Aberrations in the Diurnal Rhythms of Plasma Glucose, Plasma Insulin, Liver Glycogen, and Hepatic Glycogen Synthase and Phosphorylase Activities in Genetically Diabetic (db/db) Mice

1985 ◽  
Vol 17 (11) ◽  
pp. 572-575 ◽  
Author(s):  
W. Roesler ◽  
C. Helgason ◽  
M. Gulka ◽  
R. Khandelwal
Keyword(s):  
Plasma Glucose ◽  
Plasma Insulin ◽  
Glycogen Synthase ◽  
Liver Glycogen ◽  
Diurnal Rhythms ◽  
Hepatic Glycogen ◽  
Glucose Plasma

Differential effect of hyperglycemia and hyperinsulinemia on pathways of hepatic glycogen repletion

1991 ◽  
Vol 260 (5) ◽  
pp. E731-E735 ◽  
Author(s):  
G. I. Shulman ◽  
R. A. DeFronzo ◽  
L. Rossetti
Keyword(s):  
Portal Vein ◽  
Plasma Glucose ◽  
Plasma Insulin ◽  
Glycogen Synthesis ◽  
Liver Glycogen ◽  
Hepatic Glycogen ◽  
Group Iii ◽  
Group I ◽  
Group Ii ◽  
Glycogen Repletion

To delineate the roles of hyperglycemia and insulin on the direct vs. indirect pathways of liver glycogen synthesis, we performed euglycemic (group I; n = 8), hyperglycemic (group II; n = 9), and euglycemic pharmacological hyperinsulinemic clamp studies (120 min) with an infusion of [1-13C]glucose in chronically catheterized conscious rats after a 24-h fast. Portal vein plasma glucose concentrations and portal vein plasma insulin concentrations, respectively, obtained at the end of the study in groups I-III were as follows: group I 110 +/- 4 mg/dl, 29 +/- 7 ng/ml; group II 219 +/- 7 mg/dl, 24 +/- 7 ng/ml; and group III 112 +/- 9 mg/dl, 174 +/- 25 ng/ml. Mean liver glycogen concentrations at the end of the three studies were 0.68 +/- 0.07, 1.22 +/- 0.08 (P less than 0.001 compared with groups I and III), and 0.60 +/- 0.17 g/100 g wet wt liver in groups I-III respectively, which yielded hepatic glycogen synthetic rates of 0.16 +/- 0.03, 0.41 +/- 0.04 (P less than 0.001 compared with groups I and III), and 0.13 +/- 0.08 mumol glucosyl U.g liver-1.min-1 in groups I-III, respectively. From the enrichments of 13C in the C-1 and C-6 positions of the glucosyl unit in glycogen compared with the enrichment in the C-1 position in portal vein glucose as determined by 13C- and 1H-NMR, the amount of glycogen synthesized by the direct pathway was calculated to be 18 +/- 2, 41 +/- 3 (P less than 0.0001 compared with groups I and III), and 17 +/- 3% in groups I-III, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Glycemic and Insulinemic Response to Preexercise Carbohydrate Feedings

1994 ◽  
Vol 4 (1) ◽  
pp. 46-53 ◽  
Author(s):  
John G. Seifert ◽  
Greg L. Paul ◽  
Dennis E. Eddy ◽  
Robert Murray
Keyword(s):  
Plasma Glucose ◽  
Plasma Insulin ◽  
Glucose Solution ◽  
Physiological Responses ◽  
Metabolic Responses ◽  
Moderate Intensity ◽  
Baseline Values ◽  
Glucose Plasma ◽  
Insulinemic Response

The effects of preexercise hyperinsulinemia on exercising plasma glucose, plasma insulin, and metabolic responses were assessed during 50 min cycling at 62%. Subjects were fed a 6% sucrose/glucose solution (LCHO) or a 20% maltodextrin/glucose solution (HCHO) to induce changes in plasma insulin. During exercise, subjects assessed perceived nauseousness and lightheadedness. By the start of exercise, plasma glucose and plasma insulin had increased. In the LCHO trial, plasma glucose values significantly decreased below the baseline value at 30 min of exercise. However, by 40 min, exercise plasma glucose and insulin values were similar to the baseline value. Exercise plasma glucose and insulin did not differ from baseline values in the HCHO trial. Ingestion of LCHO or HCHO was not associated with nausea or lightheadedness. It was concluded that the hyperinsulinemia induced by preexercise feediigs of CHO did not result in frank hypoglycemia or adversely affect sensory or physiological responses during 50 min of moderate-intensity cycling.

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

scholarly journals Comparison of the Effects of Acarbose and TZQ-F, a New Kind of Traditional Chinese Medicine to Treat Diabetes, Chinese Healthy Volunteers

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Huang Yuhong ◽  
Fu Wenxu ◽  
Li Yanfen ◽  
Liu Yu ◽  
Li Ziqiang ◽  
...  
Keyword(s):  
Chinese Medicine ◽  
Traditional Chinese Medicine ◽  
Adverse Events ◽  
Plasma Glucose ◽  
Plasma Insulin ◽  
Double Blind ◽  
C Peptide ◽  
Treatment Of Diabetes ◽  
Glucose Plasma ◽  
Gastrointestinal Adverse Events

Ethnopharmacological Relevance. TZQ-F has been traditionally used in Traditional Chinese Medicine as a formula for the treatment of diabetes.Aim of the Study. This study aims to compare the pharmacologic effects and gastrointestinal adverse events between TZQ-F and acarbose.Methods. The double-blind randomized placebo-controlled fivefold crossover study was performed in 20 healthy male volunteers. Plasma glucose, plasma IRI, and plasma C-peptide were measured to assess the pharmacologic effects. Flatus and bowel activity were measured to assess the adverse event of gastrointestinal effect.Results. 3 and 4 tablets of TZQ decreased theCmaxof plasma glucose compared with that of the previous day and with placebo. 3 tablets also decreasedCmaxof plasma C-peptide compared with placebo. 4 tablets increasedCmaxof plasma insulin after breakfast and the AUC of plasma C-peptide after breakfast and dinner. 2 tablets did not decrease plasma glucose and elevated theCmaxand AUC of C-peptide after breakfast and dinner, respectively. Acarbose 50 mg decreased theCmaxof plasma insulin and C-peptide after breakfast and theCmaxof plasma glucose and C-peptide after dinner. The subjects who received TZQ did not report any abdominal adverse events.Conclusions. 3 tablets of TZQ have the same effects as the acarbose.

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.

Lack of defect in insulin action on hepatic glycogen synthase and phosphorylase in insulin-resistant monkeys

1998 ◽  
Vol 274 (6) ◽  
pp. G1005-G1010
Author(s):  
Heidi K. Ortmeyer ◽  
Noni L. Bodkin
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Muscle Glycogen ◽  
Rhesus Monkeys ◽  
Insulin Action ◽  
Glycogen Phosphorylase ◽  
Glycogen Synthase ◽  
Liver Glycogen ◽  
Hepatic Glycogen ◽  
Insulin Resistant

It is well known that an alteration in insulin activation of skeletal muscle glycogen synthase is associated with insulin resistance. To determine whether this defect in insulin action is specific to skeletal muscle, or also present in liver, simultaneous biopsies of these tissues were obtained before and during a euglycemic hyperinsulinemic clamp in spontaneously obese insulin-resistant male rhesus monkeys. The activities of glycogen synthase and glycogen phosphorylase and the concentrations of glucose 6-phosphate and glycogen were measured. There were no differences between basal and insulin-stimulated glycogen synthase and glycogen phosphorylase activities or in glucose 6-phosphate and glycogen contents in muscle. Insulin increased the activities of liver glycogen synthase ( P < 0.05) and decreased the activities of liver glycogen phosphorylase ( P ≤ 0.001). Insulin also caused a reduction in liver glucose 6-phosphate ( P = 0.05). We conclude that insulin-resistant monkeys do not have a defect in insulin action on liver glycogen synthase, although a defect in insulin action on muscle glycogen synthase is present. Therefore, tissue-specific alterations in insulin action on glycogen synthase are present in the development of insulin resistance in rhesus monkeys.

Altered hepatic glycogen metabolism and glucoregulatory hormones during sepsis

1976 ◽  
Vol 230 (5) ◽  
pp. 1296-1301 ◽  
Author(s):  
RT Curnow ◽  
EJ Rayfield ◽  
DT George ◽  
TV Zenser ◽  
FR DeRubertis
Keyword(s):  
Cyclic Amp ◽  
Portal Vein ◽  
Glycogen Synthase ◽  
Glycogen Metabolism ◽  
Liver Glycogen ◽  
Hepatic Glycogen ◽  
In Situ Perfusion ◽  
Glucoregulatory Hormones

Levels of glucose, insulin, and glucagon in portal vein plasma and of liver glycogen and cyclic AMP and activities of glycogen synthase and phosphorylase in liver were assayed in control (CONT) rats and rats infected (INF) with Diplococcus pneumoniae. In INF rats compared with CONT rats, insulin and glucagon levels were higher (8,12,24 h). Activity of synthase I was lower (8, 12, 24 h) and of phosphorylase higher (12 and 24 h) in INF rats. Cyclic AMP levels were higher in INF rats at 12 and 24 h. Total synthase activity was lower in INF rats at 24 h. Glucose given intravenously increased glycogen less in INF than in CONT rats and activated synthase and inactivated phosphorylase in all animals except at 24 h in INF rats. However, in situ perfusion of the livers at 24 h with glucose in buffer decreased phosphorylase activities in all animals and increased synthase I activities in CONT but not INF rats.

Penetration of peripheral glucose and insulin into cerebrospinal fluid in rats

1988 ◽  
Vol 255 (2) ◽  
pp. R200-R204 ◽  
Author(s):  
A. B. Steffens ◽  
A. J. Scheurink ◽  
D. Porte ◽  
S. C. Woods
Keyword(s):  
Cerebrospinal Fluid ◽  
Plasma Glucose ◽  
Plasma Insulin ◽  
Glucose Solution ◽  
Base Line ◽  
Jugular Veins ◽  
Left And Right ◽  
Freely Moving ◽  
Ad Libitum ◽  
Glucose Plasma

In this study the penetration of plasma insulin and glucose into the cerebrospinal fluid (CSF) was investigated. Rats were implanted with cannulas in the cisterna magna and into the left and right jugular veins. Freely moving rats were intravenously infused during 4 h with either glucose solution (10 mg/min) or saline. Before, during, and after the infusions, simultaneous blood and CSF samples were taken. Infusion of glucose led to an immediate rise of both plasma glucose and insulin. Although CSF glucose followed plasma glucose within 10 min, CSF insulin was unchanged until 40 min. After termination of the glucose infusion, levels of all substances returned to base line within 10 min. Twenty-four-hour food deprivation resulted in a significant decrease of plasma glucose, plasma insulin, CSF glucose, and CSF insulin. At the onset of eating after deprivation, an increase of plasma glucose and insulin occurred within 10 min, whereas CSF glucose was delayed between 10 and 40 min, after which ad libitum values were attained or surpassed. CSF insulin always remained below ad libitum levels. It is concluded that 1) glucose and insulin penetrate into the CSF and 2) CSF insulin and glucose can fulfill a putative feedback in homeostatic control of food intake and body weight.

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