Mike Montemarano, Associate Editor 03.08.21
Throughout the world, high intake of fructose has increased substantially, especially through sugar-sweetened beverages, processed foods, and sweets. The phenomenon has been associated with a rise in a wide range of conditions, including obesity, type 2 diabetes, and non-alcoholic fatty liver disease, and scientific understanding of how high fructose concentrations effect health on a cellular level is limited.
However, a team of researchers at Swansea University recently published a study in the journal Nature Communications which identified one of the cellular mechanisms by which fructose might prevent proper functioning of people’s immune systems, during an in vitro study of monocytes (white blood cells).
According to the study, high fructose concentrations reprogrammed cellular metabolic pathways to favor glutaminolysis and oxidative metabolism, two processes which support increased inflammatory cytokine production in both human monocytes and mouse macrophages. Additionally, these cells treated with fructose relied heavily on oxidative metabolism and mitochondrial inhibition.
Inflammation of this kind could go on to damage cells and tissues, contribute to organs and body systems not working as they should, and could lead to disease, the authors of the study said.
Because obesity is associated with low-level inflammation, the research also brings a deeper understanding as to how fructose could be linked to diabetes and obesity.
“It is clear that fructose levels fluctuate throughout health and disease,” the authors of the study concluded. “With the increased prevalence of high fructose diets in the Western world, understanding the impact of fructose on human health is critical. Fructose contributes to numerous metabolic disorders such as obesity, cancer, and non-alcoholic fatty liver disease; however, to date, our understanding of its impact on the immune system is lacking.”
“In addition, our work using metabolic inhibitors shows that fructose treatment leaves cells metabolically inflexible and acutely vulnerable to further metabolic challenge,” the authors continued. “This highlights a potential vulnerability of human monocytes exposed to fructose when facing metabolically challenging environments, such as during bacterial infection (including sepsis) or in the tumor microenvironment, particularly in those individuals with a high fructose diet.”
However, a team of researchers at Swansea University recently published a study in the journal Nature Communications which identified one of the cellular mechanisms by which fructose might prevent proper functioning of people’s immune systems, during an in vitro study of monocytes (white blood cells).
According to the study, high fructose concentrations reprogrammed cellular metabolic pathways to favor glutaminolysis and oxidative metabolism, two processes which support increased inflammatory cytokine production in both human monocytes and mouse macrophages. Additionally, these cells treated with fructose relied heavily on oxidative metabolism and mitochondrial inhibition.
Inflammation of this kind could go on to damage cells and tissues, contribute to organs and body systems not working as they should, and could lead to disease, the authors of the study said.
Because obesity is associated with low-level inflammation, the research also brings a deeper understanding as to how fructose could be linked to diabetes and obesity.
“It is clear that fructose levels fluctuate throughout health and disease,” the authors of the study concluded. “With the increased prevalence of high fructose diets in the Western world, understanding the impact of fructose on human health is critical. Fructose contributes to numerous metabolic disorders such as obesity, cancer, and non-alcoholic fatty liver disease; however, to date, our understanding of its impact on the immune system is lacking.”
“In addition, our work using metabolic inhibitors shows that fructose treatment leaves cells metabolically inflexible and acutely vulnerable to further metabolic challenge,” the authors continued. “This highlights a potential vulnerability of human monocytes exposed to fructose when facing metabolically challenging environments, such as during bacterial infection (including sepsis) or in the tumor microenvironment, particularly in those individuals with a high fructose diet.”
