Nat Commun: Be healthy and eat less sugar!

Fructose is a simple sugar, the sweetest sugar among all natural sugars.

On February 22, local time, researchers from the University of Swansea, the University of Bristol, and the Francis Crick Institute jointly published an article entitled " Fructose reprogrammes glutamine-dependent oxidative metabolism to Nature Communications" in "Nature Communications".

As we all know, the immune system has an important position in the human body.

The researchers cultured activated human monocytes in vitro, then incubated them with fructose, glucose, and galactose, and stimulated the monocytes with lipopolysaccharide (LPS).

The study found that the baseline glycolysis level of fructose-treated monocytes was low, only slightly higher than that of the sugar-free control group.

Fructose mimics a metabolic pattern similar to nutrient restriction

In view of the unique metabolic characteristics of human monocytes exposed to fructose, the researchers analyzed the effect of fructose on monocyte function.

To determine whether the production of cytokines is transcriptionally regulated, the researchers performed RNA sequencing (RNA-seq) analysis on monocytes treated with glucose or fructose and stimulated by LPS.

Fructose promotes more inflammatory phenotypes

Since glutamine-derived carbon enters the tricarboxylic acid cycle (TCA) to help TCA-mediated amino acid synthesis, researchers speculate that fructose may increase glutamine-mediated atherosclerosis.

Studies have found that fructose-treated monocytes can incorporate glutamine-derived carbon into TCA cycle intermediates and amino acids.

Fructose treatment induces a faster metabolic cycle

In order to further study the effect of fructose exposure on inflammation in the body, the researchers subsequently constructed a mouse LPS systemic inflammation model.

LPS systemic inflammation model

All in all, the results of this study highlight the metabolic plasticity of human monocytes in response to fructose exposure and clarify the metabolic mechanism of fructose-induced inflammation.

Original source:

Jones, N.