The AKT1 gene codes for an enzyme related to muscle building and metabolism. Some of us carry a particular version of this gene that is linked to better resting metabolic factors and greater increases in VO2 max in response to aerobic exercise. Your FitnessGenes result tells you which version of this gene you carry.


The AKT1 gene contributes to the expression of the AKT1 enzyme (also known as PKB-α), which is an important molecule involved in the regulation of multiple processes including muscle growth and metabolism. It is believed to be a mediator of insulin function and enhances glucose uptake in muscle, fat cells and liver cells, amongst others. One particular version of this gene is believed to affect our baseline metabolic processes and response to exercise. Experiments have shown that increased expression of the AKT1 gene has an anabolic (growth) effect on muscle and bone, while reduced expression has a catabolic (breakdown) effect on fat.

Global population distribution:

Source: 1000 Genome Project. Global averages for both sexes

AKT1: GG

59%

AKT1: TG

34%

AKT1: TT

7%

More about AKT1

THE EFFECT OF AKT1 ON MUSCLE HYPERTROPHY AND NO PRODUCTION

Although the impact of the different genotypes on the levels of AKT1 produced remains unclear, evidence from animal experiments indicates that AKT1 plays an important role in muscle hypertrophy and atrophy. For example, a study with mice that lack the AKT1 gene (and thus produce no AKT1 enzyme at all) showed that these animals are up to 20% smaller than normal mice. This suggests that increased AKT1 expression in muscle cells has a hypertrophic effect. Specifically, research indicates that the state of AKT1 affects the activation of mTOR - a regulator of muscle growth - leading to increases in muscle fibre size through protein synthesis. In addition, AKT1 inactivates a family of transcription factors (proteins that bind to DNA and affect how it is read), which prevents the induction of atrophy signals.

AKT1 also influences blood flow and vasodilation by increasing endothelial cell nitric oxide (NO) production.

ROLE IN METABOLIC SYNDROME

Mice and human studies suggest the version of this gene you carry may influence your risk of developing metabolic syndrome. In one mouse study, Akt1 ‘knock-out’ mice had decreased blood glucose levels, improved glucose tolerance and insulin sensitivity. This suggests lower AKT1 expression could be beneficial for lowering metabolic syndrome susceptibility. Although we do not yet know what effect the different genotypes have on AKT1 expression levels directly, studies have indicated that the T allele appears to provide a protective effect against metabolic syndrome, especially in men, and carriers in multiple studies have been found to have lower fasting glucose, fasting insulin and triglyceride levels. As a result, it is proposed that the T allele is associated with lower AKT1 expression – although this reduced expression may only be limited to fat cells.

THE EFFECT OF AKT1 IN UNTRAINED INDIVIDUALS AND THE IMPACT OF AEROBIC EXERCISE

In a recent study, the effects of the AKT1 genetic variation were determined in healthy but untrained individuals aged 50-75. In men, it showed that the GG genotype had lower VO2 max, lower insulin function and higher % body fat and % subcutaneous fat than T allele carriers. However, in women none of these variables differed between genotypes. Despite this disadvantage, men with the GG genotype seemed to respond to exercise training more effectively than men with the T allele, highlighted by significantly greater improvements in insulin sensitivity and glucose levels. However,the change in VO2 max was not as great as that of the T allele carriers (presumably reflecting the actions of AKT1 on skeletal and cardiac muscle). For the women in this study, carrying a T allele appeared to provide an advantage in aerobic exercise training. Despite a similar baseline, those with a T allele had greater improvements in fasting glucose and insulin sensitivity than GG individuals as a result of training, although both groups saw a significant increase in VO2 max.

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