# In ovo myo-inositol administration: impacts on growth performance and metabolic profiles in broiler chickens

## TL;DR

Administering myo-inositol to chicken eggs affects post-hatch growth and metabolism, with potential sex-specific differences.

## Contribution

This study explores the effects of in ovo myo-inositol administration on broiler chickens' metabolism and growth, revealing sex-specific metabolic changes.

## Key findings

- In ovo myo-inositol administration did not affect hatchability but reduced body weight and weight gain in broilers.
- Metabolomic changes suggest altered mitochondrial β-oxidation and amino acid metabolism in MI-treated chickens.
- Sex-specific differences in plasma metabolites suggest distinct metabolic responses to in ovo MI administration.

## Abstract

Myo-inositol (MI) plays key roles in cellular signaling, membrane structure, and metabolic regulation, with its effects in poultry primarily explored through direct dietary MI supplementation. In this study, we aimed to assess the effects of in ovo MI administration on post-hatch performance and metabolism of broiler chickens. A total of 480 fertilized Ross 308 eggs were divided into four groups and, on day 17 of incubation, were injected with 12 μmol/mL MI (MI 12), 24 μmol/mL MI (MI 24), 0.9% saline (positive control, PC), or left non-injected (negative control, NC). After hatching, broilers were group-housed in floor pens (8 pens per treatment), with 12 birds per pen, and fed a standard diet for 35 days. At d 35, one bird per pen was slaughtered, sex was identified, and blood and tissues were collected to assess MI concentrations, the expression of inositol monophosphatase 1 (IMPase 1) and myo-inositol oxygenase (MIOX), and plasma metabolite profiles. There was no adverse effect of MI in ovo administration on hatchability and body weight (BW) of hatchlings. During the growing period, BW was lower in MI-injected groups from day 14 onward, along with reduced average daily weight gain; however, no differences were observed in the feed conversion ratio. The survival rate was higher in MI-injected groups during days 0–21, with a positive trend until the end of the experiment. MI concentrations in plasma and tissues, along with the expression of IMPase 1 and MIOX, were not altered by treatment. Plasma metabolomics revealed higher C2 and C9 acylcarnitines, threonine, and sarcosine, along with lower serotonin, and notable changes in phosphatidylcholines and sphingolipids in MI-injected versus no-MI groups, potentially reflecting alterations in mitochondrial β-oxidation pathways, diacylglycerol-associated signaling, amino-acid-related metabolism, and peripheral serotonin metabolism. Sex-specific differences in plasma MI and metabolite profiles were detected, with male birds demonstrating reduced plasma MI concentrations, Fisher ratio, and carnosine levels, indicative of a metabolic state possibly associated with higher anabolic pressure or subclinical inflammatory activation. These findings highlight the potential of in ovo MI administration to induce subtle but persistent metabolic reprogramming and underscore the need for further studies to clarify its long-term consequences for metabolic resilience and performance in both sexes.