# Maternal Exposure to Microplastics and High-Fructose Diet Induces Offspring Hypertension via Disruption of H2S Signaling, Gut Microbiota, and Metabolic Networks

## TL;DR

Exposure to microplastics and a high-fructose diet during pregnancy can raise offspring blood pressure by disrupting hydrogen sulfide signaling and gut microbiota.

## Contribution

This study reveals the combined effects of maternal microplastic exposure and high-fructose diet on offspring hypertension through H2S signaling and gut microbiota disruption.

## Key findings

- Maternal high-fructose diet or microplastic exposure increases offspring blood pressure with additive effects when combined.
- Microplastic exposure reduces hydrogen sulfide production and causes kidney injury in offspring.
- Both exposures alter gut microbiota and metabolic pathways linked to blood pressure regulation.

## Abstract

Maternal consumption of a high-fructose (HF) diet or exposure to microplastics (MPs) can each independently affect kidney development and increase the risk of hypertension in adult offspring, yet their combined impact remains poorly understood. Dysregulation of hydrogen sulfide (H2S) signaling and alterations in gut microbiota are potential mediators of this programming. Pregnant rats received either standard chow or a 60% HF diet, with half of each group additionally exposed to sulfate-modified MPs (1 mg/L) with a 5 μm diameter throughout pregnancy and lactation. Male offspring were divided into four groups (n = 7–8 per group): control, HF, MP, and HF+MP. Maternal HF or MP exposure raised offspring blood pressure (BP), with additive effects when combined, and MP exposure caused renal injury. MP treatment also suppressed renal H2S-generating enzymes and reduced H2S production. Both HF and MP exposures altered gut microbial composition linked to BP regulation and induced metabolic changes in taurine/hypotaurine and sulfur pathways, suggesting impaired H2S production. These results indicate that maternal HF and MP exposures interfere with H2S signaling, gut microbiota, and metabolic programming, highlighting the H2S signaling as a potential target to reduce long-term kidney and cardiometabolic risks.