Nature versus nurture is a phrase with which many of us are familiar. Our genes (nature) are responsible for many of our traits, but environmental influences (nurture) also have a role to play.
When it comes to obesity and type 2 diabetes, the general conviction is that consistently consuming more calories than what we burn each day, leads to weight gain and obesity, both of which predisposes us to develop type 2 diabetes. But when we change our lifestyle and lose weight, our fat cells and pancreas usually recover.
However, this simplistic explanation raises more questions that have been left unanswered. For example, why do some people lose weight more quickly than others, even if they follow the same diet or exercise regimen? Why do some people develop type 2 diabetes while others do not, even when their genetic risk is similar?
Researchers now believe that epigenetics, a relatively new branch of genetics, could hold the answer. Epigenitics is the study of changes in gene function without any alterations to the genetic code, or genome itself. Gene function is determined by the genetic information stored in the DNA as long complex sequence of four bases — adenine, guanine, thymine and cytosine.
DNA methylation is a type of epigenetic modification that occurs when small chemical tags called methyl groups attach to cytosine bases in the DNA code. This methylation switches a gene off. We inherit some epigenetic markers from our parents, but many occur spontaneously and change during our lifetime, fashioning each of us with a unique epigenome.
Recently, researchers from Lund University in Sweden reviewed studies with human participants that investigated how DNA methylation contributes to obesity and type 2 diabetes. When comparing the DNA methylation sites in pancreatic islets — the structures that produce insulin — from people with type 2 diabetes and those without the condition, the study identified nearly 26,000 regions that were different between the two groups. It is unclear at this point whether these changes are the cause or effect of type 2 diabetes.
The researchers found that a 5-day high-fat diet overfeeding, mimicking the diet seen in many obese people, changed both the gene expression and methylation patterns in human skeletal muscle and adipose tissue. Equally important, they discovered that it was easier to induce methylation changes by overfeeding than to reverse them by a control diet.
They found that exercise also affects the epigenome. Both single sessions and long-term exercise changed DNA methylation in skeletal muscle and fat, but the gene targets were different. This could explain why different people respond differently to exercise. As we age, our epigenome continues to alter, pointing the finger at aging as also another driving factor in epigenetic changes.
The researchers suggest that using DNA methylation at known risk sites in the genome as biomarkers could be used to help identify those individuals at higher risk of developing obesity and type 2 diabetes, and then using pharmacological agents to change the methylation pattern.
While the debate on whether nature or nurture is behind obesity and type 2 diabetes remains unresolved, it is important to remember that DNA methylation is only one type of epigenetic modification. With the research field slowly emerging from its infancy, there are bound to be some interesting discoveries on the horizon.