Paternal eNOS Deficiency Affects Glucose Homeostasis and Liver Glycogen Content in Male Offspring Without Inheritance of eNOS Deficiency Itself

2021 ◽  
Author(s):  
Berthold Hocher ◽  
Yong-Ping Lu ◽  
Christoph Reichetzeder ◽  
Xiaoli Zhang ◽  
Oleg Tsuprykov ◽  
...  
Keyword(s):  
Glucose Homeostasis ◽  
Glycogen Content ◽  
Liver Glycogen ◽  
Male Offspring ◽  
Liver Glycogen Content

Hypothalamic HSP10 Impacts Mitochondrial Dynamics, Insulin Signaling, and Liver Glycogen Content

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 1801-P
Author(s):  
KRISTINA WARDELMANN ◽  
JOSÉ PEDRO CASTRO ◽  
MICHAELA RATH ◽  
JÜRGEN WEIß ◽  
ANNETTE SCHUERMANN ◽  
...  
Keyword(s):  
Insulin Signaling ◽  
Glycogen Content ◽  
Mitochondrial Dynamics ◽  
Liver Glycogen ◽  
Liver Glycogen Content

BIOCHEMICAL STUDIES ON SOCKEYE SALMON DURING SPAWNING MIGRATION: XII. LIVER GLYCOGEN

1960 ◽  
Vol 38 (1) ◽  
pp. 553-558 ◽  
Author(s):  
Violet M. Chang ◽  
D. R. Idler
Keyword(s):  
Sex Differences ◽  
Sockeye Salmon ◽  
Glycogen Content ◽  
Steroid Hormone ◽  
Liver Glycogen ◽  
Spawning Migration ◽  
Energy Expenditures ◽  
Liver Glycogen Content ◽  
Biochemical Studies ◽  
River Migration

Liver glycogen levels were determined for a pure stock of sockeye salmon (Oncorhynchus nerka) taken at three locations during spawning migration. The liver glycogen content of the male was found to be consistently greater than that of the female throughout the entire river migration. In both sexes liver glycogen decreased during the earlier phase of migration, but increased during the later stage so that the levels at the spawning grounds were approximately twice those at the mouth of the river. The changes which occur are discussed in relation to sex differences, energy expenditures, and plasma steroid hormone levels.

Liver glycogen-induced enhancements in hypoglycemic counterregulation require neuroglucopenia.

2021 ◽  
Author(s):  
Shana O Warner ◽  
Abby M Wadian ◽  
Marta S. Smith ◽  
Ben Farmer ◽  
Yufei Dai ◽  
...  
Keyword(s):  
Glycogen Content ◽  
Hormone Secretion ◽  
Control Period ◽  
Liver Glycogen ◽  
Saline Infusion ◽  
Glucose Levels ◽  
Liver Glycogen Content ◽  
Patients With Diabetes ◽  
Arterial Plasma ◽  
The Brain

Iatrogenic hypoglycemia is a prominent barrier to achieving optimal glycemic control in patients with diabetes, in part due to dampened counterregulatory hormone responses. It has been demonstrated that elevated liver glycogen content can enhance these hormonal responses through signaling to the brain via afferent nerves, but the role that hypoglycemia in the brain plays in this liver glycogen effect remains unclear. During the first 4hrs of each study, the liver glycogen content of dogs was increased by using an intraportal infusion of fructose to stimulate hepatic glucose uptake (HG; n=13), or glycogen was maintained near fasting levels with a saline infusion (NG; n=6). After a 2hr control period, during which the fructose/saline infusion was discontinued, insulin was infused intravenously for an additional 2hrs to bring about systemic hypoglycemia in all animals, whereas brain euglycemia was maintained in a subset of the HG group by infusing glucose bilaterally into the carotid and vertebral arteries (HG-HeadEu; n=7). Liver glycogen content was markedly elevated in the two HG groups (43±4, 73±3 and 75±7 mg/g in NG, HG and HG-HeadEu, respectively). During the hypoglycemic period, arterial plasma glucose levels were indistinguishable between groups (53±2, 52±1 and 51±1 mg/dL, respectively), but jugular vein glucose levels were kept euglycemic (88±5 mg/dL) only in the HG-HeadEu group. Glucagon and epinephrine responses to hypoglycemia were higher in HG compared to NG, whereas despite the increase in liver glycogen, neither increased above basal in HG-HeadEu. These data demonstrate that the enhanced counterregulatory hormone secretion that accompanies increased liver glycogen content requires hypoglycemia in the brain.

Influence de la thiourée sur la charge en glycogéne du foie de l'embryon de poulet

Development ◽  
1971 ◽  
Vol 25 (3) ◽  
pp. 377-384
Author(s):  
Nicole Daugéras
Keyword(s):  
Chick Embryo ◽  
Glycogen Content ◽  
Antithyroid Drug ◽  
Liver Glycogen ◽  
Thyroid Activity ◽  
Glycogen Level ◽  
Glycogen Concentration ◽  
Liver Glycogen Content ◽  
Thyroid Glands ◽  
Embryo Liver

Influence of thiourea on the glycogen content of the liver of the chick embryo In the developing chick embryo, liver glycogen appears on the sixth day of incubation. The glycogen content increases from the sixth day, but decreases on the twelfth day before increasing again. This decrease on day 12 might be related to the onset of thyroid activity, which would be responsible for an increased rate of utilization of the substrates. An antithyroid drug, thiourea, has been injected on day 6·0. The liver glycogen concentration of the thiourea-treated chick embryos was determined from the tenth to the fifteenth days and compared with that of the control embryos. (i) On days 11 and 12 the liver glycogen concentration of the injected embryos is higher than that of the controls. (ii) On day 13 the liver glycogen level of treated embryos decreases; this decrease might be correlated with possible functional activity of the thyroid glands if their biosynthesis is no longer inhibited by the thiourea injection or with thyroid hormones possibly coming from the yolk. (iii) On days 14 and 15 no difference is observed between the liver glycogen content of the thiourea-treated embryos and that of the controls.

Effect of Corn Oil on Liver Glycogen Content and Blood Glucose-6-phosphatase Dehydrogenase in Toads Treated with DMBA

1999 ◽  
Vol 3 (1) ◽  
pp. 31-34
Author(s):  
N.E. Abdelmeguid . ◽  
I. A. Sadek . ◽  
J. M. Sorour . ◽  
A. A. Attia .
Keyword(s):  
Blood Glucose ◽  
Glycogen Content ◽  
Corn Oil ◽  
Liver Glycogen ◽  
Liver Glycogen Content

Adrenodemedullation affects endurance but not hepatic fructose 2,6-bisphosphate

1988 ◽  
Vol 254 (4) ◽  
pp. R572-R577 ◽  
Author(s):  
H. T. Yang ◽  
R. L. Hammer ◽  
T. L. Sellers ◽  
J. Arogyasami ◽  
D. T. Carrell ◽  
...  
Keyword(s):  
Blood Lactate ◽  
Adrenal Medulla ◽  
Endurance Exercise ◽  
Glycogen Content ◽  
Vastus Lateralis ◽  
Liver Glycogen ◽  
Glycogen Depletion ◽  
Epinephrine Infusion ◽  
Liver Glycogen Content

Sham-operated (SHAM) and saline (ADM-S)- or epinephrine (ADM-E)-infused adrenodemedullated rats were run on a treadmill (21 m/min, 15% grade) for 80 min or until exhaustion. ADM-S rats had significantly lower endurance run times (116 +/- 6 min) than ADM-E rats (136 +/- 8 min) and SHAM rats (150 +/- 6 min). Liver glycogen content dropped from 56 +/- 4 to 10 +/- 2 mg/g in SHAM and from 54 +/- 4 to 18 +/- 5 mg/g in ADM-S and to 20 +/- 8 mg/g in ADM-E rats at 80 min. Liver glycogen was depleted in all rats at exhaustion. Liver fructose 2,6-bisphosphate was decreased markedly in exercising rats, and the extent of decrease was not influenced by adrenodemedullation or by epinephrine infusion. ADM-S rats showed impaired glycogen depletion in the white vastus lateralis and soleus muscles, hypoglycemia, and low blood lactate at 80 min and at exhaustion. Infusion of epinephrine into ADM rats reversed these deficiencies. These data indicate that the adrenal medulla is unessential for normal endurance exercise as long as liver glycogen is available. After liver glycogen is depleted, epinephrine from the adrenal medulla prevents hypoglycemia and is essential for allowing continuation of exercise.

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.

Body glucose as fuel for thermogenesis in the white rat exposed to cold

1960 ◽  
Vol 199 (6) ◽  
pp. 1051-1055 ◽  
Author(s):  
Florent Depocas ◽  
Roberto Masironi
Keyword(s):  
Plasma Glucose ◽  
Turnover Rate ◽  
Glycogen Content ◽  
Liver Glycogen ◽  
Turnover Time ◽  
Cold Environments ◽  
Warm Environment ◽  
White Rats ◽  
Liver Glycogen Content ◽  
Carbohydrate Catabolism

Various parameters of glucose metabolism were measured with C14-glucose in unanesthetized warm- and cold-acclimated rats at 30° and 6°C. Exposure of warm-acclimated rats to cold was associated with a decrease in turnover time of plasma glucose, no change in glucose pool size and space, an increase in rates of turnover and oxidation of body glucose, an increase in the ratio of the oxidation rate to the turnover rate, no change in percentage of respiratory CO2 derived from glucose oxidation, and a decrease in liver glycogen content. Approximately reversed changes were observed in cold-acclimated rats transferred from a cold to a warm environment except in the values of turnover time of plasma glucose and terminal liver glycogen content which underwent smaller changes. It is concluded that cold-induced thermogenesis in white rats, whether acclimated to warm or cold environments, is associated with an increase in carbohydrate catabolism proportionate to the increase in energy metabolism.

Selected Contribution: Evidence that the decrease in liver glycogen is associated with the exercise-induced increase in IGFBP-1

2002 ◽  
Vol 93 (2) ◽  
pp. 798-804 ◽  
Author(s):  
Jean-Marc Lavoie ◽  
Yovan Fillion ◽  
Karine Couturier ◽  
Pierre Corriveau
Keyword(s):  
Blood Glucose ◽  
Glycogen Content ◽  
Liver Glycogen ◽  
Lower Blood Glucose ◽  
Insulin Levels ◽  
Liver Glycogen Content ◽  
Lower Blood ◽  
Lipid Response ◽  
Exercise Induced ◽  
Fasted Rats

The purpose of the present study was to test the hypothesis that the exercise-induced increase in insulin-like growth factor binding protein (IGFBP)-1 is not always linked to a decrease in blood glucose level and to examine whether the decreasing levels of liver glycogen during exercise may be associated with the increase in IGFBP-1. Three groups of rats were submitted to a 70-min treadmill exercise. One group of rats was fed normally, and the two other groups had their food intake restricted by 50% (50% fast) the night before the experiment. One of these two 50% fasted groups of rats was infused (intravenously) with glucose throughout exercise to maintain euglycemia. Exercise in noninfused 50% fasted rats, compared with the normally fed rats, resulted in significantly lower blood glucose ( minute 70) and insulin levels, significantly lower liver glycogen content, no change in IGF-I, and significantly higher increases in free fatty acid, glycerol, β-hydroxybutyrate, and IGFBP-1. Maintenance of euglycemia during exercise in glucose-infused 50% fasted rats reduced to a large extent the decrease in insulin levels but only slightly attenuated the lipid response and the IGFBP-1 response seen in noninfused 50% fasted rats. Comparisons of all individual liver glycogen and IGFBP-1 values revealed that liver glycogen values were highly ( P < 0.001) predictive of the IGFBP-1 response during exercise ( R = 0.564). The present results indicate that the IGFBP-1 response during exercise is not always linked to a decrease in plasma glucose and suggest that the increase in IGFBP-1 during exercise may be related to the decrease in liver glycogen content.

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