Stress and Metabolic Hormones Do Not Promote Cardiac Glycogenolysis In Vitro In Rainbow Trout


Meeting Abstract

P3.9  Saturday, Jan. 5  Stress and Metabolic Hormones Do Not Promote Cardiac Glycogenolysis In Vitro In Rainbow Trout SORENSEN, OJ*; RODNICK, KJ; Idaho State University; Idaho State University soreolav@isu.edu

Increased swimming activity and or environmental hypoxia raises epinephrine, cortisol, and cortisone levels in fishes. Seasonal changes, maturation, and dietary changes such as fasting, or increased carbohydrate uptake can alter glucagon levels. In mammals, these hormones promote cardiac glycogenolysis and increase contractility. However, the effects of these hormones on cardiac glycogen metabolism in teleost fish are largely unknown. Hence, we investigated the effects of these hormones on glycogen metabolism in cardiac tissue of rainbow trout. METHODS: Ventricle strips from 10-12 month old males and females (n=6-9) were incubated in oxygenated (99.5% O2; 0.5% CO2) Ringers with glucose (5 mM) in a reciprocating bath at 14°C. Epinephrine (10 µM), cortisol (10 nM), cortisone (10 nM), or glucagon (500-5000 pg/ml) was added to non-contracting strips for 60 min. Tissue was freeze clamped before (initial values) and at the end of the experiments and stored at -80°C until free glucose and glycogen were assayed. RESULTS: For both sexes, hormone treatment did not affect glycogen or free glucose concentrations in non-contracting ventricle strips. However, initial glycogen and free glucose fell 6 (NS) and 16% (P<0.01) in males and only 1 (NS) and 10% (P<0.05) in females, respectively, compared with controls. CONCLUSIONS: In non-contracting ventricle strips, stress hormones did not reduce cardiac glycogen and free glucose levels in male and female rainbow trout while levels dropped during tissue processing. This reduction may have been due to a temporary hypoxic state of the tissue and supports previous findings that female cardiac tissue maintains free glucose and glycogen levels better than males in vitro. Funded by NSF EPSCoR EPS 0447689.

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