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|Title:||Developing a model for intestinal ammonia handling in rainbow trout|
|Authors:||Rubino, Julian G.|
|Advisor:||Wood, Chris M.|
|Keywords:||ammonia;intestine;sodium;NKCC;ammonia transport;fish;Biology;Cellular and Molecular Physiology;Comparative and Evolutionary Physiology;Systems and Integrative Physiology;Biology|
|Abstract:||<p>Ammonia is the primary nitrogenous waste product in teleost fish, which is produced primarily through protein metabolism. Fish experience natural elevations in internal ammonia loads, including during digestion where luminal ammonia concentrations in the intestine rise substantially. Furthermore, the intestine may absorb a portion of this ammonia, despite it being toxic to the fish. Based on this, <em>in vitro </em>techniques were employed in order to develop a model for teleost intestinal ammonia handling.</p> <p>Ammonia absorption and endogenous ammonia production occur along the entire length of the intestine. However, section-specific differences exist in terms of both endogenously produced ammonia and ammonia flux rates, with the highest rates in the anterior and mid intestine. Feeding stimulated an increase in production rates in all intestinal sections. Overall, ammonia originating from the gut may account for up to 42% of post-prandial whole-fish ammonia excretion. This could partly be attributed to the increased activity of the ammonia-producing enzyme glutamate dehydrogenase, and decreased activity of the ammonia-fixing glutamine synthetase. Furthermore, gut tissue ammonia concentrations surpassed typical chyme concentrations and were well regulated independent of high luminal ammonia, suggesting active transport across the intestinal epithelium.</p> <p>Seawater (60%) acclimation caused no substantial changes in the ammonia handling properties of the intestine. Ammonia transport in the intestine of both freshwater and seawater trout appears to occur via active means, coupled to Na<sup>+</sup>/K<sup>+</sup> ATPase activity. Specifically, this involves Na<sup>+</sup> linked transport through substitution of NH<sub>4</sub><sup>+</sup> for K<sup>+ </sup>on the apical Na<sup>+</sup>/K<sup>+</sup>/2Cl<sup>-</sup> co-transporter occurring predominantly in the anterior and mid intestine, and solvent drag through fluid transport (osmotically driven by active NaCl absorption) in all sections. Additionally, Rhesus glycoprotein mediated ammonia transport likely occurs through basolateral Rhbg1, supporting previous molecular evidence. Overall this thesis illuminates the quantitative importance and mechanisms of gut ammonia transport in fish, and highlights future research avenues.</p>|
|Appears in Collections:||Open Access Dissertations and Theses|
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