4.7 Article

The effects of galactooligosaccharide on systemic and mucosal immune response, growth performance and appetite related gene transcript in goldfish (Carassius auratus gibelio)

Journal

FISH & SHELLFISH IMMUNOLOGY
Volume 55, Issue -, Pages 479-483

Publisher

ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.fsi.2016.06.020

Keywords

Galactooligosaccharide (GOS); Prebiotic; Appetite; Ghrelin; Skin mucus; Immune response; Goldfish

Funding

  1. GUASNR

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The present study investigates the effects of supplementation of goldfish (Carassius auratus gibelio) diet with galactooligosaccharide (GOS) on serum immune response, mucosal immune parameters as well as appetite-related (Ghrelin) and immune-related (TNF-1 alpha and TNF-2 alpha) genes expression. One hundred and eighty fish with an average weight of 4.88 +/- 0.28 g were stocked in twelve 500-L fiberglass tank assigned to four treatments repeated in triplicates. Fish were fed on experimental diets contain 0.5, 1 and 2% GOS for 6 weeks. Supplementation of diet with GOS had no remarkable effect on goldfish growth performance (P > 0.05). Evaluation of serum innate immune parameters revealed that supplementation of diet with GOS significantly elevated total protein, Albumin, Globulins, Lysozyme and Alkaline phosphatase activity as well as agglutination compared to control group in a dose dependent manner (P < 0.0.5). Also, Fish fed 2% GOS supplemented diet showed increased skin mucus immune response (total protein and lysozyme activity) compared other groups (P < 0.0.5); except in case of ALP activity. Molecular, studies on appetite (ghrelin) and inflammatory cytokine (TNF-1 alpha and TNF-2 alpha) genes expression revealed remarkably decrease and increase, respectively in GOS fed fish (P < 0.0.5). These results showed immunomodulatory effects of dietary GOS on serum and skin mucus response as well as expression of inflammatory cytokines in goldfish, though this supplement decreased appetite gene expression and had no effect on growth performance. (C) 2016 Elsevier Ltd. All rights reserved.

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