Abstract
Abstract
Consumption of ultra-processed food (UPF) is increasing and is causally linked with noncommunicable disease onset, however specific compounds within UPFs that influence disease risk remain poorly defined. The acronym ‘SCars’, for Stable Carbonyl Adducts, is introduced herein as an umbrella term encompassing advanced glycation end-products (AGEs), advanced lipoxidation end-products (ALEs), and other carbonyl-derived modifications. These molecules arise as products of spontaneous carbonyl chemistry, a reaction accelerated by industrial food processing. Dietary SCars have been associated with metabolic dysfunction; however, their impact on microbiome composition during windows of developmental vulnerability has not been well studied. Puberty in mice represents a period of developmental plasticity during which the gut microbiome is susceptible to dietary exposures. We tested whether transient exposure to high levels of dietary SCars during puberty remodels the developing gut microbiome. Using metagenomic sequencing of fecal samples from mice exposed to high-SCars or control diets, we found that high-SCars exposure profoundly impacted microbial community structure and metabolic potential. Dietary SCars reduced microbial diversity and depleted short-chain fattyacid producing taxa while enriching pathways related to membrane remodeling, branched-chain amino acid biosynthesis, and nucleotide anabolism. These data identify SCars as features of UPFs capable of reprogramming the developing gut microbiota.