Comparative study on the effects of glutamic acid and glutamine in promoting intestinal development in chicks through...

This study evaluated the effects of glutamic acid (Glu) and glutamine (Gln) on the intestinal development of layer chicks with lipopolysaccharide (LPS)-induced damage.

A total of 240 healthy 0-d-old Hy-Line Brown chicks were randomly assigned to 4 treatments, each with 6 replicates. At 8 and 11 d of age, all birds (except for the control group) received two administrations of LPS. The LPS-challenged birds were divided into three dietary treatment groups: a basal diet (without additives), a 0.05% Glu-supplemented diet, and a 0.20% Gln-supplemented diet.

The LPS challenge induced intestinal injury and suppressed intestinal development in layer chicks, as evidenced by reduced growth performance, poor intestinal parameters, and morphology (p<0.05). Compared to the LPS group, dietary supplementation with 0.05% Glu and 0.20% Gln enhanced average daily gain (ADG), average daily feed intake, body weight (BW), and intestinal development parameters (including length, weight, villus height, and villus height/crypt depth) of duodenum, jejunum and ileum (p<0.05). These results could be attributed to upregulated mRNA expression levels of Mucin-2, Ecadherin, Dclk-1, Vil-1, Lysozyme, ChgA, Lgr-5, Bmi-1, ATP5F1AZ, and β-catenin (p<0.05). Furthermore, dietary supplementation with 0.20% Gln outperformed 0.05% Glu in enhancing BW, ADG, and ileum parameters (weight, length, epithelial cell count, and energy metabolism) (p<0.05). Additionally, intestinal organoids supplemented with 10 μM Gln had higher mean area, E-cadherin gene expression, and ATP content compared with those treated with 5 μM Glu in vitro (p<0.05).

Dietary supplementation with 0.05% Glu and 0.20% Gln could improve growth performance, intestinal development, and repair intestinal damage in layer chicks through enhanced epithelial proliferation and differentiation. Moreover, 0.20% Gln performed better than 0.05% Glu, which may be attributed to superior energy metabolism.