3H-galactose and 3H-glucose incorporation into newly synthesized hepatic glycogen in control-fed rats

1986 ◽  
Vol 44 ◽  
pp. 292-293
Author(s):  
J.E. Michaels ◽  
S.A. Garfield ◽  
J.T. Hung ◽  
S.S. Smith ◽  
R.R. Cardell
Keyword(s):  
Biochemical Analysis ◽  
Glycogen Synthesis ◽  
Hepatic Glycogen ◽  
Electron Microscopic ◽  
Once Daily ◽  
Tail Vein ◽  
Tracer Dose ◽  
Glucose Incorporation ◽  
Wet Weight

3H-galactose (gal) and 3H-glucose (glu) were compared to determine which compound was preferable for pulse labeling newly formed hepatic glycogen. Control fed rats were used to achieve substantial and consistent levels of hepatic glycogen and to stimulate glycogen synthesis.Rats fed once daily for 4 hr achieved hepatic glycogen levels > 3% wet weight liver prior to injection by tail vein of a tracer dose of 3H-gal or 3H-glu. The rats were sacrificed 15-120 min later and liver was prepared by routine techniques for light (LM) and electron microscopic (EM) radioautography (RAG) and biochemical analysis.

Distribution of newly formed hepatic glycogen in adrenalectomized rats as observed by radioautography after injection of 3H-galactose

1984 ◽  
Vol 42 ◽  
pp. 228-229
Author(s):  
J. E. Michaels ◽  
J. T. Hung ◽  
E. L. Cardell ◽  
R. R. Cardell
Keyword(s):  
Glycogen Synthesis ◽  
Hepatic Glycogen ◽  
Electron Microscopic ◽  
Routine Procedures ◽  
Silver Grains ◽  
Synthetic Glucocorticoid ◽  
Adrenalectomized Rats

In order to study early events of glycogen synthesis, we have used adrenalectomized (ADX) rats fasted overnight and injected with the synthetic glucocorticoid dexamethasone (DEX) to stimulate glycogen synthesis. Rats were given DEX 0-5 hr prior to sacrifice and injected with 2 mCi 3H-galactose 1 hr prior to sacrifice. Liver was prepared for light (LM) and electron microscopic (EM) radioautography by routine procedures.The concentration of silver grains over hepatic cytoplasm was measured in LM radioautographs using a Zeiss Videoplan. The hepatocytes were categorized as unlabeled if no silver grains (gr) were present, lightly labeled (<10gr/100 μm2 cytoplasm) or intensely labeled (>10 gr/1002 μm cytoplasm). Although very few hepatocytes showed heavy labeling after 1 hr treatment with DEX, by 2 hr after DEX treatment 8% of the cells distributed throughout the lobule were intensely labeled.

Synergistic effects of oPL and insulin on glycogen metabolism in fetal rat hepatocytes

1984 ◽  
Vol 247 (6) ◽  
pp. E714-E718
Author(s):  
M. Freemark ◽  
S. Handwerger
Keyword(s):  
Synergistic Effects ◽  
Fetal Liver ◽  
Glycogen Synthesis ◽  
Rat Hepatocytes ◽  
Glycogen Metabolism ◽  
Placental Lactogen ◽  
Maximum Effect ◽  
Hepatic Glycogen ◽  
Response Curves ◽  
Glucose Incorporation

The interactions between ovine placental lactogen (oPL) and insulin in the regulation of fetal liver glycogen metabolism have been studied in cultured hepatocytes from fetal rats on day 20 of gestation. Both oPL (0.75–22.5 micrograms/ml) and insulin (0.01–1 microM) stimulated dose-dependent increases in [14C]glucose incorporation into glycogen. However, the dose-response curves for the two hormones were not parallel and the maximum effect of oPL was 3.4 times greater than that of insulin (P less than 0.001). The two hormones had synergistic effects on [14C]glucose incorporation at low concentrations and additive effects at maximum concentrations. Ovine growth hormone (oGH) also stimulated [14C]glucose incorporation into glycogen but with a potency only 12.3% that of oPL. Cycloheximide (20 microM) abolished the stimulation of [14C]glucose incorporation by insulin (1 microM), oPL (5 micrograms/ml), and oGH (100 micrograms/ml). Although the glycogenic actions of oPL and insulin may depend on new protein synthesis, the results of these studies suggest that these hormones stimulate glycogen synthesis in fetal liver by different mechanisms. Because the glycogenic actions of oPL are potentiated by insulin, these hormones may act in concert to promote hepatic glycogen storage in the fetus.

Hepatic Glycogen Synthesis in Adrenalectomized Rats After Short- and Longterm Stimulation by Dexamethasone Observed by Light and Electron Microscopic Radioautography

1985 ◽  
Vol 43 ◽  
pp. 554-555
Author(s):  
J.E. Michaels ◽  
S.A. Garfield ◽  
S.S. Smith ◽  
J.T. Hung ◽  
R.R. Cardell
Keyword(s):  
Glycogen Synthesis ◽  
Hepatic Glycogen ◽  
Short Term ◽  
Electron Microscopic ◽  
Short And Long Term ◽  
Routine Procedures ◽  
Electron Microscopic Radioautography ◽  
Fasted Rats ◽  
Adrenalectomized Rats

The effects on glycogen synthesis of short- and long-term stimulation with dexamethasone (DEX) were studied in adrenalectomized, overnight-fasted rats by light (LM) and electron microscopic (EM) radioautography (RAG). Rats were injected with DEX 3 hr (short-term) or 14 hr (long-term) prior to labeling by intravenous injection of 2 mCi 3H-galactose, a glycogen precursor. Liver was prepared for LM and EM RAG by routine procedures.Short-term rats were sacrificed 1, 6 and 12 hr after labeling. One hr after injection of label (Fig. 1) equal percentages (44%) of heavily (> 10 grains/100 μm2 hepatocyte cytoplasm) and lightly (<10 grains/100 μm2 cytoplasm) labeled hepatocytes were evident. Six hr after labeling, heavily labeled cells increased slightly as labeled and unlabeled glycogen became evident. The appearance of unlabeled glycogen was evidence that glycogen synthesis continued between 1 and 6 hr, as circulating label fell to a level below that necessary for radioautographic labeling to occur. Twelve hr after labeling (Fig. 2) the percentage of heavily labeled hepatocytes (31%) decreased to less than at one hour as unlabeled glycogen increased. These results indicated that although glycogen synthesis had continued, some loss of label had occurred.

The glucose-galactose paradox in neonatal murine hepatic glycogen synthesis

1989 ◽  
Vol 257 (5) ◽  
pp. E697-E703 ◽  
Author(s):  
C. Kunst ◽  
R. Kliegman ◽  
C. Trindade
Keyword(s):  
Blood Glucose ◽  
Glycogen Synthesis ◽  
Hepatic Glycogen ◽  
Glycemic Response ◽  
Preferential Utilization ◽  
Glucose Incorporation ◽  
Old Rats ◽  
Direct Incorporation ◽  
Glucose Recycling

In adults glucose incorporation to glycogen is indirect after recycling from lactate. In neonates galactose entry to glycogen exceeds that for glucose, but the pathway is unknown. The pathway of hexose incorporation to glycogen was studied in 5-7-day-old rats and 6-h-old rats injected intraperitoneally (IP) with either double-labeled [6-3H]glucose (nonrecycling), [U-14C]glucose (recycling), or [6-3H]glucose and [U-14C]galactose in saline. In another group of pups, 1 g/kg of glucose or galactose was administered in addition to tracers to determine glycemia and net glycogen synthesis between 15 and 180 min after injection. Blood glucose increased from 3.4 +/- 0.4 to 8.5 +/- 1.5 mM in 5-7-day-old pups in response to IP glucose; there was no glycemic response to galactose, although galactose levels increased from 0.5 to 6.3 mM at 15 min. Hepatic glycogen increased after IP glucose from 14 +/- 2 at 15 min to 30 +/- 3 at 120 min (P less than 0.01), whereas after IP galactose glycogen was 44 +/- 6 mumol/g at 120 min (P less than 0.05). After IP glucose, 3H and 14C disintegration per minute in glycogen increased slowly with 14C exceeding 3H at 120 and 180 min. In contrast IP [14C]galactose resulted in a much greater peak of 14C incorporation into glycogen. The ratio of 3H to 14C in glycogen relative to the injectate after IP glucose decreased from 0.69 +/- 0.12 to 0.36 +/- 0.03 (P less than 0.01) between 15 to 180 min, whereas the ratio after galactose was 0.20 +/- 0.007 to 0.15 +/- 0.02 at these times. The 6-h-old pups also demonstrated augmented incorporation of [14C]galactose in glycogen relative to [3H-14C]glucose. In contrast to 5-7-day-old pups there was no evidence of glucose recycling in 6-h-old pups. In conclusion galactose entry into glycogen exceeds that for glucose and is not dependent on recycling. Direct incorporation of galactose exceeds that for direct incorporation from [3H]glucose, suggesting a preferential utilization of galactose for neonatal glycogen synthesis.

scholarly journals Effects of Meal Fructose/Glucose Composition on Postprandial Glucose Appearance and Hepatic Glycogen Synthesis in Healthy Subjects

2021 ◽  
Vol 10 (4) ◽  
pp. 596
Author(s):  
Cristina Barosa ◽  
Rogério T. Ribeiro ◽  
Rita Andrade ◽  
João F. Raposo ◽  
John G. Jones
Keyword(s):  
Plasma Glucose ◽  
Healthy Subjects ◽  
Glycogen Synthesis ◽  
Krebs Cycle ◽  
Hepatic Glycogen ◽  
Indirect Pathway ◽  
Metabolic Complications ◽  
Glucose Ratio ◽  
Dietary Fructose ◽  
P Sources

Dietary fructose overshadows glucose in promoting metabolic complications. Intestinal fructose metabolism (IFM) protects against these effects in rodents, by favoring gluconeogenesis, but the extent of IFM in humans is not known. We therefore aimed to infer the extent of IFM by comparing the contribution of dietary fructose to systemic glucose and hepatic glycogen appearance postprandially. Twelve fasting healthy subjects ingested two protein meals in random order, one supplemented with 50 g 5/95 fructose/glucose (LF) and the other with 50 g 55/45 fructose/glucose (HF). Sources of postprandial plasma glucose appearance and hepatic glycogen synthesis were determined with deuterated water. Plasma glucose excursions, as well as pre- and post-meal insulin, c-peptide, and triglyceride levels were nearly identical for both meals. The total gluconeogenic contribution to plasma glucose appearance was significantly higher for HF versus LF (65 ± 2% vs. 34 ± 3%, p < 0.001). For HF, Krebs cycle anaplerosis accounted for two-thirds of total gluconeogenesis (43 ± 2%) with one-third from Triose-P sources (22 ± 1%). With LF, three-quarters of the total gluconeogenic contribution originated via Krebs cycle anaplerosis (26 ± 2%) with one-quarter from Triose-P sources (9 ± 2%). HF and LF gave similar direct and indirect pathway contributions to hepatic glycogen synthesis. Increasing the fructose/glucose ratio had significant effects on glucose appearance sources but no effects on hepatic glycogen synthesis sources, consistent with extensive IFM. The majority of fructose carbons were converted to glucose via the Krebs cycle.

scholarly journals Glycogen synthesis in the perfused liver of adrenalectomized rats

1976 ◽  
Vol 156 (3) ◽  
pp. 585-592 ◽  
Author(s):  
P D Whitton ◽  
D A Hems
Keyword(s):  
Intact Animal ◽  
Glycogen Synthesis ◽  
Hepatic Metabolism ◽  
Hepatic Glycogen ◽  
Perfused Liver ◽  
Short Term ◽  
Glycogen Accumulation ◽  
Glycogen Deposition ◽  
Adrenalectomized Rats

1. A total loss of capacity for net glycogen synthesis was observed in experiments with the perfused liver of starved adrenalectomized rats. 2. This lesion was corrected by insulin or cortisol in vivo (over 2-5h), but not by any agent tested in perfusion. 3. The activity of glycogen synthetase a, and its increase during perfusion, in the presence of glucose plus glucogenic substrates, were proportional to the rate of net glycogen accumulation. 4. This complete inherent loss of capacity for glycogen synthesis after adrenalectomy is greater than any defect in hepatic metabolism yet reported in this situation, and is not explicable by a decrease in the rate of gluconegenesis (which supports glycogen synthesis in the liver of starved rats). The short-term (2-5h) stimulatory effect of glucocorticoids in the intact animal, on hepatic glycogen deposition, may be mediated partly through insulin action, although neither insulin or cortisol appear to act directly on the liver to stimulate glycogen synthesis.

Use of deuterium labelled glucose in evaluating the pathway of hepatic glycogen synthesis

1989 ◽  
Vol 159 (2) ◽  
pp. 522-527 ◽  
Author(s):  
Michael N. Goodman ◽  
Lorianne K. Masuoka ◽  
Jeffrey S. deRopp ◽  
A.Daniel Jones
Keyword(s):  
Glycogen Synthesis ◽  
Hepatic Glycogen

Glucose: a direct or indirect precursor of hepatic glycogen synthesis in parenterally fed patients?

1989 ◽  
Vol 17 (5) ◽  
pp. 922-923
Author(s):  
RODERICK F. G. J. KING ◽  
DAVID ALEXANDER ◽  
MICHAEL J. McMAHON
Keyword(s):  
Glycogen Synthesis ◽  
Hepatic Glycogen

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.

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