Abstract
Ultra-processed foods have known negative implications for health; however, their effect on skeletal development has never been explored. Here, we show that young rats fed ultra-processed food rich in fat and sugar suffer from growth retardation due to lesions in their tibial growth plates. The bone mineral density decreases significantly, and the structural parameters of the bone deteriorate, presenting a sieve-like appearance in the cortices and poor trabecular parameters in long bones and vertebrae. This results in inferior mechanical performance of the entire bone with a high fracture risk. RNA sequence analysis of the growth plates demonstrated an imbalance in extracellular matrix formation and degradation and impairment of proliferation, differentiation and mineralization processes. Our findings highlight, for the first time, the severe impact of consuming ultra-processed foods on the growing skeleton. This pathology extends far beyond that explained by the known metabolic effects, highlighting bone as a new target for studies of modern diets.
Highlights
The vertebrate skeleton has evolved as a dynamic system that serves numerous functions, such as protecting internal organs, creating attachment sites for muscles to produce locomotion, providing a reservoir for minerals, and serving as a hematopoietic niche
In the proliferative zone (PZ), chondrocytes are arranged in longitudinal columns, where they rapidly proliferate and deposit typical cartilage extracellular matrix (ECM) components, especially collagen type 2 (Col2) and aggrecan (Acan)
Extensive consumption of processed food and soft drinks is endemic in the modern era, with many known metabolic implications.[11]
Summary
To study the link between UPF consumption and postnatal Effect of UPF on GP organization skeletal development, we conducted a 6-week-long in vivo trial in Abnormal bone phenotypes may stem from interference with young female rats (3 weeks to 9 weeks of age) This time frame the EO process in the GP2. Enlargement of the GP and the different proportions of Surprisingly, growth in the UPF + CSD group was the proliferative vs nonproliferative regions in the GP were retarded, caloric intake (derived from both food and the caloric observed in the UPF + CSD rats (Fig. 2e). These results suggested soft drink) was significantly higher (Fig. 1d). That in the control group at both time points
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