scholarly journals Defective activation by glucose of hepatic glycogen synthesis in the obese hyperglycaemic mouse

1983 ◽  
Vol 216 (2) ◽  
pp. 491-494 ◽  
Author(s):  
S A Smith ◽  
M A Cawthorne ◽  
A L Levy ◽  
D L Simson
Keyword(s):  
Glycogen Synthase ◽  
Glycogen Synthesis ◽  
Fold Increase ◽  
Hepatic Glycogen ◽  
Oral Glucose ◽  
Oral Glucose Load ◽  
Glucose Load ◽  
No Activation ◽  
Sustained Activation

The administration of an oral glucose load to 24 h-starved lean (+/?) male C57BL/6 mice produced a rapid, 7-fold increase in the rate of hepatic glycogen synthesis and a sustained activation of glycogen synthase. In contrast, glucose produced only a small (4.5-fold), short-lived increase in hepatic glycogen synthesis in genetically obese (ob/ob) mice and no activation of glycogen synthase.

Contribution of net hepatic glycogen synthesis to disposal of an oral glucose load in humans

Metabolism ◽  
2001 ◽  
Vol 50 (5) ◽  
pp. 598-601 ◽  
Author(s):  
Kitt F. Petersen ◽  
Gary W. Cline ◽  
David P. Gerard ◽  
Inger Magnusson ◽  
Douglas L. Rothman ◽  
...  
Keyword(s):  
Glycogen Synthesis ◽  
Hepatic Glycogen ◽  
Oral Glucose ◽  
Oral Glucose Load ◽  
Glucose Load

Mechanism of delayed hepatic glycogen synthesis after an oral galactose load vs. an oral glucose load in adult rats

1992 ◽  
Vol 263 (1) ◽  
pp. E42-E49 ◽  
Author(s):  
C. B. Niewoehner ◽  
B. Neil
Keyword(s):  
Glucose Concentration ◽  
Glycogen Synthesis ◽  
Liver Glycogen ◽  
Hepatic Glycogen ◽  
Oral Glucose ◽  
Glucose Load ◽  
Adult Rats ◽  
Glycogen Accumulation ◽  
Glucose Administration

We have compared the effects of administration of oral galactose or glucose (1 g/kg) to 24-h fasted rats to examine the mechanism by which galactose regulates its own incorporation into liver glycogen in vivo. Liver glycogen increased to a maximum more slowly after galactose than after glucose administration (0.14 vs. 0.29 mumol.g liver-1.min-1). Glycogen accumulation after the galactose load was 70% of that after the glucose load (149 vs. 214 mumol), and the net increase in liver glycogen represented the same proportion (24 vs. 22%) of added carbohydrate after urinary loss of galactose was accounted for. Slower glycogen accumulation after galactose vs. glucose loading could not be explained by galactosuria, by differences in the active forms of synthase or phosphorylase, by end product (glycogen) inhibition of synthase phosphatase, or by different concentrations of the known allosteric effectors of synthase R plus I and phosphorylase a. Similar increases in glucose 6-phosphate were observed after both hexoses. AMP and ADP increased only transiently after galactose administration, and ATP, UTP, and Pi concentrations were unchanged. The UDP-glucose concentration decreased, whereas the UDP-galactose concentration increased two- to threefold after galactose but not glucose administration. The UDP-glucose pyrophosphorylase reaction is inhibited competitively by UDP-galactose. This could explain the decreased UDP-glucose concentration and the reduced rate of glycogen synthesis after galactose was given.

scholarly journals The activity of glycogen synthase phosphatase limits hepatic glycogen deposition in the adrenalectomized starved rat

1983 ◽  
Vol 214 (2) ◽  
pp. 539-545 ◽  
Author(s):  
M Bollen ◽  
G Gevers ◽  
W Stalmans
Keyword(s):  
Phosphatase Activity ◽  
Protein Phosphatase ◽  
Glycogen Synthase ◽  
Glycogen Synthesis ◽  
Hepatic Glycogen ◽  
Complete Inactivation ◽  
Glycogen Deposition ◽  
Initial Recovery ◽  
No Activation

Hepatocytes from adrenalectomized 48 h-starved rats responded to increasing glucose concentrations with a progressively more complete inactivation of phosphorylase. Yet no activation of glycogen synthase occurred, even in a K+-rich medium. Protein phosphatase activities in crude liver preparations were assayed with purified substrates. Adrenalectomy plus starvation decreased synthase phosphatase activity by about 90%, but hardly affected phosphorylase phosphatase activity. Synthase b present in liver extracts from adrenalectomized starved rats was rapidly and completely converted into the a form on addition of liver extract from a normal fed rat. Glycogen synthesis can be slowly re-induced by administration of either glucose or cortisol to the deficient rats. In these conditions there was a close correspondence between the initial recovery of synthase phosphatase activity and the amount of synthase a present in the liver. The latter parameter was strictly correlated with the measured rate of glycogen synthesis in vivo. The decreased activity of synthase phosphatase emerges thus as the single factor that limits hepatic glycogen deposition in the adrenalectomized starved rat.

Relationship between insulin response to oral glucose load and creatinine clearance

Diabetes ◽  
1975 ◽  
Vol 24 (12) ◽  
pp. 1066-1071 ◽  
Author(s):  
K. Yasuda ◽  
T. Sato ◽  
T. Furuyama ◽  
K. Yashinaga
Keyword(s):  
Creatinine Clearance ◽  
Insulin Response ◽  
Oral Glucose ◽  
Oral Glucose Load ◽  
Glucose Load

The disposal of an oral glucose load in healthy subjects. A quantitative study

Diabetes ◽  
1985 ◽  
Vol 34 (6) ◽  
pp. 580-588 ◽  
Author(s):  
E. Ferrannini ◽  
O. Bjorkman ◽  
G. A. Reichard ◽  
A. Pilo ◽  
M. Olsson ◽  
...  
Keyword(s):  
Quantitative Study ◽  
Healthy Subjects ◽  
Oral Glucose ◽  
Oral Glucose Load ◽  
Glucose Load

Enhanced Insulin Response to Oral Glucose Load in Patients with Angina Pectoris Associated with ST Segment Elevation in the Absence of Epicardial Coronary Arterial Obstruction

Angiology ◽  
1998 ◽  
Vol 49 (9) ◽  
pp. 815-826 ◽  
Author(s):  
Shigeo Takata ◽  
Atsuhiro Shimakura ◽  
Satoru Sakagami ◽  
Yukio Nakamura ◽  
Hitoshi Ohkuwa ◽  
...  
Keyword(s):  
Angina Pectoris ◽  
Insulin Response ◽  
Oral Glucose ◽  
Oral Glucose Load ◽  
Glucose Load ◽  
St Segment Elevation ◽  
St Segment

scholarly journals Sitagliptin improves glycaemic excursion after a meal or after an oral glucose load in J apanese subjects with impaired glucose tolerance

2015 ◽  
Vol 17 (11) ◽  
pp. 1033-1041 ◽  
Author(s):  
K. Kaku ◽  
T. Kadowaki ◽  
Y. Terauchi ◽  
T. Okamoto ◽  
A. Sato ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Impaired Glucose Tolerance ◽  
Oral Glucose ◽  
Oral Glucose Load ◽  
Glucose Load

Acute Effect of Chili Consumption on Thermogenesis and Glycemic Response Following Oral Glucose Load in Men

2020 ◽  
Vol 19 (3) ◽  
pp. 288-294
Author(s):  
Muriel Ávila-Seguel ◽  
Constanza Márquez-Urrizola ◽  
Gislaine Granfeldt ◽  
Katia Saez-Carrillo ◽  
Javad Sharifi-Rad ◽  
...  
Keyword(s):  
Acute Effect ◽  
Chili Pepper ◽  
Oral Glucose ◽  
Glycemic Response ◽  
Oral Glucose Load ◽  
Glucose Load ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Post Test ◽  
Quasi Experimental

Hypoglycemic and thermogenic effects are attributed to the capsaicinoid compounds (capsaicin). The aim of this study was to evaluate the acute effect of the consumption of 5g of chili pepper on thermogenesis and the glycemic response. In a pretest-post-test quasi-experimental study, the energy expenditure (EE) of 15 healthy men was evaluated by using indirect calorimetry at rest and with the consumption of 5g of Capsicum annum. In addition, the glycemic response after an oral glucose load was evaluated. After the consumption of C. annum, there was a significant increase in the EE of all the participants during the first few seconds postchili consumption. In sedentary participants, the consumption of chili pepper caused a significant decrease of blood glucose levels. The consumption of chili pepper has a potential immediate thermogenic effect during the first few seconds and, in sedentary people, it has a potential hypoglycemic effect.

Hepatic glycogen in humans. I. Direct formation after oral and intravenous glucose or after a 24-h fast

1989 ◽  
Vol 257 (2) ◽  
pp. E145-E157 ◽  
Author(s):  
J. Radziuk
Keyword(s):  
Glucose Infusion ◽  
Hepatic Glycogen ◽  
Oral Glucose ◽  
Metabolic Clearance ◽  
Glucose Load ◽  
Fasting Period ◽  
Intravenous Glucose ◽  
Glucose Loading ◽  
Constant Rate ◽  
Direct Formation

The formation of hepatic glycogen by the direct pathway is assessed in humans 1) after a 12-h fast and oral loading (100 g) or 2) intravenous infusion (90 g) and 3) after a 24-h fast and the same oral glucose load. The methodology used is based on the double tracer method. [3–3H]glucose is infused at a constant rate for the determination of the metabolic clearance of glucose. [1–14C]glucose is administered with the glucose load. One hour after absorption or the intravenous glucose infusion is terminated, a glucagon infusion is initiated to mobilize the glycogen labeled with [1-14C]glucose and formed during the absorptive period. At this time a third tracer, [6-3H]glucose, is administered to measure glucose clearance. It was found that after the 12-h fast and oral glucose loading 7.2 +/- 1.1 g of hepatic glycogen appears to be formed directly from glucose compared with 8.4 +/- 1.0 g after the same load and a 24-h fast and 8.5 +/- 0.4 g after a 12-h fast and an equivalent intravenous glucose infusion. When the amount of label ([14C]glucose) mobilized that was not corrected for metabolic recycling was calculated, the data suggested that the amount of glycogen formed by gluconeogenic pathways was probably at least equal to that formed by direct uptake. It was also approximately 60% greater after a 24-h fast. It can be concluded that the amount of hepatic glycogen formed directly from glucose during glucose loading is not significantly altered by the route of entry or the extension of the fasting period to 24 h. The data suggest, however, that gluconeogenetic formation of glycogen increases with fasting.

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