The work provides novel genetic insights into dietary preferences and opens the possibility of targeting SI to selectively reduce sucrose intake at the population level.
The study was led by Dr. Peter Aldiss, now a group leader in the School of Medicine at the University of Nottingham, alongside Assistant Professor Mette K Andersen, at the Novo Nordisk Foundation Centre for Basic Metabolic Research in Copenhagen and Professor Mauro D’Amato at CIC bioGUNE in Spain and LUM University in Italy. It also involves scientists internationally from Copenhagen, Greenland, Italy and Spain as part of the ‘Sucrase-isomaltase working group’.
Dr Aldiss said: “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.
“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.”
The team of experts began by investigating the dietary behaviours in mice lacking the SI gene. Here, mice developed a rapid reduction in sucrose intake, and preference. This was confirmed in two large population-based cohorts involving 6,000 individuals in Greenland and 134,766 in the UK BioBank.
The team took a nutrigenetics approach to understand how genetic variation in the SI gene impacts sucrose intake and preference in humans. Strikingly, individuals with a complete inability to digest dietary sucrose in Greenland consumed significantly less sucrose-rich foods whilst individuals with a defective, partially functional SI gene in the UK, liked sucrose-rich foods less.
“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,” says Dr 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.”
