Contribution of net hepatic glycogenolysis to glucose production during the early postprandial period

1996 ◽  
Vol 270 (1) ◽  
pp. E186-E191 ◽  
Author(s):  
K. F. Petersen ◽  
T. Price ◽  
G. W. Cline ◽  
D. L. Rothman ◽  
G. I. Shulman
Keyword(s):  
Magnetic Resonance ◽  
Glycogen Content ◽  
Hepatic Glucose Production ◽  
Liver Volume ◽  
Glucose Production ◽  
Liver Glycogen ◽  
Whole Body ◽  
Hepatic Glycogen ◽  
Resonance Spectroscopy ◽  
13C Nuclear Magnetic Resonance

Relative contributions of net hepatic glycogenolysis and gluconeogenesis to glucose production during the first 12 h of a fast were studied in 13 healthy volunteers by noninvasively measuring hepatic glycogen content using 13C nuclear magnetic resonance spectroscopy. Rates of net hepatic glycogenolysis were calculated by multiplying the change in liver glycogen content with liver volume determined by magnetic resonance imaging. Rates of gluconeogenesis were calculated as the difference between rates of glucose production determined with an infusion of [6,6-2H]-glucose and net hepatic glycogenolysis. At 6 P.M. a liquid mixed meal (1,000 kcal; 60% as glucose) was given, to which [2-2H]glucose was added to trace glucose absorption. Hepatic glycogen content was measured between 11 P.M. and 1 A.M. and between 3 and 6 A.M. At 11 P.M. the concentration was 470 mM and it decreased linearly during the night. The mean liver volume was 1.47 +/- 0.06 liters. Net hepatic glycogenolysis (5.8 +/- 0.8 mumol.kg body wt-1.min-1) accounted for, on average, 45 +/- 6% and gluconeogenesis for 55 +/- 6% of the rate of whole body glucose production (12.6 +/- 0.6 mumol.kg body wt-1.min-1). In conclusion, this study shows that, even early in the phase of the postabsorptive period when liver glycogen stores are maximal, gluconeogenesis contributes approximately 50% to hepatic glucose production.

Influence of prior exercise and liver glycogen content on the sensitivity of the liver to glucagon

2002 ◽  
Vol 92 (1) ◽  
pp. 188-194 ◽  
Author(s):  
Victoria Matas Bonjorn ◽  
Martin G. Latour ◽  
Patrice Bélanger ◽  
Jean-Marc Lavoie
Keyword(s):  
Glucose Utilization ◽  
Glycogen Content ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Liver Glycogen ◽  
Hepatic Glycogen ◽  
Prior Exercise ◽  
Hepatic Glucose ◽  
Increased Sensitivity ◽  
Glucagon And Insulin

The purpose of the present study was to test the hypothesis that a prior period of exercise is associated with an increase in hepatic glucagon sensitivity. Hepatic glucose production (HGP) was measured in four groups of anesthetized rats infused with glucagon (2 μg · kg−1 · min−1 iv) over a period of 60 min. Among these groups, two were normally fed and, therefore, had a normal level of liver glycogen (NG). One of these two groups was killed at rest (NG-Re) and the other after a period of exercise (NG-Ex; 60 min of running, 15–26 m/min, 0% grade). The two other groups of rats had a high hepatic glycogen level (HG), which had been increased by a fast-refed diet, and were also killed either at rest (HG-Re) or after exercise (HG-Ex). Plasma glucagon and insulin levels were increased similarly in all four conditions. Glucagon-induced hyperglycemia was higher ( P < 0.01) in the HG-Re group than in all other groups. HGP in the HG-Re group was not, however, on the whole more elevated than in the NG-Re group. Exercised rats (NG-Ex and HG-Ex) had higher hyperglycemia, HGP, and glucose utilization than rested rats in the first 10 min of the glucagon infusion. HG-Ex group had the highest HGP throughout the 60-min experiment. It is concluded that hyperglucagonemia-induced HGP is stimulated by a prior period of exercise, suggesting an increased sensitivity of the liver to glucagon during exercise.

scholarly journals Contributions of net hepatic glycogenolysis and gluconeogenesis to glucose production in cirrhosis

1999 ◽  
Vol 276 (3) ◽  
pp. E529-E535 ◽  
Author(s):  
Kitt Falk Petersen ◽  
Martin Krssak ◽  
Victor Navarro ◽  
Visvanathan Chandramouli ◽  
Ripudaman Hundal ◽  
...  
Keyword(s):  
Magnetic Resonance ◽  
Glycogen Content ◽  
Glucose Production ◽  
Hepatic Glycogen ◽  
Resonance Spectroscopy ◽  
Contributing Factors ◽  
Control Subjects ◽  
Igf I ◽  
The Difference ◽  
C Nmr

Net hepatic glycogenolysis and gluconeogenesis were examined in normal ( n = 4) and cirrhotic ( n = 8) subjects using two independent methods [13C nuclear magnetic resonance spectroscopy (NMR) and a2H2O method]. Rates of net hepatic glycogenolysis were calculated by the change in hepatic glycogen content before (∼11:00 PM) and after (∼7:00 AM) an overnight fast using13C NMR and magnetic resonance imaging. Gluconeogenesis was calculated as the difference between the rates of glucose production determined with an infusion of [6,6-2H2]glucose and net hepatic glycogenolysis. In addition, the contribution of gluconeogenesis to glucose production was determined by the2H enrichment in C-5/C-2 of blood glucose after intake of2H2O (5 ml/kg body water). Plasma levels of total and free insulin-like growth factor I (IGF-I) and IGF-I binding proteins-1 and -3 were significantly decreased in the cirrhotic subjects ( P < 0.01 vs. controls). Postprandial hepatic glycogen concentrations were 34% lower in the cirrhotic subjects ( P = 0.007). Rates of glucose production were similar between the cirrhotic and healthy subjects [9.0 ± 0.9 and 10.0 ± 0.8 μmol ⋅ kg body wt−1 ⋅ min−1, respectively]. Net hepatic glycogenolysis was 3.5-fold lower in the cirrhotic subjects ( P = 0.01) and accounted for only 13 ± 6% of glucose production compared with 40 ± 10% ( P = 0.03) in the control subjects. Gluconeogenesis was markedly increased in the cirrhotic subjects and accounted for 87 ± 6% of glucose production vs. controls: 60 ± 10% ( P = 0.03). Gluconeogenesis in the cirrhotic subjects, as determined from the2H enrichment in glucose C-5/C-2, was also increased and accounted for 68 ± 3% of glucose production compared with 54 ± 2% ( P = 0.02) in the control subjects. In conclusion, cirrhotic subjects have increased rates of gluconeogenesis and decreased rates of net hepatic glycogenolysis compared with control subjects. These alterations are likely important contributing factors to their altered carbohydrate metabolism.

Effect of liver glycogen content on glucose production in running rats

1989 ◽  
Vol 66 (1) ◽  
pp. 318-322 ◽  
Author(s):  
J. Vissing ◽  
J. L. Wallace ◽  
H. Galbo
Keyword(s):  
Plasma Glucose ◽  
Glycogen Content ◽  
Hepatic Glucose Production ◽  
Plasma Concentrations ◽  
Glucose Production ◽  
Liver Glycogen ◽  
Treadmill Running ◽  
Hepatic Glycogen ◽  
Hepatic Glucose ◽  
Exercise Induced

The influence of supranormal compared with normal hepatic glycogen levels on hepatic glucose production (Ra) during exercise was investigated in chronically catheterized rats. Supranormal hepatic glycogen levels were obtained by a 24-h fast-24-h refeeding regimen. During treadmill running for 35 min at a speed of 21 m/min, Ra and plasma glucose increased more (P less than 0.05) and liver glucogen breakdown was larger in fasted-refed compared with control rats, although the stimuli for Ra were higher in control rats, the plasma concentrations of insulin and glucose being lower (P less than 0.05) in control compared with fasted-refed rats. Also, plasma concentrations of glucagon and both catecholamines tended to be higher and muscle glycogenolysis lower in control compared with fasted-refed rats. Lipid metabolism was similar in the two groups. The results indicate that hepatic glycogenolysis during exercise is directly related to hepatic glycogen content. The smaller endocrine glycogenolytic signal in face of higher plasma glucose concentrations in fasted-refed compared with control rats is indicative of metabolic feedback control of glucose mobilization during exercise. However, the higher exercise-induced increase in Ra, plasma glucose, and liver glycogen breakdown in fasted-refed compared with control rats indicates that metabolic feedback mechanisms are not able to accurately match Ra to the metabolic needs of working muscles.

Time course of insulin action on tissue-specific intracellular glucose metabolism in normal rats

1998 ◽  
Vol 274 (4) ◽  
pp. E642-E650 ◽  
Author(s):  
Sietse J. Koopmans ◽  
Lawrence Mandarino ◽  
Ralph A. Defronzo
Keyword(s):  
Insulin Action ◽  
Time Course ◽  
Hepatic Glucose Production ◽  
Glycogen Synthesis ◽  
Glucose Production ◽  
Liver Glycogen ◽  
Whole Body ◽  
Glucose Disposal ◽  
Muscle Glycogen Synthesis ◽  
The Face

We investigated the time course of insulin action in conscious rats exposed to constant physiological hyperinsulinemia (∼100 mU/l) while maintaining euglycemia (∼100 mg/dl) for 0, 0.5, 2, 4, 8, or 12 h. [3-3H]glucose was infused to quantitate whole body glucose disposal (rate of disappearance, Rd), glycolysis (generation of3H2O in plasma), hepatic glucose production (HGP), and skeletal muscle and liver glycogen synthesis ([3-3H]glucose incorporation into glycogen and time-dependent change in tissue glycogen concentration). The basal Rd, which equals HGP, was 6.0 ± 0.3 mg ⋅ kg−1 ⋅ min−1. With increased duration of hyperinsulinemia from 0 to 0.5 to 2 to 4 h, Rd increased from 6.0 ± 0.3 to 21.0 ± 1.1 to 24.1 ± 1.5 to 26.6 ± 0.6 mg ⋅ kg−1 ⋅ min−1( P < 0.05 for 2 and 4 h vs. 0.5 h). During the first 2 h the increase in Rd was explained by parallel increases in glycolysis and glycogen synthesis. From 2 to 4 h the further increase in Rd was entirely due to an increase in glycolysis without change in glycogen synthesis. From 4 to 8 to 12 h of hyperinsulinemia, Rd decreased by 19% from 26.6 ± 0.6 to 24.1 ± 1.1 to 21.6 ± 1.8 mg ⋅ kg−1 ⋅ min−1( P < 0.05 for 8 h vs. 4 h and 12 h vs. 8 h). The progressive decline in Rd, in the face of constant hyperinsulinemia, occurred despite a slight increase (8–14%) in glycolysis and was completely explained by a marked decrease (64%) in muscle glycogen synthesis. In contrast, liver glycogen synthesis increased fourfold, indicating an independent regulation of muscle and liver glycogen synthesis by long-term hyperinsulinemia. In the liver, during the entire 12-h period of insulin stimulation, the contribution of the direct (from glucose) and the indirect (from C-3 fragments) pathways to net glycogen formation remained constant at 77 ± 5 and 23 ± 5%, respectively. HGP remained suppressed throughout the 12-h period of hyperinsulinemia.

scholarly journals Sucrose ingestion after exhaustive exercise accelerates liver, but not muscle glycogen repletion compared with glucose ingestion in trained athletes

2016 ◽  
Vol 120 (11) ◽  
pp. 1328-1334 ◽  
Author(s):  
Cas J. Fuchs ◽  
Javier T. Gonzalez ◽  
Milou Beelen ◽  
Naomi M. Cermak ◽  
Fiona E. Smith ◽  
...  
Keyword(s):  
Muscle Glycogen ◽  
Glycogen Content ◽  
Liver Volume ◽  
Liver Glycogen ◽  
Resonance Spectroscopy ◽  
Time Treatment ◽  
Liver Glycogen Content ◽  
Glucose Ingestion ◽  
Postexercise Recovery ◽  
Glycogen Repletion

The purpose of this study was to assess the effects of sucrose vs. glucose ingestion on postexercise liver and muscle glycogen repletion. Fifteen well-trained male cyclists completed two test days. Each test day started with glycogen-depleting exercise, followed by 5 h of recovery, during which subjects ingested 1.5 g·kg−1·h−1 sucrose or glucose. Blood was sampled frequently and 13C magnetic resonance spectroscopy and imaging were employed 0, 120, and 300 min postexercise to determine liver and muscle glycogen concentrations and liver volume. Results were as follows: Postexercise muscle glycogen concentrations increased significantly from 85 ± 27 (SD) vs. 86 ± 35 mmol/l to 140 ± 23 vs. 136 ± 26 mmol/l following sucrose and glucose ingestion, respectively (no differences between treatments: P = 0.673). Postexercise liver glycogen concentrations increased significantly from 183 ± 47 vs. 167 ± 65 mmol/l to 280 ± 72 vs. 234 ± 81 mmol/l following sucrose and glucose ingestion, respectively (time × treatment, P = 0.051). Liver volume increased significantly over the 300-min period after sucrose ingestion only (time × treatment, P = 0.001). As a result, total liver glycogen content increased during postexercise recovery to a greater extent in the sucrose treatment (from 53.6 ± 16.2 to 86.8 ± 29.0 g) compared with the glucose treatment (49.3 ± 25.5 to 65.7 ± 27.1 g; time × treatment, P < 0.001), equating to a 3.4 g/h (95% confidence interval: 1.6-5.1 g/h) greater repletion rate with sucrose vs. glucose ingestion. In conclusion, sucrose ingestion (1.5 g·kg−1·h−1) further accelerates postexercise liver, but not muscle glycogen repletion compared with glucose ingestion in trained athletes.

Mobilization of Glucose From the Liver During Exercise and Replenishment Afterward

2005 ◽  
Vol 30 (3) ◽  
pp. 292-303 ◽  
Author(s):  
R. Richard Pencek ◽  
Patrick T. Fueger ◽  
Raul C. Camacho ◽  
David H. Wasserman
Keyword(s):  
Human Subjects ◽  
Hepatic Glucose Production ◽  
Glucose Production ◽  
Liver Glycogen ◽  
Hepatic Glycogen ◽  
Glycogen Depletion ◽  
Hepatic Glucose Metabolism ◽  
Carbohydrate Feeding ◽  
Hepatic Glucose ◽  
Glucagon And Insulin

The liver is anatomically well situated to regulate blood glucose. It is positioned downstream from the pancreas, which releases the key regulatory hormones glucagon and insulin. It is also just downstream from the gut, permitting efficient extraction of ingested glucose and preventing large excursions in systemic glucose after a glucose-rich meal. The position of the liver is not as well situated from the standpoint of experimentation and clinical assessment, as its primary blood supply is impossible to access in conscious human subjects. Over the last 20 years, to study hepatic glucose metabolism during and after exercise, we have utilized a conscious dog model which permits sampling of the blood that perfuses (portal vein, artery) and drains (hepatic vein) the liver. Our work has demonstrated the key role of exercise-induced changes in glucagon and insulin in stimulating hepatic glycogenolysis and gluconeogenesis during exercise. Recently we showed that portal venous infusion of the pharmacological agent 5'-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside leads to a marked increase in hepatic glucose production. Based on this, we propose that the concentration of AMP may be a component of a physiological pathway for stimulating hepatic glucose production during exercise. Insulin-stimulated hepatic glucose uptake is increased following exercise by an undefined mechanism that is independent of liver glycogen content. The fate of glucose taken up by the liver is critically dependent on hepatic glycogen stores, however, as glycogen deposition is greatly facilitated by prior glycogen depletion. Key words: pancreas, carbohydrate, feeding, exertion, AICAR

Early glycogenolysis and late glycogenesis in human liver after intravenous administration of galactose

1996 ◽  
Vol 270 (1) ◽  
pp. G14-G19 ◽  
Author(s):  
R. Fried ◽  
N. Beckmann ◽  
U. Keller ◽  
R. Ninnis ◽  
G. Stalder ◽  
...  
Keyword(s):  
Magnetic Resonance ◽  
Competitive Inhibition ◽  
Glycogen Synthesis ◽  
Liver Volume ◽  
Hepatic Glycogen ◽  
Resonance Spectroscopy ◽  
Hepatic Glucose Output ◽  
Glycogen Concentration ◽  
Hepatic Glucose ◽  
Glucose Output

Galactose is incorporated by a different metabolic pathway than glucose. Its contribution to glycogen synthesis has not been studied in humans. We administered galactose (0.5 g/kg iv) to overnight-fasted normal human volunteers and examined its effects on hepatic glycogen synthesis and hepatic glucose output (HGO). Hepatic glycogenesis was assessed noninvasively, determining glycogen concentration by 13C magnetic resonance spectroscopy (MRS) and liver volume by magnetic resonance imaging. HGO was determined by [6,6-2H2]glucose and gluconeogenesis calculated by adding the amount of hepatic glycogenesis to the HGO. After galactose administration, liver glycogen concentration (baseline 254 +/- 11 mmol/l) decreased in the first 45 min to 207 +/- 15 mmol/l (P < 0.05) and increased thereafter to 313 +/- 7 mmol/l (P < 0.01). Net hepatic glycogenesis was 101 +/- 12 mmol over 150 min. HGO (baseline 14.3 +/- 1.9 mumol.kg-1.min-1) increased threefold in the first 15 min and then returned to baseline. The average rate of gluconeogenesis was 12.3 mumol.kg-1.min-1. Intravenous galactose leads to an increase in hepatic glycogen and hepatic glucose output in normal humans. Competitive inhibition of UDP-glucose pyrophosphorylase by UDP-galactose could explain the apparent glycogenolysis observed early after galactose administration. 13C MRS in combination with a stable isotope tracer is a noninvasive and safe method to study hepatic carbohydrate metabolism in humans.

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