Reduced fasting periods increase intestinal permeability in chickens

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Feed restriction is a common practice in chicken meat production where birds are usually fasted prior to slaughter to minimize carcass contamination with intestinal contents during processing. During the depopulation process, some birds in the same shed are often deprived of feed for up to 12 hr (Allen et al., 2008; Delezie, Swennen, Buyse, & Decuypere, 2007). Additionally, broiler breeders are often deprived of feed for weight management and production (Najafi, Zulkifli, Soleimani, & Kashiani, 2015). Fasting for periods of up to 24 hr has been shown to increase stress measured by increased corticosterone levels (Najafi, Zulkifli, Soleimani, & Goh, 2016) and affect intestinal morphology (reduced crypt depth and increased mucin production; Burkholder, Thompson, Einstein, Applegate, & Patterson, 2008; Thompson & Applegate, 2006). Studies have shown a reduction in villus height due to fasting, possibly due to reduced cell proliferation and migration rates (Ferraris & Carey, 2000). Fasting during thinning in poultry productions also increased in vivo risk of Campylobacter colonization (Allen et al., 2008) and ex vivo attachment of Salmonella enteritidis in the ileum (Burkholder et al., 2008) and can potentially be harmful for human health and food safety. Recently, fasting for 19.5 hr in 21‐day‐old broiler chickens (Gilani et al., 2016a) and 24 hr in 7 days old broiler chickens (Kuttappan et al., 2015; Vicuna et al., 2015) has been shown to increase intestinal permeability (IP). Increased IP is the increased passage of intestinal contents from the lumen to blood and may lead to reduced performance and compromised health (Gilani, Howarth, Kitessa, Forder, et al., 2016). However, the effects of short‐term fasting periods of 4.5 and 9 hr have yet to be investigated.
Glutamine is a non‐essential amino acid, deposited in skeletal muscle (Stachowicz‐Stencel & Synakiewicz, 2012), and provides a substrate for intestinal cell proliferation. Studies have shown that glutamine improves IP in in vitro human cell cultures (Le Bacquer, Laboisse, & Darmaun, 2003), in a weaning stress model in pigs (Wang, Zhang, et al., 2015) and a mucositis model in rats (Beutheu et al., 2014) by regulating tight junction protein expression as reviewed by Wang, Wu et al. (2015). Limited in vitro studies in chickens have also shown that glutamine improves barrier integrity (Awad & Zentek, 2015; Awad et al., 2015). In the aforementioned studies, glutamine was administered post‐challenge, while glutamine as a preventative treatment has also been utilized as reviewed by (Andrade et al., 2015; Wang, Wu, et al., 2015). In brief, glutamine has been shown to maintain IP in mice when fed before a heat stress challenge (Soares et al., 2014). Similarly, feeding glutamine before an exercise and intestinal ischaemia challenge maintained IP in humans (Zuhl et al., 2014) and rats (Wang, Niu, et al., 2015). However, the role of glutamine in gut permeability in chickens has yet to be explored. There are a few published scientific papers regarding biomarkers of increased IP in chickens. Fluorescein isothiocyanate dextran (FITC‐d) has recently been utilized as permeability marker in chickens (Kuttappan et al., 2015; Vicuna et al., 2015), and we have recently utilized FITC‐d and lactulose, rhamnose and mannitol sugar methods (Gilani et al., 2016a). Both methods were utilized and compared in the current study.
The main objectives of this study were to investigate whether reduced fasting periods of 4.5, 9 and 19.5 hr increased intestinal permeability as measured by two different methods (lactulose/rhamnose/mannitol ratio and the fluorescein isothiocyanate dextran (FITC‐d) test), and to determine whether glutamine supplementation before fasting at 38 days of age ameliorated increased IP in chickens.
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