# Evaluation of Alterations in Nutrient Utilization and Intestinal Health in Response to Heat Stress in Pekin Ducks Based on a Pair-Feeding Experimental Design

## TL;DR

Heat stress in Pekin ducks reduces nutrient use and gut health, with reduced feed intake being a key factor in these effects.

## Contribution

This study characterizes the impact of heat stress on nutrient utilization and gut health in Pekin ducks using a pair-feeding design.

## Key findings

- Heat stress reduces dietary energy, protein, and fat utilization in Pekin ducks.
- Heat stress causes gut barrier dysfunction and microbiota changes, worsening intestinal health.
- Reduced feed intake is a primary driver of gut health deterioration under heat stress.

## Abstract

As global temperatures rise, heat stress (HS) is becoming a prevalent stressor with deleterious consequences for duck growth and health. Under HS conditions, birds reduce feed intake (FI) and undergo physiological adaptations to mitigate heat production or enhance heat dissipation, yet HS effects on nutrient utilization and gut health in meat ducks—particularly under pair-fed experimental designs—remain poorly characterized. This study investigated alterations in nutrient utilization, standardized ileal amino acid digestibility, and intestinal health parameters in Pekin ducks exposed to HS. The results demonstrated that HS induces intestinal barrier dysfunction and microbiota dysbiosis, thereby impairing gut health and consequently reducing dietary nutrient utilization. Critically, although reduced FI constitutes an adaptive mechanism to limit metabolic heat load, data indicate this FI reduction represents a primary driver of intestinal health compromise in HS-exposed Pekin ducks.

The objective of this study was to investigate alterations in nutrient utilization, standardized ileal digestibility of amino acids (SIDAA), and intestinal health in response to heat stress (HS) in Pekin ducks. A total of 240 healthy 28-day-old male Pekin ducks were randomly allocated to three groups: a normal control (NC) group, an HS group, and a pair-fed (PF; provided an amount of feed equal to that consumed by the HS group to eliminate the effects of feed intake) group, each with eight replicate cages of ten birds. The results showed that HS significantly reduced the apparent utilization of dietary energy, ether extract, and crude protein compared to both the NC and PF groups (p < 0.05), but yielded comparable SIDAA to the PF group. The HS group exhibited reduced mRNA levels of EAAT3 and PepT1, along with elevated mRNA levels of CAT1, GLUT5, and FATP6 in the jejunum compared to the NC or PF groups, respectively (p < 0.05). Furthermore, HS resulted in a significant deterioration of jejunal morphology and goblet cell count compared to the NC and PF groups (p < 0.05). Serum fluorescein isothiocyanate-dextran levels were significantly higher in HS ducks than in NC ducks (p < 0.05), but did not differ from PF ducks. At order-level classification of ileal mucosal microbiota, HS markedly increased the relative abundance of Bacillales, Deferribacterales, and Actinomycetales versus NC (p < 0.05), while significantly decreasing Bifidobacteriales abundance relative to PF (p < 0.05). Collectively, HS induces a leaky gut and microbiota dysbiosis that compromises gut health, thereby reducing dietary nutrient utilization in Pekin ducks. The observed reduction in feed intake constitutes a primary driver of intestinal health deterioration in heat-stressed Pekin ducks.