Adrenal, Hypophyseal and Pancreatic Hormones in the Liver Glycogen Response to Low Atmospheric Pressure

1957 ◽  
Vol 191 (2) ◽  
pp. 342-344
Author(s):  
L. L. Langley ◽  
C. H. Gunthorpe
Keyword(s):  
Atmospheric Pressure ◽  
Liver Glycogen ◽  
Diabetic Rats ◽  
Pancreatic Hormones ◽  
Minimal Dose ◽  
Significant Difference ◽  
Hypophysectomized Rats ◽  
Low Atmospheric Pressure ◽  
Glycogen Deposition ◽  
Adrenalectomized Rats

The administration of 3 cc of adrenocortical extract (Upjohn) to adrenalectomized rats fasted at sea-level fails to cause liver glycogen deposition. Such animals under low atmospheric pressure accumulate about 1% liver glycogen. Adrenalectomized-hypophysectomized rats maintained on a minimal dose of hypophyseal extract, given 3 cc of adrenocortical extract and stressed do not deposit liver glycogen. These results suggest that the hypophyseal hormones function not only to control the adrenal cortices under these conditions, but also may contribute directly to the observed carbohydrate alterations. When larger doses of hypophyseal hormones are used there is a significant difference in liver glycogen between the stressed and nonstressed groups indicating the possible implication of still another agent, perhaps insulin, since alloxan diabetic rats do not accumulate liver glycogen in response to low atmospheric pressure.

Carbohydrate metabolism of mice exposed to simulated changes in gravity

1964 ◽  
Vol 207 (2) ◽  
pp. 411-414 ◽  
Author(s):  
Jiro Oyama ◽  
William T. Platt
Keyword(s):  
Blood Glucose ◽  
Carbohydrate Metabolism ◽  
Exposure Time ◽  
Liver Glycogen ◽  
Critical Function ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Significant Difference ◽  
Glycogen Deposition ◽  
Adrenal Corticosterone

Unrestrained mice were centrifuged for varying periods ranging from 0.5 to 10 hr at 2.5, 5, and 10 x gravity. Liver glycogen and blood glucose levels increased significantly depending on the g load and exposure time. Adrenalectomy completely abolished the glycogen deposition response. The glycogen response was a critical function of the age of mice; unweaned mice did not respond. Blood corticosterone increased significantly prior to the deposition of glycogen. Centrifuged fed mice deposited three times the amount of glycogen of fasted mice. There was no significant difference in the amount of glycogen deposited in centrifuged mice previously starved for 1, 2, or 3 days. It is concluded that the increased glycogen deposited following centrifugation is effected by an increased elaboration of adrenal corticosterone.

THE EFFECT OF INSULIN ON THE DISTRIBUTION OF GLUCOSE BETWEEN THE BLOOD PLASMA AND THE LIVER IN ALLOXAN-DIABETIC AND ADRENALECTOMIZED RATS

1963 ◽  
Vol 41 (1) ◽  
pp. 2431-2439 ◽  
Author(s):  
G. Hetenyi Jr. ◽  
F. K. Kopstick ◽  
L. J. Retelstorf
Keyword(s):  
Cell Membrane ◽  
Blood Plasma ◽  
Liver Cell ◽  
Liver Glycogen ◽  
Liver Cells ◽  
Diabetic Rats ◽  
Hepatic Cell ◽  
Very High ◽  
Adrenalectomized Rats

In diabetic rats the concentration of glucose in the liver was less than in the plasma. The relative accumulation of glucose in the liver cell after the injection of insulin was also found to be significantly less in previously untreated diabetic than in normal rats. Pretreatment with insulin restored the response to normal. Experiments with labeled glucose indicated that the rate at which glucose is carried through the hepatic cell membrane is very high compared to the rate at which glucose is being formed in the liver cells in diabetic rats. The relatively small amount of glucose accumulating after insulin in livers of diabetic rats originates from the plasma. In adrenalectomized rats which have very little liver glycogen, the relative accumulation of glucose in liver cells, following the injection of insulin, was less than that in normals. These experiments indicate that in normal rats a large part of the glucose retained in the liver after the injection of insulin originates from non-labeled endogenous hepatic sources, presumably glycogen.

THE EFFECT OF INSULIN ON THE DISTRIBUTION OF GLUCOSE BETWEEN THE BLOOD PLASMA AND THE LIVER IN ALLOXAN-DIABETIC AND ADRENALECTOMIZED RATS

1963 ◽  
Vol 41 (12) ◽  
pp. 2431-2439 ◽  
Author(s):  
G. Hetenyi Jr. ◽  
F. K. Kopstick ◽  
L. J. Retelstorf
Keyword(s):  
Cell Membrane ◽  
Blood Plasma ◽  
Liver Cell ◽  
Liver Glycogen ◽  
Liver Cells ◽  
Diabetic Rats ◽  
Hepatic Cell ◽  
Very High ◽  
Adrenalectomized Rats

In diabetic rats the concentration of glucose in the liver was less than in the plasma. The relative accumulation of glucose in the liver cell after the injection of insulin was also found to be significantly less in previously untreated diabetic than in normal rats. Pretreatment with insulin restored the response to normal. Experiments with labeled glucose indicated that the rate at which glucose is carried through the hepatic cell membrane is very high compared to the rate at which glucose is being formed in the liver cells in diabetic rats. The relatively small amount of glucose accumulating after insulin in livers of diabetic rats originates from the plasma. In adrenalectomized rats which have very little liver glycogen, the relative accumulation of glucose in liver cells, following the injection of insulin, was less than that in normals. These experiments indicate that in normal rats a large part of the glucose retained in the liver after the injection of insulin originates from non-labeled endogenous hepatic sources, presumably glycogen.

CARBOHYDRATE METABOLISM IN THE ISOLATED DIAPHRAGM OF ADRENALECTOMIZED RATS AS AFFECTED BY EXPOSURE TO ADRENALINE IN VIVO AND IN VITRO

1960 ◽  
Vol XXXV (IV) ◽  
pp. 551-559 ◽  
Author(s):  
P. R. Bouman ◽  
W. Dermer
Keyword(s):  
Glucose Uptake ◽  
Carbohydrate Metabolism ◽  
Second Stage ◽  
Initial Stage ◽  
Significant Difference ◽  
Glycogen Deposition ◽  
Glucose Assimilation ◽  
Adrenalectomized Rats

ABSTRACT Hemidiaphragms of adrenalectomized rats which had been nembutalized prior to decapitation, were incubated under aerobic conditions and the glucose uptake and glycogen deposition were measured. Addition of adrenaline in vitro induced marked glycogen degradation and a relative small decrease in glucose uptake. Pretreatment with adrenaline in vivo, however, appeared to increase glycogen deposition in vitro while glucose uptake increased to an equivalent extent. This effect was attributed to the low initial glycogen content induced by this treatment. Double exposure to adrenaline by administering this substance both in vivo and in vitro, neither affected glucose uptake nor glycogen deposition as compared with untreated control diaphragms. However, there was a significant difference in the glycogen level at which both groups metabolized, this level being extremely low in diaphragms doubly exposed to adrenaline. It was concluded that the action of adrenaline on muscular carbohydrate metabolism consists basically of three different stages: 1. A temporary initial stage during which glucose assimilation is inhibited secondarily to glycogen degradation. 2. A second stage, in which the occurrence of inhibition of glucose assimilation is determined by the fact whether in the corresponding control tissue the glucose uptake is raised in favour of glycogen deposition. 3. A stage of recovery induced by discontinuing the exposure to adrenaline. This stage is characterized by glycogen deposition and an equivalent rise in glucose assimilation.

scholarly journals Influence of hormones on the nicotinamide nucleotide coenzymes of adipose tissue

1967 ◽  
Vol 105 (3) ◽  
pp. 1013-1018 ◽  
Author(s):  
Patricia McLean ◽  
A. L. Greenbaum ◽  
J. Brown ◽  
K. R. Greenslade
Keyword(s):  
Growth Hormone ◽  
Adipose Tissue ◽  
Lipid Synthesis ◽  
Total Content ◽  
Diabetic Rats ◽  
Tissue Protein ◽  
Significant Difference ◽  
Hypophysectomized Rats ◽  
Reduced Forms ◽  
Fat Pads

The concentrations of the oxidized and reduced forms of the nicotinamide nucleotides were measured in the epididymal fat pads of normal, alloxan-diabetic and hypophysectomized rats. In both alloxan-diabetic rats and hypophysectomized rats the weight of the adipose tissue fell, as did the total content of NADH and NADPH; in addition, NAD+ was decreased in the alloxan-diabetic group. Of these changes the most marked was in NADPH and this was the only significant difference when the results were expressed as nicotinamide nucleotides/mg. of tissue protein. The concentration of NADPH in the hypophysectomized rats was not altered by treatment with growth hormone but was restored to normal by treatment with thyroxine. These results are discussed in relation to the known effect of these hormonal conditions on lipid synthesis in adipose tissue.

Factors Determining the Liver Glycogenating Action of Orinase

1958 ◽  
Vol 192 (3) ◽  
pp. 514-516 ◽  
Author(s):  
W. L. Henry ◽  
John H. Kim ◽  
Alice S. Hall
Keyword(s):  
Beta Cell ◽  
Liver Glycogen ◽  
Diabetic Animal ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Protamine Zinc Insulin ◽  
Series Of Experiments ◽  
Adrenalectomized Rats

The liver glycogenating action of Orinase was studied in normal, adrenalectomized and alloxan diabetic rats. The adrenalectomized rats were studied in three groups, salt maintained, cortisone maintained and cortisone plus adrenaline maintained. The alloxan diabetic rats were studied in two groups, protamine zinc insulin (P.Z.I.) maintained and uncontrolled. Of the adrenalectomized rats only those maintained on cortisone plus adrenaline responded to Orinase administration with increased liver glycogen. The alloxan diabetic animal maintained on P.Z.I. presented increased liver glycogen after Orinase administration but the untreated alloxan diabetic rat did not. This series of experiments indicated that the liver glycogenating effect seen during Orinase administration requires the participation of adrenomedullary, adrenocortical and beta cell hormones.

scholarly journals Chronic overeating impairs hepatic glucose uptake and disposition

2015 ◽  
Vol 308 (10) ◽  
pp. E860-E867 ◽  
Author(s):  
Katie C. Coate ◽  
Guillaume Kraft ◽  
Masakazu Shiota ◽  
Marta S. Smith ◽  
Ben Farmer ◽  
...  
Keyword(s):  
Glucose Uptake ◽  
Glycogen Synthase ◽  
Glycogen Synthesis ◽  
Liver Glycogen ◽  
Hepatic Glucose Metabolism ◽  
Significant Difference ◽  
Hepatic Glucose ◽  
Glycogen Deposition ◽  
Hepatic Glucose Uptake ◽  
Glycogen Phosphorylase Activity

Dogs consuming a hypercaloric high-fat and -fructose diet (52 and 17% of total energy, respectively) or a diet high in either fructose or fat for 4 wk exhibited blunted net hepatic glucose uptake (NHGU) and glycogen deposition in response to hyperinsulinemia, hyperglycemia, and portal glucose delivery. The effect of a hypercaloric diet containing neither fructose nor excessive fat has not been examined. Dogs with an initial weight of ≈25 kg consumed a chow and meat diet (31% protein, 44% carbohydrate, and 26% fat) in weight-maintaining (CTR; n = 6) or excessive (Hkcal; n = 7) amounts for 4 wk (cumulative weight gain 0.0 ± 0.3 and 1.5 ± 0.5 kg, respectively, P < 0.05). They then underwent clamp studies with infusions of somatostatin and intraportal insulin (4× basal) and glucagon (basal). The hepatic glucose load was doubled with peripheral (Pe) glucose infusion for 90 min (P1) and intraportal glucose at 4 mg·kg−1·min−1 plus Pe glucose for the final 90 min (P2). NHGU was blunted ( P < 0.05) in Hkcal during both periods (mg·kg−1·min−1; P1: 1.7 ± 0.2 vs. 0.3 ± 0.4; P2: 3.6 ± 0.3 vs. 2.3 ± 0.4, CTR vs. Hkcal, respectively). Terminal hepatic glucokinase catalytic activity was reduced nearly 50% in Hkcal vs. CTR ( P < 0.05), although glucokinase protein did not differ between groups. In Hkcal vs. CTR, liver glycogen was reduced 27% ( P < 0.05), with a 91% increase in glycogen phosphorylase activity ( P < 0.05) but no significant difference in glycogen synthase activity. Thus, Hkcal impaired NHGU and glycogen synthesis compared with CTR, indicating that excessive energy intake, even if the diet is balanced and nutritious, negatively impacts hepatic glucose metabolism.

Carbohydrate metabolism in rats with chronic uremia

1960 ◽  
Vol 198 (4) ◽  
pp. 797-799 ◽  
Author(s):  
Nancy G. Boucot ◽  
Elizabeth K. Nurser ◽  
John P. Merrill
Keyword(s):  
Carbohydrate Metabolism ◽  
Liver Glycogen ◽  
Glucose Absorption ◽  
Hepatic Glycogen ◽  
Glucose Content ◽  
Chronic Uremia ◽  
Significant Difference ◽  
Uremic Syndrome ◽  
Glycogen Deposition

In order to evaluate the effects of the chronic uremic syndrome upon some aspects of carbohydrate metabolism in vivo, determinations of gastric and intestinal glucose absorption, and of hepatic glycogen deposition were made in 39 chronically uremic rats and in 49 litter-mate controls. A surgical method for producing chronic uremia was developed. Rats fasted for 24 hours were given a glucose gavage of standard concentration. Three hours later residual gastric and intestinal glucose content and liver glycogen content were determined. No statistically significant difference between the two groups was found in either glucose absorption from the gastrointestinal tract or in glycogen deposition.

Spirometra mansonoides: effects of plerocercoid infection on glycogen deposition in rats

1982 ◽  
Vol 56 (4) ◽  
pp. 315-322 ◽  
Author(s):  
C. K. Phares ◽  
Nguyen Duy Ai
Keyword(s):  
Skeletal Muscle ◽  
Growth Hormone ◽  
Glycogen Phosphorylase ◽  
Liver Glycogen ◽  
Light Period ◽  
Glycogen Concentration ◽  
Hypophysectomized Rats ◽  
Glycogen Deposition ◽  
Intact Rats

ABSTRACTThe effects of infection with plerocercoids of Spirometra mansonoides on tissue glycogen deposition of rats was determined. Hypophysectomized rats infected for two days had higher liver glycogen concentrations than controls and this effect was greatest after one week. Elevated liver glycogen associated with plerocercoid infection was observed in fed animals both at the beginning and at the end of the light period as well as after an overnight fast. Glycogen phosphorylase (1,4αD glucan: orthophosphate α glucosyltransferase EC 2.4.1.1.) was inhibited but glucose-6-phosphatase (EC 3.1.3.9) was unaffected in the livers of infected hypophysectomized rats. While this effect is similar to actions of both growth hormone and insulin, plerocercoid infection had no influence on glycogen of cardiac or skeletal muscle at any time. Plerocercoid infection had no effect on the glycogen concentration of any tissue of intact rats.

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