Targeted gene expression panels and microbiota analysis provide insight into the effects of alternative production diet formulations on channel catfish nutritional physiology
2018
Schroeter, Julie C. | Peterson, Brian C. | Bledsoe, Jacob | Li, Menghe | Small, Brian C.
The present research evaluated targeted gene expression panels and microbiota analysis to provide greater insight into the effects of alternatively-sourced dietary ingredients on production indices, gut health, changes in the gut microbiota and genes involved in the regulation of appetite, growth, metabolism, and intestinal inflammation. Four dietary formulations were based primarily on distinguishing protein sources: (D1-MFM) menhaden fishmeal (control), (D2-MBM) porcine meat and bone meal, (D3-SBM) soybean meal, and (D4-CSM/CGM) cottonseed meal/corn germ meal, respectively, and fed to channel catfish for 12 weeks. Differences in feed conversion ratio (FCR), specific growth rate, feed intake, body condition, weight gain, proximal intestine histology, intestinal microbiota composition, and quantitative gene expression were analyzed. FCR was significantly (P < 0.05) increased in D2–4 relative to D1-MFM; however, other production indices were unaffected by treatment. Dietary treatment also had no effect on intestinal histology (P < 0.05). Effects of alternative dietary formulations on the gut microbiota were minimal, although when using Chao1, a significant effect of dietary treatment was detected (P = 0.0497) on gut-associated microbiota richness estimates. D3-SBM caused diet-specific differences (P < 0.05) in the expression of neuropeptide Y, peptide YY, and D2-MBM, D3-SBM, and D4-CSM/CGM resulted in differences in α-amylase, insulin receptor-a, glucose-6-phosphate-dehydrogenase, glucocorticoide receptor 1, and glucocorticoide receptor 2, relative to D1-MFM. These changes likely relate to differences in diet-mediated regulation of appetite and glucose metabolism, and perhaps the modulation of gut passage rate. By evaluating the molecular regulation of these pathways, as well as surveying the gut-associated microbiota, effects not detectable in short-term feeding trials may be elucidated which explain subtle differences in performance, such as FCR, as observed in the present study.
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