These foods not only shorten your lifespan, but also make you more addicted

The Maillard reaction is a non-enzymatic browning that is widely present in the food industry. It is a reaction between reducing sugars and amino acids and proteins. It can produce some delicious substances and eventually generate dark brown macromolecules, such as melanoidins.

Foods rich in advanced glycation end products include: fried foods, grilled and barbecued foods, baked foods, foods slow-cooked for a long time, etc.

However, the Maillard reaction also occurs in all cells from prokaryotes to eukaryotes, forming advanced glycation end products (AGEs). Early studies have shown that AGEs can cause various damages to the body, including causing inflammation and oxidative damage, leading to hardening of the blood vessels, high blood pressure, kidney disease, cancer, and nervous system problems.

Recently, researchers from the Buck Institute for Research on Aging published a research paper titled "Methylglyoxal-derived hydroimidazolone, MG-H1, increases food intake by altering tyramine signaling via the GATA transcription factor ELT-3 in Caenorhabditis elegans" in the journal "eLife."

The study showed that advanced glycation end products produced by the Maillard reaction promote disease risk, shorten the lifespan of worms by 25-30%, and increase the worms' appetite for more of the same substance.

In this study, the researchers analyzed the biochemical signaling pathways that cause normal, healthy worms to overeat. By purifying advanced glycation end products, they found that two of the substances could increase worm feeding.

The analysis found that a specific mutation, the glod-4 mutation, increased food intake and was found to be mediated by a specific AGE (MG-H1). Further analysis showed that a tyramine-dependent pathway was responsible.

Furthermore, RNAseq analysis revealed that several neurotransmitter and feeding genes were upregulated in glod-4 knockdown worms.

The researchers also screened and identified tdc-1 or tyra-2/ser-2 signaling as important pathways mediating MG-H1-induced feeding in glod-4 mutants by overfeeding worms. Deficiency of tdc-1 or tyra-2/ser-2 receptors suppressed lifespan shortening and avoided the neuronal damage caused by feeding.

In the study, the researchers found that even naturally occurring AGEs, which cannot be processed, can shorten the lifespan of worms by about 25-30%.

The researchers say this study is the first to identify a signaling pathway mediated by a specific AGE molecule to enhance eating and neurodegeneration. Understanding this signaling pathway may shed light on overeating caused by an AGE-rich diet.

The researchers are currently extending this work to mice to investigate the link between AGEs and fat metabolism.

Taken together, the results suggest that the accumulation of AGEs is associated with disease promotion, increased appetite, and neurodegenerative diseases, and understanding this signaling pathway may help combat global obesity and other age-related diseases.

Paper link:

https://doi.org/10.7554/eLife.82446