study we tried to explore the genetic mechanism underlying lower EE in Africans. We screened 231 common variants with possibly harmful impact on 182 genes in the catabolic process. The genetic risk, including the total number of mutations and the sum of harmful probabilities, was calculated and analyzed for the screened variants at a population level. Results of the genetic risk among human groups showed that most Africans (3 out of 4 groups) had a significantly smaller genetic risk in the catabolic process than Europeans and Asians, which might result in higher efficiency of generating energy among Africans. In sport competitions, athletes need massive amounts of energy expenditure in a short period of time, so higher efficiency of energy generation might help make African-descendent athletes more powerful. On the other hand, higher efficiency of generating energy might also result in consuming smaller volumes of body mass. As a result, Africans might be more vulnerable to obesity compared to the other races when under the same or similar conditions. Therefore, the smaller genetic risk in the catabolic process might be at the core of understanding lower EE, more athletic capability and higher prevalence of obesity in Africans.

Figure 1. Correlation between MAF and the harm probability of SNPs (r_i) on common SNPs in ASW.

MAF is minor allele frequency. The equation of the line of best fit is f(x) = −0.4993x+0.3046, where x is MAF, correlation coefficient r² = 0.03304, and P = 2.17710⁻⁵.

Figure 2. The overall genetic risk on all screened SNPs in catabolic process.

R (subplot A) is the sum of harmful probabilities on all screened SNPs, and Num (subplot B) is the total number of mutations on all screened SNPs.

Figure 3. The genetic risk on population-shared SNPs in catabolic process.

R_p (subplot A) is the sum of harmful probabilities on population-shared SNPs, and Num_p (subplot B) is the total number of mutations on population-shared SNPs.

Figure 4. The genetic risk on population-shared and subpopulation-shared SNPs in catabolic process.

R_p+R_s (subplot A) is the sum of harmful probabilities on population-shared and subpopulation-shared SNPs, and Num_p+Num_s (subplot B) is the total number of mutations on population-shared SNPs. Genetic risk (R_p+R_s in subplot A) and the sum of mutation number (Num_p+Num_s in subplot B) at population- and subpopulation-shared SNPs on candidate genes of coronary heart disease in human groups.

Figure 5. The genetic risk on group-specific SNPs in catabolic process.

X (subplot A) is the sum of harmful probabilities on group-specific SNPs, and Num_x (subplot B) is the total number of mutations on group-specific SNPs.

Figure 6. Proportions of components in mean genetic risk in human groups.

In subplot A, R_p, R_s and X (subplot A) are the sums of harmful probabilities on population-shared, subpopulation-shared and group-specific SNPs, respectively. In subplot B, Num_p, Num_s and Num_x are the total numbers of mutations on population-shared, subpopulation-shared and group-specific SNPs, respectively.