Effect of a Partial Loss of Scales and Mucous on Carbohydrate Metabolism in Rainbow Trout (Salmo gairdneri)

1967 ◽  
Vol 24 (5) ◽  
pp. 939-953 ◽  
Author(s):  
Edgar C. Black ◽  
S. J. Tredwell

This study was undertaken to determine what part partial scaling and partial desliming might play in the survival of trout. Carbohydrate metabolism in these trout was studied and in addition, hemoglobin levels and red cell volumes were studied to serve as indicators of osmotic shifts of water.Increases in lactate were minimal and occurred during the first few hours of holding after the removal of [Formula: see text] to [Formula: see text] of the scales. There were slight changes in hemoglobin levels and red cell volumes which appeared to coincide with activity as reflected by lactate levels. There was a three- to fourfold increase in the blood glucose level of partially scaled fish. Liver glycogen levels dropped to [Formula: see text] of the air-dipped control value for fish that had been [Formula: see text] scaled and held in holding baskets for a period of 140 hr. Only one mortality occurred in all the experiments.The following conclusions were reached. Partial loss of scales or mucous does not result in the death of rainbow trout (Salmo gairdneri). Partial scaling or desliming of the fish was accompanied by a significant increase in blood glucose (p < 0.05).

1966 ◽  
Vol 23 (4) ◽  
pp. 471-485 ◽  
Author(s):  
E. Don Stevens ◽  
Edgar C. Black

The effect of intermittent severe exercise of short duration on carbohydrate metabolism was examined using unanesthetized, intact rainbow trout. The levels of muscle glycogen, muscle lactate, blood lactate, and liver glycogen were determined in fish sampled immediately after severe exercise of 3 sec to 5 min, after recovery of 3 min to 60 min, and after re-exercise of 3 sec to 5 min. It appears that rainbow trout are not well adapted to tolerate frequent exercise of short duration.


1964 ◽  
Vol 207 (2) ◽  
pp. 411-414 ◽  
Author(s):  
Jiro Oyama ◽  
William T. Platt

Unrestrained mice were centrifuged for varying periods ranging from 0.5 to 10 hr at 2.5, 5, and 10 x gravity. Liver glycogen and blood glucose levels increased significantly depending on the g load and exposure time. Adrenalectomy completely abolished the glycogen deposition response. The glycogen response was a critical function of the age of mice; unweaned mice did not respond. Blood corticosterone increased significantly prior to the deposition of glycogen. Centrifuged fed mice deposited three times the amount of glycogen of fasted mice. There was no significant difference in the amount of glycogen deposited in centrifuged mice previously starved for 1, 2, or 3 days. It is concluded that the increased glycogen deposited following centrifugation is effected by an increased elaboration of adrenal corticosterone.


1982 ◽  
Vol 60 (9) ◽  
pp. 2079-2084 ◽  
Author(s):  
G. F. Wagner ◽  
B. A. McKeown

An experiment was conducted to determine if the hyperglycemia that is observed in zinc-stressed fish is also accompanied by changes in the levels of plasma insulin and liver glycogen. Juvenile rainbow trout were exposed to three concentrations of zinc sulphate along with a control group over 31 days. Plasma glucose levels were monitored in each group over the course of the experiment. The group demonstrating the most acute and sustained hyperglycemia (0.352 ppm zinc) was then analyzed along with the controls for changes in plasma insulin (using a teleost insulin radioimmunoassay) and liver glycogen levels. Significant depressions in plasma insulin and liver glycogen levels were observed in the zinc-exposed fish when compared with the controls. These changes are discussed with respect to possible influences of epinephrine, which is elevated in stressed fish, and (or) a direct effect of zinc metal on the pancreatic beta cells.


1973 ◽  
Vol 30 (1) ◽  
pp. 31-40 ◽  
Author(s):  
Blake F. Grant ◽  
Paul M. Mehrle

In mature rainbow trout (Salmo gairdneri) receiving sublethal doses of endrin (4.3–145 × μg/kg body wt/day in 0.215–7.25 mg/kg of food) for 163 days and then forced to swim for 1 hr, the insecticide affected serum electrolytes, osmolality, total protein, cholesterol, cortisol, lactate, glucose, liver glycogen, and growth. Forced swimming alone altered 9 of 16 serum parameters examined. Apparent increases in serum Na and Cl and significant increases in osmolality and liver glycogen were directly related to dosage. A biphasic distribution of phosphate, total protein, and cholesterol with dosage was apparent. Glucose was increased about 50% by 145 μg/kg but was unaffected by lower doses. Variance analysis of zone electrophoretic patterns disclosed an in teraction between serum protein distribution and dose. Mobilization of liver glycogen was apparently inhibited by low doses and almost totally blocked by high doses. Correspondingly, trout given 14.5 μg/kg or more had lowered serum cortisol levels whereas the lowest dose elevated cortisol. Growth was inhibited appreciably by 145 μg/kg but not by lower doses. Visceral fat accumulated 4.8–8.7 μg endrin/g tissue in the 43 and 145 μg/kg exposures. We conclude that endrin caused dysfunction of physiologic processes critical to survival.


1965 ◽  
Vol 31 (2) ◽  
pp. 127-137 ◽  
Author(s):  
P. J. BENTLEY ◽  
B. K. FOLLETT

SUMMARY River lampreys regulated their blood glucose concentration when injected with glucose. Mammalian insulin decreased the blood glucose concentration in the lamprey while adrenaline, cortisol and arginine vasotocin increased it. Glucagon had no effect initially but after a delay of 4 hr. decreased the blood glucose level. Insulin and cortisol increased the liver glycogen concentration. Adrenaline decreased the muscle glycogen concentration; vasotocin increased it. Treatment with alloxan increased the blood glucose concentration. Fat and glycogen in the lamprey are stored mainly in the skeletal muscles and their histochemical distribution in muscle is described. The results are discussed in relation to the metabolism of the migrating lamprey and the evolution of the control of carbohydrate metabolism in vertebrates.


1986 ◽  
Vol 43 (10) ◽  
pp. 2017-2024 ◽  
Author(s):  
Pierre Raymond ◽  
Gérard Leduc ◽  
Jack A. Kornblatt

The exposure of rainbow trout (Salmo gairdneri) to 0.01, 0.02 and 0.03 mg HCN∙L−1 for 20 d demonstrated the biotransformation of HCN into thiocyanate which accumulated in the blood plasma which increased the duration of exposure to cyanide. Despite its transformation into thiocyanate, there is still a sufficient quantity of cyanide to inhibit cytochrome oxidase by 60–80% within the first 24 h of exposure. This level of inhibition remained stable during the 20 d of the tests and was the same at the three concentrations tested. This observation permits the prediction of effective concentration of free HCN inside the fish. The measurements of liver glycogen levels illustrate the Pasteur effect in the rainbow trout subjected to cyanide. During cyanide exposure, liver glycogen was rapidly used, particularly at 0.03 mg HCN∙L−1 whereas at 0.01 and 0.02 mg HCN∙L−1 the glycogen levels gradually came back to normal after 7–10 d of exposure.


1959 ◽  
Vol 197 (1) ◽  
pp. 47-51 ◽  
Author(s):  
R. L. Hazelwood ◽  
F. W. Lorenz

Prolonged fasting caused a rise in blood glucose which reached a maximum above the prefast level on the 6th day. Concurrently the liver glycogen, rapidly depleted at the start of the fast, was partially replaced. Blood NPN increased continuously. Thus, gluconeogenesis appeared likely not only to be responsible for the blood glucose increase but also to play a role in the restoration of liver glycogen after initial glycogenolysis due to fasting. Fasting for 48 hours increased cardiac glycogen up to three times the prefasting level; a rapid decrease in this moiety occurred with further abstinence. Glucagon and growth hormone increased the cardiac glycogen of nonfasted birds; but had little, if any, influence on the effects of fasting. The daily injection of 60–70 u of either regular or HGF-free insulin per kilogram body weight resulted in an hyperglycemic rebound 24 hours after each injection. This rebound could be blocked completely by feeding Dibenzyline.


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