Linear growth failure induced by systemic inflammation inhibiting IGF-1/IGFBP axis in rats with asymptomatic colitis

BACKGROUND: Children in poor areas show significant growth retardation that does not improve with an adequate supply of energy and nutrients, which may be related to asymptomatic intestinal infection caused by poor sanitation. Our objective was to explore the mechanism of intestinal inflammation inhibiting growth in the setting of asymptomatic colitis. METHODS: Forty-eight 3-week-old Wistar rats were randomly divided into three groups: the control group, colitis group (with asymptomatic colitis induced by 2.5% trinitrobenzenesulphonic acid) and pair-fed group (daily food intake matched to the pair in the colitis group). The linear growth was assessed, and the plasma levels of hormone and systemic cytokines were detected and compared by independent two-sample t-test or one-way ANOVA among groups. RESULTS: At d5, the increases in the body length of the control, colitis and pair-fed groups were 1.65 ± 0.34 cm, 1.10 ± 0.30 cm and 1.38 ± 0.26 cm, respectively, and the increase in the body length in the colitis group was significantly less than that in the control group (P < 0.05). There were significant differences in the levels of hormone and cytokines among three groups (P < 0.05). Compared with the control group, rats in the colitis group exhibited linear growth failure, as well as higher expression of calprotectin, tumour necrosis factor-α, interleukin-6 and insulin-like growth factor binding protein 2, lower insulin-like growth factor-1 and insulin-like growth factor binding protein 3, and lower expression of nuclear factor kappa B in hepatocytes. CONCLUSIONS: In addition to undernutrition, the systemic inflammatory response caused by asymptomatic colitis may inhibit the linear growth of rats by its influence on the insulin-like growth factor/insulin-like growth factor binding protein axis. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12876-019-1023-z) contains supplementary material, which is available to authorized users.