Abstract
SummaryCompensatory growth is a physiological phenomenon found in both humans and animals. However, the underlying mechanisms are unclear. In this study, for the first time, we investigated the role of microbiota in compensatory growth induced by protein restriction using a rat model. Weaned Sprague‐Dawley rats were fed a low protein diet (L group), a normal protein diet (N group) and a low protein diet for 2 weeks followed by a normal protein diet (LN group). The results showed that in contrast with the inhibited growth of rats in the L group, compensatory growth was observed in the LN group. Meanwhile, rats in the LN group had increased concentrations of total short chain fatty acids, particularly butyrate, and an altered bacterial composition with modified abundances of Peptostreptococcaceae, Bifidobacteriaceae, Porphyromonadaceae and Prevotellaceae in the colonic content. Furthermore, gene expression analysis indicated that the rats that experienced compensatory growth had improved barrier function and innate immune function in the colon. Our data revealed the importance of colonic microbiota in achieving compensatory growth.
Highlights
Low-birth weight neonates and malnourished children usually exhibit compensatory growth due to foetal malnutrition or postnatal protein/calorie malnutrition (Ashworth, 1969; Hack et al, 1996)
A compensatory increase in body weight was observed on post-weaning day (PWD) 28 in the LN group after rats were switched to a normal protein (NP) diet on PWD 14, the value was still lower than that in the NP diet as the control group (N group)
average daily gain (ADG) was unaffected and average daily feed intake (ADFI) was decreased in the LN group compared with the N group from PWD 14 to PWD 28
Summary
Low-birth weight neonates and malnourished children usually exhibit compensatory growth due to foetal malnutrition or postnatal protein/calorie malnutrition (Ashworth, 1969; Hack et al, 1996). According to the previous studies, the changes in circulating hormones (including growth hormone, insulin growth factor I and insulin) as well as the metabolic changes in multiple organs and tissues (including liver, pancreas, intestine, muscle and fat tissue) are believed to be causal factors or consequences of compensatory growth (Wilson and Osbourn, 1960; Hornick et al, 2000). Among these organs and tissues, the gastrointestinal tract (GIT) is crucial for host metabolism and health, because it fulfils the nutritional requirements for the whole host and is the largest endocrine and immune organ in the body (Borgstrom et al, 1979; Evans et al, 2013; Peterson and Artis, 2014). Further investigations focusing on GIT are needed to elucidate its role in compensatory growth
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