Effects of glucagon with or without insulin administration on liver glycogen metabolism

1995 ◽  
Vol 269 (2) ◽  
pp. E231-E238 ◽  
Author(s):  
N. Ercan ◽  
M. C. Gannon ◽  
F. Q. Nuttall
Keyword(s):  
Plasma Glucose ◽  
Glycogen Phosphorylase ◽  
Glycogen Metabolism ◽  
Liver Glycogen ◽  
Hepatic Glycogen ◽  
Insulin Administration ◽  
Similar Increase ◽  
Glycogen Concentration ◽  
Ad Libitum ◽  
Glucagon And Insulin

Rats fed ad libitum were given insulin alone (4 U/kg), glucagon alone (25 micrograms/kg), or insulin and glucagon sequentially. Phosphorylase a and synthase R activities, hepatic glycogen, uridine diphosphoglucose, inorganic phosphate (Pi), and plasma glucose, lactate, glucagon, and insulin concentrations were determined over the subsequent 40 min. In separate animals, muscle extraction of 2-deoxy-D-[3H]glucose also was determined. After glucagon administration, glycogen phosphorylase a and plasma glucose were increased within 5 min. However, the glycogen concentration did not decrease for 20 min. Glucagon administration to rats pretreated with insulin stimulated a similar increase in phosphorylase a activity. Again, glycogen was not degraded for 20 min. After insulin only, glycogen concentration remained unchanged. Plasma glucose decreased as expected. In each group, muscle extraction of 2-deoxy-D-[3H]glucose increased compared with the controls (P < 0.05). In summary, glucagon and/or insulin administration did not stimulate significant glycogen degradation for 20 min, even though phosphorylase was activated. The mechanism remains to be determined.

Some Effects of Prolonged Undernutrition on Carbohydrate Metabolism in Rats

1956 ◽  
Vol 187 (3) ◽  
pp. 432-436 ◽  
Author(s):  
N. S. Halmi ◽  
B. N. Spirtos
Keyword(s):  
Insulin Sensitivity ◽  
Blood Sugar ◽  
Initial Level ◽  
Liver Glycogen ◽  
Hepatic Glycogen ◽  
Glycogen Concentration ◽  
Insulin Tolerance ◽  
Lower Blood ◽  
Ad Libitum ◽  
Sugar Levels

A) Rats fed 10 gm of ground Rockland diet/day for 4–6 weeks and then fasted for 24 hours showed an enhanced insulin sensitivity as compared with ad libitum-fed rats that were fasted for the same length of time. The fasting blood sugar and liver glycogen concentrations were significantly higher in underfed animals. B) Underfed rats were fasted 24 hours, then fed 5 gm/ 100 gm body weight and tested 8 hours later. These rats exhibited a) no greater insulin sensitivity, b) lower blood sugar levels and c) a smaller rise in liver glycogen concentration than similarly treated ad libitum-fed animals. Intestinal absorption of glucose was not diminished in the undernourished rats. C) Cortisone treatment (0.5 mg/100 gm body wt/day for 5 days) abolished the insulin sensitivity of underfed rats without altering the hepatic glycogen concentration. Somatotrophin (0.5 mg Armour standard equivalent/100 gm body wt/day for 5 days) did not improve their insulin tolerance. After functional evisceration, the blood sugar fall (if expressed as percentage of the initial level) was significantly slower in underfed than in ad libitum-fed rats. However, the decline of the blood sugar level appeared to be more markedly enhanced by insulin in the underfed animals.

Control of hepatic glycogen metabolism in the rhesus monkey: effect of glucose, insulin, and glucagon administration

1975 ◽  
Vol 228 (1) ◽  
pp. 80-87 ◽  
Author(s):  
RT Curnow ◽  
EJ Rayfield ◽  
DT George ◽  
TV Zenser ◽  
F De Rubertis
Keyword(s):  
Rhesus Monkey ◽  
Glycogen Phosphorylase ◽  
Glycogen Synthase ◽  
Glycogen Metabolism ◽  
Hepatic Glycogen ◽  
Insulin Administration ◽  
Intravenous Glucose ◽  
Camp System ◽  
Effect Of Glucose ◽  
Insulin Inhibition

The effects of intravenous glucose, insulin and glucagon admininistration on the hepatic glycogen synthase and glycogen phosphorylase systems were assessed in the anesthetized rhesus monkey. Results were correlated with measurements of hepatic cyclic AMP (cAMP) concentrations and plasma glucose, insulin, and glucagon concentrations. Both glucose and insulin administration promoted significant inactivation of phosphorylase by 1 min, which was followed by more gradual activation of synthase. Neither glucose nor insulin caused significant changes in hepatic cAMP. Marked hyperglucagonemia resulting from insulin-induced hypoglycemia did not cause increases IN in hepatic cAMP, suggesting that the elevated insulin levels possibly inhibited glucagon action on the hepatic adenylate cyclase-cAMP system. Glucagon administration caused large increases in hepatic cAMP and activation of phosphorylase within 1 min, followed by more gradual inactivation of synthase when it had been previously activated by glucose. Concomitant glucose infusion, with resulting increased plasma insulin concentrations, markedly diminished the duration of hepatic cAMP elevations following glucagon adminstration, again suggesting an insulin inhibition of glucagon action on the hepatic adenylate-cAMP system.

Temporal patterns of tissue glycogen, glucose, and glycogen phosphorylase activity prior to hibernation in freeze-tolerant chorus frogs, Pseudacris triseriata

2008 ◽  
Vol 86 (10) ◽  
pp. 1095-1100 ◽  
Author(s):  
Steve C. Dinsmore ◽  
David L. Swanson
Keyword(s):  
Glycogen Phosphorylase ◽  
Threshold Level ◽  
Liver Glycogen ◽  
Critical Threshold ◽  
Hepatic Glycogen ◽  
Phosphorylase Activity ◽  
Continuous Increase ◽  
Glycogen Accumulation ◽  
Chorus Frogs ◽  
Glycogen Stores

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).

Plasma glucose concentration determines direct versus indirect liver glycogen synthesis

1986 ◽  
Vol 251 (5) ◽  
pp. E584-E590 ◽  
Author(s):  
C. H. Lang ◽  
G. J. Bagby ◽  
H. L. Blakesley ◽  
J. L. Johnson ◽  
J. J. Spitzer
Keyword(s):  
Plasma Glucose ◽  
Glucose Concentration ◽  
Infusion Rate ◽  
Glycogen Synthesis ◽  
Liver Glycogen ◽  
Glucose Infusion ◽  
Glucose Infusion Rate ◽  
Hepatic Glycogen ◽  
Glucose Load ◽  
Indirect Pathway

In the present study hepatic glycogenesis by the direct versus indirect pathway was determined as a function of the glucose infusion rate. Glycogen synthesis was examined in catheterized conscious rats that had been fasted 48 h before receiving a 3-h infusion (iv) of glucose. Glucose, containing tracer quantities of [U-14C]- and [6-3H]glucose, was infused at rates ranging from 0 to 230 mumol X min-1 X kg-1. Plasma concentrations of glucose, lactate, and insulin were positively correlated with the glucose infusion rate. Despite large changes in plasma glucose, lactate, and insulin concentrations, the rate of hepatic glycogen deposition (0.46 +/- 0.03 mumol X min-1 X g-1) did not vary significantly between glucose infusion rates of 20 and 230 mumol X min-1 X kg-1. However, the percent contribution of the direct pathway to glycogen repletion gradually increased from 13 +/- 2 to 74 +/- 4% in the lowest to the highest glucose infusion rates, with prevailing plasma glucose concentrations from 9.4 +/- 0.5 to 21.5 +/- 2.1 mM. Endogenous glucose production was depressed (by up to 40%), but not abolished by the glucose infusions. Only a small fraction (7-14%) of the infused glucose load was incorporated into liver glycogen via the direct pathway irrespective of the glucose infusion rate. Our data indicate that the relative contribution of the direct and indirect pathways of hepatic glycogen synthesis are dependent on the glucose load or plasma glucose concentration and emphasize the predominance of the indirect pathway of glycogenesis at plasma glucose concentrations normally observed after feeding.

Effects of Epinephrine on Carbohydrate Metabolism in Underfed and ad Libitum-Fed Rats

1957 ◽  
Vol 190 (2) ◽  
pp. 239-242
Author(s):  
B. N. Spirtos ◽  
R. G. Stuelke ◽  
N. S. Halmi
Keyword(s):  
Carbohydrate Metabolism ◽  
Blood Sugar ◽  
Blood Lactate ◽  
Liver Glycogen ◽  
Hepatic Glycogen ◽  
Commercial Diet ◽  
Ad Libitum ◽  
Sugar Levels ◽  
Fasted Rats

Rats fed 10 gm of a commercial diet for 4–5 weeks and fasted for 24 hours showed less rise in liver glycogen and blood sugar levels in response to the injection of epinephrine than did ad libitum-fed-fasted rats. Gastrocnemius glycogen levels were found to be higher in underfed-fasted animals and fell to the same extent as in ad libitum fed-fasted animals when epinephrine was given. Blood lactate concentrations, however, rose less markedly in the underfed-fasted group. This may have been at least partly responsible for the diminished rise in hepatic glycogen and blood sugar.

The variable clinical phenotype of three patients with hepatic glycogen synthase deficiency

2017 ◽  
Vol 30 (4) ◽  
Author(s):  
Çiğdem Seher Kasapkara ◽  
Zehra Aycan ◽  
Esma Açoğlu ◽  
Saliha Senel ◽  
Melek Melahat Oguz ◽  
...  
Keyword(s):  
Glycogen Synthase ◽  
Glucose Monitoring ◽  
Glycogen Metabolism ◽  
Liver Glycogen ◽  
Postprandial Hyperglycemia ◽  
Hepatic Glycogen ◽  
Case Presentation ◽  
Ketotic Hypoglycemia ◽  
Fasting Hypoglycemia ◽  
Lactic Acidemia

AbstractBackground:Glycogen synthase deficiency, also known as glycogenosis (GSD) type 0 is an inborn error of glycogen metabolism caused by mutations in theCase presentation:Herein we report three new cases of liver glycogen synthase deficiency (GSD0). The first patient presented at the 4 years of age with recurrent hypoglycemic seizures. The second patient who is the brother of the first patient presented at 15 months with asymptomatic incidental hypoglycemia. Glucose monitoring in both patients revealed daily fluctuations from fasting hypoglycemia to postprandial hyperglycemia and lactic acidemia. A third patient was consulted for ketotic hypoglycemia and postprandial hyperglycemia at the 5 years of age.Conclusions:Genetic analyses of the siblings revealed homozygosity for mutation c.736C>T on the

Resistance of hepatic glycogen to depletion in obese Zucker rats

1991 ◽  
Vol 69 (6) ◽  
pp. 841-845 ◽  
Author(s):  
Harry Koubi ◽  
Claude Duchamp ◽  
Alain Géloën ◽  
Alain Fréminet ◽  
Yves Minaire
Keyword(s):  
Cold Exposure ◽  
Liver Glycogen ◽  
Zucker Rats ◽  
Hepatic Glycogen ◽  
Glycogen Store ◽  
Obese Rats ◽  
Fasting And Refeeding ◽  
Obese Zucker Rats ◽  
Ad Libitum ◽  
Glycogen Stores

Glycogen stores (liver and carcass) have been studied in lean and obese Zucker rats. The animals were submitted to one of three feeding conditions: ad libitum, a 48-h fast, or a 48-h fast and food ad libitum for 24 h, and to two environmental conditions, either thermoneutrality or an acute cold exposure (2 days at 4–7 °C). After a 2-day fast at 25 °C, the liver glycogen store was reduced by 45 times in the lean rats, while it was decreased by only 3 times in the obese rats. Under these conditions, the liver glycogen store was 45 times higher in the obese than in the lean rats. After 2 days in the cold, liver glycogen store was 4.4 times higher in obese rats than in lean rats. After a 2-day fast in the cold, the liver glycogen store in the obese rats was 30 times higher than in the lean rats. In comparison to fasting at thermoneutrality, fasting in the cold did not lead to a further reduction in hepatic glycogen in obese Zucker rats. The differences observed in the mobilization of the hepatic glycogen store between obese and lean rats have not been found in the mobilization of the carcass glycogen store. Drastic conditions, such as a 2-day fast in the cold, did not exhaust the glycogen store in obese Zucker rats. The present observations point out that obese Zucker rats cannot mobilize the entire hepatic glycogen store, as seen in lean control rats. The role of this abnormality in the high hyperlipogenesis that maintains the obese state is still to be evaluated.Key words: glycogen, fasting and refeeding, cold exposure, obesity, liver.

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