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In Randomized Study, Patients at High Genetic Risk of Obesity Were Less Likely to Benefit From Exercise

NEW YORK (GenomeWeb) – People whose genetic profiles put them at high risk for obesity are less likely to respond to resistance exercise by losing weight or body fat, according to a study appearing today in the International Journal of Obesity.

More than 30 SNPs have been linked to variations in body-mass index, but how these SNPs influence weight loss or body composition changes in response to exercise is not clear.

Researchers from the University of Arizona randomized 150 women with varying genetic risks of obesity, as gauged by a score based on 21 SNPs linked to BMI, to either participate in a supervised, year-long exercise program or not. Based on this, the researchers found that women with low-risk scores were more likely to lose weight through the exercise program than women with high-risk scores.

"In a block-randomized clinical trial for resistance exercise, we find significant 
interactions of exercise with genetic risk for obesity on change in weight and body fat," Arizona's Zhao Chen and her colleagues wrote in their paper. "It appears that these interactions are not driven by any one particular SNP, but rather are the result of a collective effect of many SNPs."

Chen and her colleagues drew on a subset of the Bone Estrogen Strength Training (BEST) Study, in which post-menopausal women, both those on and not on hormone replacement therapy, were block randomized to an exercise program arm or non-exercise arm. The exercise program consisted of high-intensity resistance training and moderate impact weight-bearing exercise for an hour and fifteen minutes, three times a week, for a year.

The women were also instructed not to alter their diet or hormone therapy status during the course of the study. The researchers measured the participants' height, weight, and body composition traits at baseline and after one year.

The researchers recruited 266 women who'd completed a year of that study for additional genetic analysis, and 148 women returned the consent form with a buccal DNA sample for analysis.

Some 32 SNPs had previously been linked to BMI through a genome-wide association study meta-analysis, and Chen and her colleagues were able to genotype their cohort for 21 of those SNPs using the Sequenom Mass Array platform.

By adding all these risk alleles together and weighing them by their effect size, the researchers came up with a genetic risk score for BMI.

Using a multiple linear regression model, Chen and her colleagues found a statistically significant interaction between exercise and the genetic risk score on changes in weight, total and percent body fat, and abdominal fat from baseline measurements.

People with the highest genetic risk of obesity showed the weakest putative effect of exercise, the researchers reported.

In addition, the effect seemed to be due to the full expanse of SNPs rather than any one SNP in particular.

As BMI-associated genes are highly expressed in the hypothalamus, the researchers hypothesized that they might influence the effects of physical activity through physiological mechanisms like taste, satiety, or the regulation of energy expenditure. But uncovering just how these variants influence BMI will require additional research, the researchers said.

"Further research in other populations may eventually enable the routine use of genetic profile information in tailoring disease prevention and treatment measures," Chen and her colleagues added.