The Changes in Blood Glucose in Pleuronectes Platessa Following Capture From The Wild: A Stress Reaction

Author(s):  
C. S. Wardle

Changes in blood glucose levels in teleosts have been reviewed by a number of workers. Epple (1969) considered the regulation of glucose by the insulin of the fish pancreatic islet tissue, Nakano & Tomlinson (1967) examined the regulation of glucose by the catecholamines, Black, Robertson & Parker (1961) considered glucose in carbohydrate metabolism of teleost muscle, while knowledge of regulation of blood glucose in Chondrichthyans has recently been extended and reviewed by Patent (1968, 1970). The investigation of blood glucose levels and their control mechanisms dealt with in this paper forms part of a broader study of the changes that occur when fish are caught from the wild and placed in aquaria (Wardle, 1968, 1971, and unpublished). In this study, capture is considered as a stimulus imposed on the wild fish, which initiates a series of physiological changes that can be measured as the fish adapts to the aquarium.

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.


1972 ◽  
Vol 27 (12) ◽  
pp. 1531-1535 ◽  
Author(s):  
H. S. Ali Athar ◽  
S. Nazrul Hasnain ◽  
M. Zain-Ul-Abedin

1. Initial glycogen levels in the liver were found to be significantly higher than in the kidneys of the two species studied. The glycogen levels in kidney were however considerably higher than in some mammalian species.2. Total reducing capacity, true glucose, saccharoid fraction and titratable acidity increase gradually with concomitant decrease in the glycogen levels when liver and kidney homogenates of uromastix and liver homogenate of varanus were incubated for a period of 4 hours.3. Total reducing capacity, true glucose and the titratable acidity increase gradually, while the glycogen and the saccharoid fraction remain unchanged when the kidney homogenates of varanus are incubated for 4 hours.4. Total reducing capacity, true glucose and saccharoid fraction in the blood of uromastix are higher than in varanus. The blood glucose levels in both the species are higher than found in the mammals


PPAR Research ◽  
2010 ◽  
Vol 2010 ◽  
pp. 1-12 ◽  
Author(s):  
Annelies Peeters ◽  
Myriam Baes

Tight control of storage and synthesis of glucose during nutritional transitions is essential to maintain blood glucose levels, a process in which the liver has a central role. PPAR is the master regulator of lipid metabolism during fasting, but evidence is emerging for a role of PPAR in balancing glucose homeostasis as well. By using PPAR ligands and PPAR mice, several crucial genes were shown to be regulated by PPAR in a direct or indirect way. We here review recent evidence that PPAR contributes to the adaptation of hepatic carbohydrate metabolism during the fed-to-fasted or fasted-to-fed transition in rodents.


1976 ◽  
Vol 230 (4) ◽  
pp. 1163-1167 ◽  
Author(s):  
J Rogulski ◽  
A Pacanis ◽  
T Strzelecki ◽  
E Kaminska ◽  
S Angielski

Intraperitoneal administration of maleate produced an increase in blood alpha-ketoacid, acetoacetate, and free fatty acids. The effect of this treatment on blood glucose levels depended on whether the rats were fed or fasted. In fed rats it was accompanied by slight, transient hyperglycemia connected with depletion of liver glycogen stores. In fasted animals moderate hypoglycemia was observed. The in vivo conversion of various precursors into blood glucose was not inhibited, suggesting that maleate does not affect hepatic gluconeogenesis. Neither was a direct effect on liver glycogenolysis observed. On the other hand, maleate inhibited renal gluconeogenesis from various substrates and stimulated anerobic glycolysis in kidney cortical alices. The data are interpreted in terms of increased utilization and decreased production of glucose by the kidney followed by secondary changes in liver carbohydrate metabolism.


Cells ◽  
2018 ◽  
Vol 7 (8) ◽  
pp. 95 ◽  
Author(s):  
Yoshimitsu Kiriyama ◽  
Hiromi Nochi

Amylin, (or islet amyloid polypeptide; IAPP), a 37-amino acid peptide hormone, is released in response to nutrients, including glucose, lipids or amino acids. Amylin is co-stored and co-secreted with insulin by pancreatic islet β-cells. Amylin inhibits food intake, delays gastric emptying, and decreases blood glucose levels, leading to the reduction of body weight. Therefore, amylin as well as insulin play important roles in controlling the level of blood glucose. However, human amylin aggregates and human amylin oligomers cause membrane disruption, endoplasmic reticulum (ER) stress and mitochondrial damage. Since cytotoxicity of human amylin oligomers to pancreatic islet β-cells can lead to diabetes, the protection of pancreatic islet β cells from cytotoxic amylin is crucial. Human amylin oligomers also inhibit autophagy, although autophagy can function to remove amylin aggregates and damaged organelles. Small molecules, including β-sheet breaker peptides, chemical chaperones, and foldamers, inhibit and disaggregate amyloid formed by human amylin, suggesting the possible use of these small molecules in the treatment of diabetes. In this review, we summarize recent findings regarding the role and cytotoxicity of amylin and the protection of pancreatic islet β-cells from cytotoxicity of amylin.


2006 ◽  
Vol 31 (03) ◽  
Author(s):  
H Hager ◽  
E Giorni ◽  
A Felli ◽  
B Mora ◽  
M Hiesmayr ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document