The effects of hypophysectomy on liver glycogenolytic enzymes and starvation response in goldfish (Carassius auratus L.)

1977 ◽  
Vol 55 (8) ◽  
pp. 1297-1303 ◽  
Author(s):  
R. M. Walker ◽  
P. H. Johansen

The role of the pituitary gland in goldfish liver carbohydrate metabolism was studied by examining the effects of its removal on the livers of starved animals and on glycogenolytic enzymes.Five weeks starvation after hypophysectomy or sham operation resulted in significantly lower total liver glycogen levels compared with respective fed controls. The larger liver glycogen reserves of starved hypophysectomized fish than fed, sham-operated animals indicate gluconeogenesis is operating to produce glycogen.Glucose-6-phosphatase (EC 3.1.3.9) and glycogen phosphorylase (EC 2.4.1.1) were assayed in liver supernatant fractions from hypophysectomized and sham-operated goldfish. Hypophysectomy resulted in an apparent decline in the activity of glucose-6-phosphatase, but no change in glycogen phosphorylase, compared with sham-operated controls. Reduced glucose-6-phosphatase activity is consistent with lowered glycogenolysis as a cause of liver glycogen accumulation in hypophysectomized goldfish. It is suggested that reduced glycogenolysis could be related to reduced peripheral use of carbohydrate. The possible role of ACTH and glucocorticoids is discussed.

1977 ◽  
Vol 55 (8) ◽  
pp. 1304-1311 ◽  
Author(s):  
R. M. Walker ◽  
P. H. Johansen

At 20 °C goldfish survive anaerobic conditions for only a few hours while at 4 °C survival is extended to several days. During the course of low-temperature anaerobiosis there was a rise in blood glucose and lactate, a decline in liver glycogen concentration, and an increase in liver water content, while liver size remained constant.The better cold anaerobic survival of winter and hypophysectomized goldfish compared with spring and sham-operated animals was correlated with greater glycogen stores in the livers of the former. It is concluded that liver glycogen is a necessary energy source during cold anaerobiosis, and it is suggested that the resulting hyperglycemia may represent a mechanism to increase glycolytic energy yield. Cold anaerobiosis also resulted in elevated liver glucose-6-phosphatase (EC 3.1.3.9) activity, suggesting an increase in glycogenolysis, but no change in glycogen phosphorylase (EC 2.4.1.1) activity. While cold anaerobic survival is short term it is possible that liver glycogen may sustain goldfish for longer periods at low oxygen levels through a mixed aerobic–anaerobic metabolism.


1962 ◽  
Vol 38 (7) ◽  
pp. 345-347 ◽  
Author(s):  
Nobuo EGAMI ◽  
Hisami ETOH ◽  
Chikashi TACHI ◽  
Kazuko AOKI ◽  
Ryoichi ARAI

2008 ◽  
Vol 86 (10) ◽  
pp. 1095-1100 ◽  
Author(s):  
Steve C. Dinsmore ◽  
David L. Swanson

Freezing survival may differ among winters in chorus frogs ( Pseudacris triseriata (Wied-Neuwied, 1838)), and low freezing survival is associated with low hepatic glycogen stores. The pattern of prehibernation liver glycogen accumulation in chorus frogs is unknown. Frogs might accumulate hepatic glycogen stores until a threshold level sufficient for winter survival is attained, after which frogs enter hibernation (critical threshold hypothesis). According to this model, frogs active late in the season should only be those with low hepatic glycogen stores. Alternatively, hepatic glycogen levels might continue to increase throughout the fall as long as frogs remain active (continuous increase hypothesis). We tested these hypotheses by measuring liver and leg muscle glycogen, glucose, and glycogen phosphorylase activities in chorus frogs throughout the fall prehibernation period in southeastern South Dakota. Hepatic glycogen levels were significantly related to date and increased throughout the fall period, consistent with the continuous increase hypothesis. This suggests that hepatic glycogen levels do not serve as a cue for entrance into hibernation. Liver phosphorylase activity did not vary significantly with progression of the fall season and activity was lower than in winter, suggesting that the winter increment of phosphorylase activity requires some stimulus during hibernation (e.g., low temperatures).


1981 ◽  
Vol 200 (3) ◽  
pp. 509-514 ◽  
Author(s):  
B Bréant ◽  
S Keppens ◽  
H De Wulf

Vasopressin and alpha-adrenergic agonists are known to be potent cyclic AMP-independent Ca2+-dependent activators of liver glycogen phosphorylase. When hepatocytes are pre-incubated with increasing concentrations of vasopressin or of the alpha-agonist phenylephrine, they become progressively unresponsive to a second addition of the respective agonist. The relative abilities of six vasopressin analogues and of five alpha-agonists to activate glycogen phosphorylase and to cause subsequent desensitization are highly correlated, indicating that the same vasopressin and alpha-adrenergic receptors are involved in both responses. About 5-times-higher peptide concentrations are needed to desensitize the cells than to activate their glycogen phosphorylase, whereas the concentrations of alpha-agonists required for the desensitization are only twice those needed for the activation of phosphorylase. The desensitization is not mediated by a perturbation in the agonist-receptor interaction. It is clearly heterologous, i.e. it is not agonist-specific, and must therefore involve a mechanism common to both series of agonists. The evidence for a role of Ca2+ movements or phosphatidylinositol turnover is briefly discussed.


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