Modification of Carbohydrate Metabolism and Liver Vitellogenic Function in Brook Trout (Salvelinus fontinalis) by Exposure to Low pH

1987 ◽  
Vol 44 (3) ◽  
pp. 630-635 ◽  
Author(s):  
W. H. Tam ◽  
L. Birkett ◽  
R. Makaran ◽  
P. D. Payson ◽  
D. K. Whitney ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Brook Trout ◽  
Salvelinus Fontinalis ◽  
Acid Stress ◽  
Somatic Growth ◽  
Liver Weight ◽  
Liver Glycogen ◽  
Control Fish ◽  
Glucose Levels ◽  
Blood Glucose Levels

Brook trout (Salvelinus fontinalis), 1+ yr old, were exposed to pH 4.48 from February to December. Compared with control fish maintained at pH 7.34, acid-stressed fish generally had elevated blood glucose levels. Plasma cortisol concentration, measured only in males, was significantly increased in the acid-treated trout up to July. Although somatic growth decreased by about 30% by the end of the experiment, peritoneal fat was unchanged. During the reproductive season, female plasma levels of oestrogen and vitellogenin were the same at both pH levels. When immature fish were implanted with oestradiol-17β and then maintained for 21 d either in pH 7.34 (control) or 4.48, acid-treated fish again showed increased blood glucose levels. Liver weight increased at both pH levels, but liver glycogen was depleted and plasma vitellogenin was significantly increased by exogenous oesterogen only in control fish. It is postulated that before acclimation occurs, acid stress increases cortisol secretion, diverts nutrients normally used for growth to maintain a high blood sugar level, and affects the liver's ability to metabolize carbohydrates and synthesize vitellogenin.

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.

VARIATIONS IN GLUCAGON RESPONSE AMONG JUVENILE DIABETICS

PEDIATRICS ◽  
1963 ◽  
Vol 32 (6) ◽  
pp. 1002-1006
Author(s):  
Donnell D. Etzwiler
Keyword(s):  
Blood Glucose ◽  
Good Control ◽  
Liver Glycogen ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Juvenile Diabetics ◽  
Glycogen Stores ◽  
Initial Blood ◽  
Hyperglycemic Effect

Glucagon or a placebo preparation was administered to 65 juvenile diabetics on 74 separate occasions. When the initial blood glucose of these children showed them to be in reasonably good control, glucagon produced a hyperglycemic effect. However, when the blood glucose levels were markedly elevated, the effect of glucagon was less predictable. The depletion of liver glycogen stores and the possible effect of contaminating insulin in glucagon preparations are discussed.

Endurance training attenuates stress hormone responses to exercise in fasted rats

1982 ◽  
Vol 243 (1) ◽  
pp. R179-R184 ◽  
Author(s):  
W. W. Winder ◽  
M. A. Beattie ◽  
R. T. Holman
Keyword(s):  
Blood Glucose ◽  
Plasma Concentrations ◽  
Liver Glycogen ◽  
Stress Hormone ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Fasted State ◽  
Hormone Responses ◽  
Exercise Muscle ◽  
Fasted Rats

Endurance exercise training produces major adaptations in hormonal and metabolic responses to exercise. This study was designed to determine whether the differences in hormone response persist in the fasted condition when liver glycogen is depleted. Rats were run on a motor-driven rodent treadmill 5 days/wk for periods up to 2 h/day for 10 wk. Trained and nontrained rats were then fasted 24 h and were run for periods ranging from 0- to 60 min. At the end of 60 min of exercise muscle glycogen was higher in trained rats (2.9 +/- 0.3 vs. 1.1 +/- 0.1 mg/g). Blood glucose was maintained at higher levels in trained rats throughout the course of the exercise (3.2 +/- 0.1 vs. 2.3 +/- 0.1 mM after 60 min). Plasma concentrations of glucagon and epinephrine increased in both groups during the exercise but were significantly lower in trained animals. Differences between trained and nontrained animals in stress hormone responses to exercise persist in the fasted state and appear to be a consequence of the capacity of trained animals to maintain higher blood glucose levels.

Liver glycogen content decreases during meals in rats

1982 ◽  
Vol 243 (3) ◽  
pp. R450-R453
Author(s):  
W. Langhans ◽  
N. Geary ◽  
E. Scharrer
Keyword(s):  
Blood Glucose ◽  
Glycogen Content ◽  
Liver Glycogen ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Liver Glycogen Content ◽  
Ad Libitum ◽  
Portal Veins ◽  
Hepatic Portal

The effects of feeding on liver glycogen content and blood glucose in the hepatic and hepatic portal veins were investigated in rats. Liver glycogen content decreased about 25% during meals both in rats refed after 12 h food deprivation (23 +/- 1 to 17 +/- 1 mg glycogen/g liver) and in ad libitum-fed rats taking fully spontaneous meals (44 +/- 2 to 32 +/- 2 mg/g). Liver glycogen began to increase within 30 min after meals in ad libitum-fed rats. Hepatic vein blood glucose levels at meal onset (118 +/- 4 mg/dl in the food-deprived rats, 127 +/- 4 in ad libitum-fed rats) and at meal end (155 +/- 3 and 166 +/- 5 mg/dl, respectively) were similar in the two groups. Portal vein blood glucose increased during meals in the previously food-deprived rats (83 +/- 4 to 116 +/- 6 mg/dl) but not in the ad libitum-fed rats (127 +/- 5 to 132 +/- 3 mg/dl). Mechanisms that may elicit prandial glycogenolysis and the possible role of this effect in the production of meal ending satiety are discussed.

scholarly journals Effect of reduced dietary zinc intake on carbohydrate and Zn metabolism in the genetically diabetic mouse (C57BL/KsJ db+/db+)

1988 ◽  
Vol 60 (3) ◽  
pp. 499-507 ◽  
Author(s):  
Susan Southon ◽  
Z. Kechrid ◽  
A. J. A. Wright ◽  
Susan J. Fairweather-Tait
Keyword(s):  
Blood Glucose ◽  
Control Diet ◽  
Fasting Blood Glucose ◽  
Liver Glycogen ◽  
Diabetic Mouse ◽  
Whole Body ◽  
Diabetic Mice ◽  
Control Groups ◽  
Glucose Levels ◽  
Blood Glucose Levels

1. Male, 4–5-week-old, genetically diabetic mice (C57BL/KsJ db/db) and non-diabetic heterozygote litter-mates (C57BL/KsJ db/+)were fed on a diet containing 1 mg zinc/kg (low-Zn groups) or 54 mg Zn/kg (control groups) for 27 d. Food intakes and body-weight gain were recorded regularly. On day 28, after an overnight fast, animals were killed and blood glucose and insulin concentrations, liver glycogen, and femur and pancreatic Zn concentrations were determined.2. The consumption of the low-Zn diet had only a minimal effect on the Zn status of the mice as indicated by growth rate, food intake and femur and pancreatic Zn concentrations. In fact, diabetic mice fed on the low-Zn diet had a higher total food intake than those fed on the control diet. The low-Zn diabetic mice had higher fasting blood glucose and liver glycogen levels than their control counterparts. Fasting blood insulin concentration was unaffected by dietary regimen.3. A second experiment was performed in which the rate of loss of 65Zn, injected subcutaneously, was measured by whole-body counting in the two mouse genotypes over a 28 d period, from 4 to 5 weeks of age. The influence of feeding low-Zn or control diets was also examined. At the end of the study femur and pancreatic Zn and non-fasting blood glucose levels were determined.4. All mice fed on the low-Zn diet showed a marked reduction in whole-body 65Zn loss compared with those animals fed on the control diet. In the low-Zn groups, the loss of 65Zn from the diabetic mice was significantly greater than that from heterozygote mice. This difference was not observed in the control groups. Blood glucose levels were elevated in the low-Zn groups. Possible reasons for these observations are discussed.5. The present study demonstrates an adverse effect of reduced dietary Zn intake on glucose utilization in the genetically diabetic mouse, which occurred before any significant tissue Zn depletion became apparent.

EFFECTS OF PROGESTERONE, OESTRADIOL AND/OR CLOMIPHENE ON LIVER GLYCOGEN AND BLOOD GLUCOSE IN INTACT AND ADRENALECTOMISED RATS DURING DELAYED IMPLANTATION

1974 ◽  
Vol 76 (4) ◽  
pp. 678-688
Author(s):  
M. S. Sankaran ◽  
M. R. N. Prasad
Keyword(s):  
Blood Glucose ◽  
Clomiphene Citrate ◽  
Insulin Level ◽  
Liver Glycogen ◽  
Hepatic Glycogen ◽  
Prolonged Administration ◽  
Glucose Levels ◽  
Delayed Implantation ◽  
Blood Glucose Levels ◽  
Induced Changes

ABSTRACT Prolonged administration of progesterone alone caused significant changes in liver glycogen. Oestradiol-17β increased the liver glycogen 18 hours after the treatment. A single administration of clomiphene citrate on day 9 post-coitum (pc) inhibited the oestradiol or progesterone induced increase in hepatic glycogen. Bilateral adrenalectomy on day 3 pc abolished the changes in liver glycogen induced by progesterone, oestradiol and/or clomiphene. Administration of progesterone, oestradiol or clomiphene caused a decrease in blood glucose levels in rats during delayed implantation. Although the effects of progesterone and oestradiol on blood glucose levels were abolished by adrenalectomy, clomiphene induced changes persisted in the adrenalectomised rats. It is concluded that progesterone, oestradiol and/or clomiphene induced changes in liver glycogen are mediated through the adrenal glands. Changes in the blood glucose levels are discussed in relation to increased insulin level in the blood and also in relation to the increased glucocorticoid secretion following various treatments.

scholarly journals CREBH Maintains Circadian Glucose Homeostasis by Regulating Hepatic Glycogenolysis and Gluconeogenesis

2017 ◽  
Vol 37 (14) ◽  
Author(s):  
Hyunbae Kim ◽  
Ze Zheng ◽  
Paul D. Walker ◽  
Gregory Kapatos ◽  
Kezhong Zhang
Keyword(s):  
Blood Glucose ◽  
Glucose Homeostasis ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Liver Glycogen ◽  
Glycogen Storage ◽  
Hepatic Glycogen ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Glucose Levels ◽  
Blood Glucose Levels

ABSTRACT Cyclic AMP-responsive element binding protein, hepatocyte specific (CREBH), is a liver-enriched, endoplasmic reticulum-tethered transcription factor known to regulate the hepatic acute-phase response and lipid homeostasis. In this study, we demonstrate that CREBH functions as a circadian transcriptional regulator that plays major roles in maintaining glucose homeostasis. The proteolytic cleavage and posttranslational acetylation modification of CREBH are regulated by the circadian clock. Functionally, CREBH is required in order to maintain circadian homeostasis of hepatic glycogen storage and blood glucose levels. CREBH regulates the rhythmic expression of the genes encoding the rate-limiting enzymes for glycogenolysis and gluconeogenesis, including liver glycogen phosphorylase (PYGL), phosphoenolpyruvate carboxykinase 1 (PCK1), and the glucose-6-phosphatase catalytic subunit (G6PC). CREBH interacts with peroxisome proliferator-activated receptor α (PPARα) to synergize its transcriptional activities in hepatic gluconeogenesis. The acetylation of CREBH at lysine residue 294 controls CREBH-PPARα interaction and synergy in regulating hepatic glucose metabolism in mice. CREBH deficiency leads to reduced blood glucose levels but increases hepatic glycogen levels during the daytime or upon fasting. In summary, our studies revealed that CREBH functions as a key metabolic regulator that controls glucose homeostasis across the circadian cycle or under metabolic stress.

CHANGES IN BLOOD GLUCOSE AND LIVER CARBOHYDRATE AFTER INTRAUTERINE INJECTION OF GLUCAGON INTO FOETAL RATS

1969 ◽  
Vol 45 (3) ◽  
pp. 367-374 ◽  
Author(s):  
D. J. S. HUNTER
Keyword(s):  
Blood Glucose ◽  
Liver Glycogen ◽  
Maternal Blood ◽  
Uterine Wall ◽  
Control Group ◽  
Hepatic Glycogen ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Carbohydrate Levels ◽  
Foetal Blood

SUMMARY Maternal blood glucose, foetal blood glucose and liver carbohydrate levels were estimated after foetuses were injected with glucagon through the uterine wall on days 19½, 20½ and 21½ of gestation in the rat. Glucagon had a hyperglycaemic effect in the foetus on all the days studied but the response was greater and more rapid on day 21½ of gestation. Glucagon was shown to decrease liver glycogen on day 20½ and 21½ but again the response was more rapid and more pronounced on day 21½. The normal levels of foetal liver glycogen were similar to those previously found but the normal foetal blood glucose values are lower than previous results. Decrease in liver glycogen observed in the control group of foetuses on day 21½ of gestation together with a loss in foeto-maternal blood glucose relationship on that day of gestation suggest that on day 21½ the foetal rat develops the ability to mobilize hepatic glycogen and thereby to alter its blood glucose level independently from the mother. The significance of the low blood glucose levels found in the foetus is discussed.

Radioautographic Analysis of the Intralobular and Intracellular Distribution of Newly Formed Hepatic Glycogen After Injection of 3H-Galactose

1982 ◽  
Vol 40 ◽  
pp. 164-165
Author(s):  
J. E. Michaels ◽  
J. T. Hung ◽  
R. R. Cardell
Keyword(s):  
Blood Glucose ◽  
Blood Sugar ◽  
Liver Glycogen ◽  
Intracellular Distribution ◽  
Hepatic Glycogen ◽  
Glucose Levels ◽  
Glucocorticoid Hormone ◽  
Blood Glucose Levels ◽  
Overnight Fasting ◽  
Sugar Levels

In normal animals glycogen levels in the liver are closely related to blood sugar levels. High levels of glucose in the blood stimulate uptake of glucose by liver hepatocytes and synthesis of glycogen whereas low blood glucose levels result in breakdown of glycogen and release of glucose into the blood. After adrenalectomy and overnight fasting, liver glycogen levels in the rat are reduced to about 0.03%. The adrenalectomized rat is easily stimulated to form new glycogen by injection of a glucocorticoid hormone such as dexamethasone (DEX).

Effect of hepatic vagotomy on hormonal response to exercise in gluconeogenesis-inhibited rats

1991 ◽  
Vol 260 (1) ◽  
pp. R67-R72 ◽  
Author(s):  
S. Cardin ◽  
J. M. Lavoie ◽  
F. Trabelsi
Keyword(s):  
Blood Glucose ◽  
Vagus Nerve ◽  
Liver Glycogen ◽  
Afferent Pathway ◽  
Hormonal Response ◽  
Experimental Conditions ◽  
Hormonal Responses ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Response To Exercise

The liver, through the afferent pathway of the hepatic vagus nerve, has been reported to influence the hormonal response to exercise in adrenodemedullated rats. The present investigation was designed to evaluate the role played by gluconeogenesis in this hepatic influence. To this end, we studied the effects of a selective hepatic vagotomy on the hormonal response to a 30-min treadmill run (26 m/min, 0% grade) in adrenodemedullated rats injected with 3-mercaptopicolinic acid, a gluconeogenic inhibitor. Hepatic vagotomy was associated with small but significant higher (P less than 0.05) elevations of peripheral blood glucose levels at rest and after exercise. No significant differences were observed between hepatic-vagotomized and sham-operated rats in either resting or exercising levels of liver glycogen, portal glucose, portal and peripheral insulin and glucagon, and peripheral epinephrine and norepinephrine. All hormonal responses, with the exception of epinephrine, were either decreased or increased similarly in the two experimental conditions after exercise. These data indicate that contrary to what has been reported in rats with an intact capacity for gluconeogenesis, hepatic-vagotomized and sham-operated rats with an inhibited gluconeogenesis had similar hormonal responses to exercise. It is concluded that gluconeogenesis plays a role in the afferent neural influence exerted by the liver via the hepatic vagus nerve in the regulation of hormonal response to exercise.

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