Scientists from multiple countries have discovered a genetic variation that affects sucrose intake and preference. This groundbreaking study could pave the way for new strategies to combat obesity and type 2 diabetes.
In a new study, published today in the journal Gastroenterology, researchers have uncovered a genetic variation that could explain why some people crave sugary treats more than others. This discovery opens up exciting possibilities for developing new treatments to curb sugar intake and combat related health issues, such as obesity and type 2 diabetes.
The study, led by Peter Aldiss, a group leader in the School of Medicine at the University of Nottingham, was conducted alongside Mette K. Andersen, an assistant professor at the Novo Nordisk Foundation Centre for Basic Metabolic Research in Copenhagen, and Mauro D’Amato, a professor at CIC bioGUNE in Spain and at LUM University in Italy. It also involved scientists from Denmark, Greenland and Spain as part of the “Sucrase-isomaltase working group.”
“Excess calories from sugar are an established contributor to obesity and type 2 diabetes. In the UK, we consume 9-12% of our dietary intake from free sugars, such as sucrose, with 79% of the population consuming up to three sugary snacks a day. At the same time, genetic defects in sucrose digestion have been associated with irritable bowel syndrome, a common functional disorder affecting up to 10% of the population,” Aldiss said in a news release.
The team began their investigation by studying mice lacking the SI (sucrase-isomaltase) gene, which revealed reduced sucrose intake and preference. These findings were corroborated by large population-based cohorts, including 6,000 individuals in Greenland and 134,766 from the UK BioBank. The study utilized a nutrigenetics approach to understand how variations in the SI gene influence sucrose intake and preference in humans.
Their findings were particularly striking. Individuals in Greenland with a complete inability to digest dietary sucrose consumed significantly less sucrose-rich foods, while those in the UK with a partially functional SI gene exhibited a decreased liking for sugary foods.
“Now, our study suggests that genetic variation in our ability to digest dietary sucrose may impact not only how much sucrose we eat, but how much we like sugary foods,” Aldiss added.
This realization could have far-reaching implications. By targeting the SI gene, it might be possible to develop therapies aimed at reducing sucrose consumption at a population level.
“These findings suggest that genetic variation in our ability to digest dietary sucrose can influence our intake, and preference, for sucrose-rich foods whilst opening up the possibility of targeting SI to selectively reduce sucrose intake at the population level,” added Aldiss. “In the future, understanding how defects in the SI gene act to reduce the intake, and preference, of dietary sucrose will facilitate the development of novel therapeutics to help curb population-wide sucrose intake to improve digestive and metabolic health.”
This pioneering research holds promise not only for enhancing our understanding of dietary behaviors but also for addressing major public health challenges. By uncovering how genetic factors influence sugar consumption, researchers hope to pave the way for innovative treatments that could significantly improve global health outcomes.