Reduced fasting periods increase intestinal permeability in chickens

Abstract

SummaryFasting of up to 24 hr has been shown to increase intestinal permeability (IP) in chickens.The aim of this study was to determine whether fasting duration of 4.5 and 9 hr increased IP and whether l-glutamine (a non-essential amino acid) supplementation before fasting provided some protection of barrier function as shown in other species.Ross 308 male broilers (n = 96) were fed either a control diet or the same diet supplemented with 1% glutamine from d0 to d38 post-hatch. On d37, the birds were assigned to single-bird metabolism cages and were fasted for either 0, 4.5, 9 or 19.5 hr.This study design was 2 × 4 factorial with two levels of glutamine and four levels of fasting. Birds in the 0-hr fasting group had free access to feed. All birds had ad libitum access to water. To measure IP on day 38, following their respective fasting periods, birds were administered two separate oral gavages of fluorescein isothiocyanate dextran (FITC-d) followed by lactulose, mannitol and rhamnose (LMR) sugars, 60 min apart. Whole blood was collected from the jugular vein 90 min post-LMR sugar gavage. FITC-d and L/M/R ratios were measured by spectrophotometry and highperformance ionic chromatography respectively. Lipopolysaccharide (LPS) endotoxins in plasma of the birds fed the control diet were also measured using chicken-specific LPS antibody ELISA. Serum FITC-d and plasma L/M and L/R ratios for 4.5, 9 and 19.5 hr were significantly (p < .05) higher compared to the non-fasting group. However, IP was not different in the glutamine-supplemented group (p > .05) compared to the control group. LPS concentrations measured by the ELISA were below the detectable range. We conclude that fasting periods of 4.5 and 9 hr increased IP compared to non-fasted birds and dietary glutamine supplementation did not ameliorate changes in IP. K E Y W O R D Sfluorescein isothiocyanate dextran, glutamine, lipopolysaccharides, feed withdrawal and sugar ratio

Gene expression and morphological changes in the intestinal mucosa associated with increased permeability induced by short‐term fasting in chickens

“…Interestingly, Gilani et al (2017) have shown that 4.5, 9 and 19.5 hr fasting increased IP linearly, as measured by increased serum FITC-d concentrations in blood, suggesting that the villus morphology in the current study did not directly correlate with the increased IP. This phenomenon has been observed in other studies.…”

“…Gilani et al. () have shown that these fasting periods increased IP, as measured by FITC‐d. Also these results were inconsistent with the studies in other species.…”

“…Gilani et al. () have shown that fasting for as little as 4.5 and 9 hr increased IP in chickens. In these studies, increased IP was measured by fluorescein isothiocyanate dextran (FITC‐d) or lactulose rhamnose and mannitol (LMR) sugars, which pass through tight junctions between enterocytes (Gilani, Howarth, Kitessa, Forder et al., ).…”

“…Long-term fasting has been demonstrated to negatively affect the intestinal morphology in chickens (Thompson & Applegate, 2006;Yamauchi, Kamisoyama, & Isshiki, 1996;Yamauchi, Yamamoto, & Ishiki, 1995) and, recently, has been shown to increase intestinal permeability Kuttappan et al, 2015;Vicuna et al, 2015). Gilani et al (2017) have shown that fasting for as little as 4.5 and 9 hr increased IP in chickens. In these studies, increased IP was measured by fluorescein isothiocyanate dextran (FITC-d) or lactulose rhamnose and mannitol (LMR) sugars, which pass through tight junctions between enterocytes .…”

“…As fasting periods of 4.5, 9 and 19.5 hr have been shown to increase IP in chickens (Gilani et al., ), the objectives of this study were to investigate the associated effects of fasting of chickens for 0, 4.5, 9 and 19.5 hr on mRNA expression of TJP including claudin‐1, claudin‐3, occludin, JAM, E‐cadherin, ZO‐1, ZO‐2 and expression of genes associated with cellular protection and inflammation such as HSP‐70, IAP, GLP‐2, mTOR, FABP‐6 and MUC‐2, and villus‐crypt architecture of enterocytes.…”