Our immune system plays a vital role: It protects us from harmful substances, cell changes, and germs. And it has been a part of many conversations since the start of COVID-19. Now, a new study by Swansea scientists in collaboration with researchers at the University of Bristol and the Francis Crick Institute in London has shown that consuming a diet high in fructose might prevent the proper functioning of our immune systems in ways that have, until now, largely been unknown.
Their study, “Fructose reprograms glutamine-dependent oxidative metabolism to support LPS-induced inflammation,” is published in Nature Communications.
Fructose is a type of simple sugar that makes up 50% of table sugar. It is found in sugary drinks and sweeteners, and it’s not news that consuming an excessive amount of fructose is unhealthy. However, understanding the impact of fructose on the immune system of people who consume it in high levels, has been limited until now.
“Fructose intake has increased substantially throughout the developed world and is associated with obesity, type 2 diabetes, and non-alcoholic fatty liver disease,” the researchers wrote. “Currently, our understanding of the metabolic and mechanistic implications for immune cells, such as monocytes and macrophages, exposed to elevated levels of dietary fructose is limited. Here, we show that fructose reprograms cellular metabolic pathways to favor glutaminolysis and oxidative metabolism, which are required to support increased inflammatory cytokine production in both LPS-treated human monocytes and mouse macrophages.”
The new study demonstrates that fructose causes the immune system to become inflamed and that process produces more reactive molecules which are associated with inflammation. This inflammation can go on to damage cells and tissues and contribute to organs and body systems not working and may lead to disease.
“Although able to rewire their metabolic pathways upon exposure to fructose, the cells are left metabolically inflexible and vulnerable to further metabolic challenge. Importantly, we show that fructose exposure ex vivo promotes elevated cytokine production in both human and mouse mononuclear phagocytes and that a high fructose diet promotes an inflammatory phenotype in vivo, attributing pathophysiological relevance to our findings,” noted the researchers.
The findings also provide a better understanding of how fructose is related to diabetes and obesity.
“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 wellbeing,” said Nick Jones, PhD, lecturer, biomedical sciences, Swansea University’s Medical School.
“Our results have highlighted the metabolic plasticity of human monocytes in response to fructose exposure and have elucidated the metabolic mechanisms supporting fructose-induced inflammation,” concluded the researchers.
Their findings highlight the importance of the microenvironment in shaping the innate immune response and may lead to further studies in areas such as cancer and infectious diseases.