Effect of enteral glutamine supplementation for low-birth-weight infants on weight gain patterns and levels of fecal secretory immunoglobulin A

Abstract

Aim: Glutamine is needed for optimal cell growth and for the immune system, especially in the enterocytes of gut mucosal immune responses. Low birth weight makes infants susceptible to glutamine depletion because nutrition is limited in the first week of life. To determine the effect of enteral glutamine supplementation on weight gain patterns and fecal secretory immunoglobulin A. Material and Methods:This study is a double-blind, randomized controlled trial. Infants were randomly assigned to the glutamine group and placebo group. The glutamine group was supplemented with glutamine 400 mg/kg/day for 14 days, and placebo group received glucose 400 mg/kg/day for 14 days. The infants were observed for 30 days. Return-to-birth-weight, weight gain velocity, and fecal secretory immunoglobulin A levels were monitored during the study. Results: Thirty-seven low-birth-weight infants were randomly assigned to the glutamine and placebo groups. The glutamine group had a shorter return-to-birth-weight time than the placebo group (8.1±0.9 vs. 11.0±1.6 days) and faster weight gain velocity (20.0±1.8 vs. 15.5±2.2 g/ kg/day) (p<0.001). Secretory immunoglobulin A levels after glutamine supplementation were higher than in the placebo group (0.456±0.057 vs. 0.376±0.035 mg/g) (p<0.001). Levels of secretory immunoglobulin A after treatment in each group were increased. However, there was a significant difference before and after supplementation between the glutamine and placebo groups (0.247±0.024 vs. 0.140±0.016 mg/g) (p<0.001). Conclusion: Enteral glutamine supplementation in low-birth-weight infants accelerates return to birth weight, increases the weight gain velocity, and the levels of fecal secretory immunoglobulin A.

Free amino acids in human milk: a potential role in early life growth and immunity

“…We have previously confirmed earlier findings that the total protein and TAA content in HM decreases in the first 2 to 3 months of lactation, and that levels remain relatively stable thereafter [22]. The decreasing protein and TAA levels in HM are indicated to correlate with the infant's changing requirements for growth and might prevent overfeeding of AAs, as milk volume intake increases with progressing lactation [23].…”

“…The nutrient composition of HM is considered insufficient for preterm infants with a low birthweight [22,23]. As human hindmilk is more energy-dense and contains more fat than foremilk, exclusively feeding hindmilk to preterm infants is used in practice to obtain a higher rate of weight gain [23,24].…”

“…The nutrient composition of HM is considered insufficient for preterm infants with a low birthweight [22,23]. As human hindmilk is more energy-dense and contains more fat than foremilk, exclusively feeding hindmilk to preterm infants is used in practice to obtain a higher rate of weight gain [23,24]. The present study indicates that this practice provides the preterm infant with higher levels of protein, which might suit the increased protein requirements of preterm infants to achieve improved growth and neurodevelopment [25].…”

“…extra-nutritional components with biological activity) that are uniquely present in HM can be important contributors to these benefits. This is evidenced by the ability of certain bioactive components in HM to influence growth and inhibit allergic sensitization to cow's milk and other foods in animals [22][23][24][25][26][27][28], and is further supported by correlations observed between their levels in HM and outcomes of growth and food allergy in infancy [29][30][31][32][33][34][35][36][37][38][39]. Given the importance of these outcomes for optimal health throughout life, it is of great interest to continue research on the composition of bioactive components in HM and their potential roles in these benefits associated with HM feeding.…”

“…immunity. These characteristics correlate with an increased susceptibility to infections and allergies in the neonatal period [23,24]. This susceptibility is further enhanced by an immature intestinal barrier and an incomplete intestinal microbial colonization at birth [23].…”