Is DNA to blame for obesity?

Obesity is a complex disease that is influenced by a combination of genetic, environmental factors and lifestyle. While the exact genetic basis of obesity is not fully understood, research has identified some genes that play a role in the predisposition of humans to obesity.

The first evidence for the genetic background of obesity was in studies of twins where it was shown that the 70-90% of monozygotic twins show a similar fat masswhile in dizygotic twins, the percentage is reduced to 35-40%.

Also, studies of adopted individuals showed a strong correlation of BMI adopted children with their biological parents but not with foster parents.

The main factor that determines the mass of adipose tissue is leptin. Leptin is a hormone produced by fat cells and exerts its action in the hypothalamus. Leptin has ανορεξιογόνο action, however, the overweight and obese people show resistance to the action of leptin and while they have high levels , it causes anorexia. The gene LEPR (leptin receptor) encodes a receptor that is involved in signaling pathways that regulate appetite and energy balance. Mutations in this gene can disrupt the signaling of leptin, leading to increased food intake and obesity.

Another important gene for the genetic basis of obesity is the MCR4 (receptor melanocortin 4). The gene that is associated with the regulation of intake and expenditure of energy. Mutations in this gene are common in families with obese individuals and is responsible for the most common form of μονογονιδιακής obesity has been found until today. Variations in the gene MCR4 have been associated with increased appetite and decreased energy expenditure, leading to weight gain and obesity.

Very large studies of correlation of the entire genome that have been made, have revealed the first gene and the polymorphisms of the exhibit strong correlation with obesity. This gene is the FTO (fat mass and obesity – associated gene) and its role was not fully understood until the past decade but is now one of the most extensively studied genes associated with obesity. Mutations of this gene have been associated with increased Body Mass Index and a higher risk of obesity. The gene FTO is believed to affect appetite and energy expenditure. Mice in which deletion of the FTO gene showed a significant reduction of adipose tissue, while mice with overexpression of the gene showed obesity and metabolic syndrome.

In addition, epigenetic factors such as DNA methylation and modifications ιστόνης can also affect the expression of genes associated with obesity. These modifications, can also be affected by environmental factors such as diet, exercise and stress.

Therefore, it is important to note that while obesity has a strong genetic component, lifestyle factors such as diet, physical activity, and socioeconomic status also contribute significantly to the development of obesity.

Finally, there are about 25 genetic syndromes associated with obesity such as Prader-Willi, Bardet-Biedl (BBS), Alstrom, 16p (micro) deletion syndrome.