Effects of compound 48/80 on hepatic glycogen and glucose‐6‐phosphatase early in the diurnal cycle of the rat

Abstract

The amount and distribution of glycogen as well as the activity of glucose-6-phosphatase (G-6-Pase) in the livers of rats were analyzed by biochemical and/or histochemical techniques. During the first 5 hr of the light cycle, livers of rats were sampled prior to and 30 min following an injection of compound 48/80 or Ringer's solution. Glycogen decreased significantly in response to sampling; however, treatment with compound 48/80 provoked an additional significant decrease in hepatic glycogen. These differences occurred irrespective of the time during the 5 hr that this was studied. The livers of the majority of the rats treated with compound 48/80 displayed a periportal distribution of glycogen, while those treated with Ringer's showed a more uniform pattern. Hepatic G-6-Pase activity was unchanged in either the Ringer's or compound 48/80 treated rats. These results indicated that (1) the significant glycogenolytic response occurs independently of the amount of glycogen present, (2) G-6-Pase activity is not affected within 30 min following the stimulation of glycogenolysis, (3) variation in glycogen patterns during depletion depends on the nature of the stimulus and/or degree of response, and (4) the amount of glycogen available for release is limited.

Compound 48/80, a mast cell degranulator, causes oxidative damage by enhancing vitamin C synthesis via reduced glutathione depletion and lipid peroxidation through neutrophil infiltration in rat livers

“…(9) It is also known that enhanced glycogenolysis in the liver of rats treated once with C48/80 is independent of the content of glycogen stored in the tissue. (10) Therefore, these findings and the above-described results allow us to suggest that, in the liver of rats with a single C48/80 treatment, H 2 O 2 generation and lipid peroxidation are enhanced following VC synthesis via GSH depletion-dependent glycogenolysis, resulting in the occurrence of oxidative damage.…”

“…(9) It has also been shown in rats treated once with C48/80 that C48/80-induced glycogenolysis in the liver is independent of the content of glycogen stored in the tissue. (10) Furthermore, it has been shown that degranulation of mast cells existing in the liver tissue of rats treated once with C48/80 is not associated with glycogen depletion in the tissue. (11) Braun et al (12) have reported that depletion of reduced glutathione (GSH) induces glycogenolysis, resulting in stimulated VC synthesis in isolated mouse hepatocytes.…”

Elevated Blood Glucose after Compound 48/80 Treatment Is Not Related to Hepatic Mast Cell Degranulation in Rats

“…Systemic hypotension has been implicated as the effector of numerous compound 48/80-mediated responses, e.g., the increased release of renin from juxtaglomerular cells of the kidney (34). Hypotension and reduced perfusion also have been postulated to provoke anoxia in the liver which in turn might trigger hyperglycemia and glycogenolysis (35). However, data reported in other manuscripts suggested that glycogenolysis and hyperglycemia are independent of changes in systemic blood pressure and hepatic blood flow (14,16).…”