High levels of fructose consumption causes inflammation in the immune system and damages cells that contribute to the healthy functioning of organs and body systems, according to researchers at the University of Swansea, UK. 

The study authors say the findings uncover biological mechanisms behind the long-established connection between fructose and diseases such as obesity and diabetes.

“Research into different components of our diet can help us understand what might contribute to inflammation and disease and what could be best harnessed to improve health and well-being,” says Nick Jones, a researcher at Swansea University. 

Fructose is commonly found in products like sugary drinks, confectionery and processed foods. According to the researchers, consumption of fructose has steadily risen throughout the western world, largely driven by elevated levels of sucrose and high fructose corn syrup in F&B. 

This is thought to have exacerbated various non-communicable diseases, including non-alcoholic fatty liver disease. 

Emma Vincent of the Bristol Medical School, a researcher on the study, explains that the recent findings are “exciting” as they bring researchers closer to understanding why some diets lead to ill health.

The researchers hope their findings will contribute to disease prevention.Blood and mice 
Now published in Nature Communications, the researchers used both human blood samples and mice to investigate how fructose acts on the body in different ways. 

Peripheral blood was taken from human volunteers and cultured. Blood monocytes’ purity was then measured regularly and analyzed for flow cytometry.

The hind legs of mice were also used to extract bone marrow and red blood cells, which were then cultured separately. 

The exposure strategies helped isolate the impact of fructose on inflammation without interference from whole-body metabolism.

“We investigated how activated human monocytes and mouse macrophages respond metabolically and functionally to fructose exposure,” reads the study. 

The findings demonstrate that mononuclear phagocytes from both species are metabolically plastic in engaging in an alternative carbon source’s metabolism and reprogram cellular pathways to favor oxidative metabolism. 

Although able to rewire their metabolic pathways upon exposure to fructose, the cells are left “metabolically inflexible” and vulnerable to further metabolic challenge. 

The findings also show that fructose exposure ex vivo promotes elevated cytokine production in both human and mouse mononuclear phagocytes. A high fructose diet was shown to promote an inflammatory phenotype in vivo.

Further investigations 
The researchers are lauding the results for highlighting the metabolic plasticity of human monocytes in response to fructose exposure and elucidating the metabolic mechanisms supporting fructose-induced inflammation. 

“These findings highlight the importance of the microenvironment in shaping the innate immune response and could form the foundations of investigations for therapies in areas as diverse as cancer and infectious diseases,” concludes the study.