Liver glycogen and glyceride glycerol formation as compared with glucose synthesis in 24h-starved virgin and pregnant rats

1983 ◽  
Vol 11 (6) ◽  
pp. 730-731 ◽  
Author(s):  
ANTONIO ZORZANO ◽  
EMILIO HERRERA
Keyword(s):  
Liver Glycogen ◽  
Pregnant Rats ◽  
Glucose Synthesis ◽  
Glycerol Formation

scholarly journals Pregnancy and pentobarbital anaesthesia modify hepatic synthesis of acylglycerol glycerol and glycogen from gluconeogenic precursors during fasting in rats

1988 ◽  
Vol 256 (2) ◽  
pp. 487-491 ◽  
Author(s):  
A Zorzano ◽  
E Herrera
Keyword(s):  
Late Pregnancy ◽  
Liver Glycogen ◽  
Control Group ◽  
Hepatic Glycogen ◽  
Dihydroxyacetone Phosphate ◽  
Pregnant Rats ◽  
Glucose Synthesis ◽  
Marked Accumulation ◽  
Fasted Rats ◽  
Hepatic Synthesis

1. Incorporation of gluconeogenic precursors into blood glucose and hepatic glycogen and acylglycerol glycerol was examined in 24 h-fasted virgin rats by using a flooding procedure for substrate administration. At 10 min after their intravenous injection, the conversion of alanine or glycerol into liver glycogen or acylglycerol glycerol was proportional to glucose synthesis. 2. In 24 h-fasted 21-day-pregnant rats, the incorporation of alanine and glycerol into hepatic acylglycerol glycerol was markedly enhanced compared with the control group. In addition, during fasting at late pregnancy, the proportion of substrates directed to acylglycerol glycerol as compared with the fraction incorporated into glucose was augmented. 3. In pentobarbital-treated fasted rats, the incorporation of both alanine and pyruvate into circulating glucose and into hepatic glycogen and acylglycerol glycerol was increased. Pentobarbital treatment increased the proportion of substrates incorporated into liver glycogen, compared with the fraction appearing in circulating glucose. These changes were concomitant with a marked accumulation of glycogen. 4. The data indicate that, during fasting, gluconeogenesis provides glucose as well as hepatic glycogen and acylglycerol glycerol, independently of whether the substrates enter gluconeogenesis at the level of pyruvate or dihydroxyacetone phosphate.

Effect of maternal exercise on fetal liver glycogen late in gestation in the rat

1986 ◽  
Vol 60 (4) ◽  
pp. 1254-1258 ◽  
Author(s):  
K. I. Carlson ◽  
H. T. Yang ◽  
W. S. Bradshaw ◽  
R. K. Conlee ◽  
W. W. Winder
Keyword(s):  
Fetal Liver ◽  
Metabolic Stress ◽  
Liver Glycogen ◽  
Moderate Intensity ◽  
Blood Levels ◽  
Pregnant Rats ◽  
Maternal Liver ◽  
Maternal Exercise ◽  
Glucose Plasma ◽  
Glucagon And Insulin

To determine the effect of maternal exercise on fetal liver glycogen content, fed and fasted rats that were pregnant for 20.5 or 21.5 days were run on a rodent treadmill for 60 min at 12 m/min with a 0% grade or 16 m/min up a 10% grade. The rats were anesthetized by intravenous injection of pentobarbital sodium, and fetal and maternal liver and plasma samples were collected and frozen. Fetal liver glycogenolysis did not occur as a result of maternal exercise. Fetal blood levels of lactate increased 22–60%, but glucose, plasma glucagon, and insulin were unchanged during maternal exercise. Maternal liver glycogen decreased as a result of exercise in all groups of rats except the fasted 20.5-day-pregnant group. Plasma free fatty acids increased in all groups and blood lactate increased in fed (20.5 days) and fasted (21.5 days) pregnant rats. Maternal glucose, glucagon, and insulin values remained constant during exercise. The fetus appears to be well-protected from metabolic stress during moderate-intensity maternal exercise.

The mechanism by which glucagon induces the release of amino acids from muscle and its relevance to fasting

1977 ◽  
Vol 196 (1124) ◽  
pp. 347-365 ◽  
Keyword(s):  
Amino Acids ◽  
Blood Glucose ◽  
Skeletal Muscles ◽  
Muscle Protein ◽  
Liver Glycogen ◽  
Blood Levels ◽  
Hepatic Glycogen ◽  
Systemic Injection ◽  
Arterial Blood ◽  
Glucose Synthesis

A raised level of glucagon was attained rapidly, and maintained steadily, for an hour or more in the circulation of fed, or of fasted, rabbits. During this time the concentrations of 18 amino acids, of glucose and of insulin, were measured in samples of arterial blood and of blood leaving the skeletal muscles, taken simultaneously. The glucagon raised the level of glucose in the arterial blood, while, at the same time, decreasing the levels of most of the amino acids. The rate of release of amino acids from the skeletal muscles increased during this time. When the store of hepatic glycogen had been depleted by a previous injection of glucagon, or by fasting, glucagon still caused a rise in blood glucose, but the rise was less, and was less well sustained, than that seen when the glycogen stores of the liver were normal. The second injection of glucagon, or fasting, caused the glycogen depleted liver to convert certain amino acids, obtained from the blood, into glucose, lowering the blood levels of these amino acids. The muscles now released amino acids. There was no detectable difference in the release of amino acids from muscle whether glucagon was given systemically or into the artery supplying the muscles. However, a systemic injection of L-alanine, together with glucagon, abolished the fall in the level of amino acids in the blood, and suppressed their release from muscle. During fasting a steady fall in the blood levels of five amino acids occurred, probably due to their use by the liver for glucose synthesis; the temporary rise in the levels of other amino acids, which are not readily used for glucose synthesis, seems to be due to their concomitant release, from the breakdown of muscle protein. We conclude that the elevated level of glucagon, which is found in fasting, ensures that an acceptable level of the blood glucose is maintained by means of two mechanisms; first by releasing glucose from liver glycogen, and then, when fasting is prolonged, by causing the liver to synthesize glucose from certain of the amino acids in the blood, thus decreasing their concentration in the blood. This fall in the levels of these amino acids in the blood is, we believe, the stimulus which leads first to the release of amino acids from the muscles, and then to the breakdown of muscle protein to replace these released amino acids, and thus to maintain a continuous supply of these amino acids for glucose synthesis.

DYNAMICS OF HEPATIC GLYCOGEN: OESTROGEN AND PREGNANCY

1972 ◽  
Vol 71 (2) ◽  
pp. 385-392 ◽  
Author(s):  
P. K. Paul
Keyword(s):  
Food Intake ◽  
Serum Cholesterol ◽  
Liver Glycogen ◽  
Steroid Treatment ◽  
Hepatic Glycogen ◽  
Pregnant Rats ◽  
Oestrogen Treatment ◽  
Cholesterol Levels ◽  
Glycogen Deposition ◽  
Intact Rats

ABSTRACT The effects of oestradiol (0.5 μ/rat/day) given for a variable period on rat liver were investigated, and the results were compared with those of untreated pregnant rats at different stages of pregnancy. The part played by the adrenal under these conditions was also investigated. Oestrogen treatment for 14 and 21 days in intact rats reduced the liver glycogen. A corresponding reduction in food intake was noted during these days. However, a rebound rise in liver glycogen occurred after 28 days of oestrogen administration. In contrast, the ovariectomized animals did not show any change in liver glycogen following steroid treatment. During pregnancy the total liver glycogen increased after the first week, but returned to the normal level on day twenty one. The adrenal and serum cholesterol levels in oestrogen treated and pregnant rats remained low except for an increase in serum cholesterol on day 21 of gestation and 7 days after oestrogen treatment. The study suggests that continued oestrogen treatment of non-pregnant rats probably maintains some endogenous factor(s) (progesterone) for about 21 days, which antagonizes the effect of oestrogen administration on hepatic glycogen deposition. The implications of liver glycogen changes during pregnancy in relation to progesterone levels and dietary intake are discussed.

scholarly journals Neonatally induced diabetes: liver glycogen storage in pregnant rats

2012 ◽  
Vol 55 (2) ◽  
pp. 251-256
Author(s):  
Isabela Lovizutto Iessi ◽  
Aline Bueno ◽  
Yuri Karen Sinzato ◽  
Ana Paula Machado Spada ◽  
Marilza Vieira Cunha Rudge ◽  
...  
Keyword(s):  
Liver Glycogen ◽  
Glycogen Storage ◽  
Pregnant Rats

Glycogen Storage in Fetuses of Trained Pregnant Rats

1997 ◽  
Vol 22 (4) ◽  
pp. 384-393 ◽  
Author(s):  
Pamela E. Houghton ◽  
Michelle F. Mottola ◽  
Jamie Mezzapelli ◽  
Richard Vandermolen ◽  
Paul D. Christopher
Keyword(s):  
Fetal Heart ◽  
Fetal Liver ◽  
Exercise Program ◽  
Liver Glycogen ◽  
Glycogen Storage ◽  
Control Group ◽  
Pregnant Rats ◽  
Glycogen Concentration ◽  
Fetal Organs ◽  
Key Words Exercise Training

The purpose was to determine if running 30 m/min on a 10° incline, 60 min/day for 5 days/week altered fetal glycogen storage in prepregnancy trained rats. Animals that exercised for 3 weeks prior to pregnancy either continued the same exercise program until Day 19 of gestation (pregnant running group [PR]), or ceased exercising at conception (pregnant controls [PC]). A separate set of animals did not exercise either before or during pregnancy (pregnant nonrunning control group [PNRC]). On Day 20 of gestation, fetal organs and placenta were weighed and analyzed for glycogen concentration. Glycogen concentrations were not different in either fetal liver, heart, or placenta of PR rats compared to PNRC animals. However, fetal liver glycogen concentration was significantly lower in the fetal heart and liver of PC animals compared to glycogen measured in both PNRC and PR animals (p < .0.5). These results suggest that exercise of this intensity does not compromise fetal glycogen storage in trained pregnant rats. However, chronic prepregnancy exercise and then abrupt cessation of exercise at conception may compromise fetal growth and development. Key words: exercise training, pregnancy, fetal glycogen

Modification of Pineal Ultrastructure by Exogenous Hormones

1967 ◽  
Vol 25 ◽  
pp. 170-171
Author(s):  
R. A. Turner ◽  
A. E. Rodin ◽  
D. K. Roberts
Keyword(s):  
Electron Microscopy ◽  
Endoplasmic Reticulum ◽  
Rough Endoplasmic Reticulum ◽  
Estradiol Benzoate ◽  
Female Rats ◽  
List Type ◽  
Type Number ◽  
Pregnant Rats ◽  
Gonadal Atrophy ◽  
Pineal Ultrastructure

There have been many reports which establish a relationship between the pineal and sexual structures, including gonadal hypertrophy after pinealectomy, and gonadal atrophy after injection of pineal homogenates or of melatonin. In order to further delineate this relationship the pineals from 5 groups of female rats were studied by electron microscopy:ControlsPregnant ratsAfter 4 weekly injections of 0.1 mg. estradiol benzoate.After 8 daily injections of 150 mcgm. melatonin (pineal hormone).After 8 daily injections of 3 mg. serotonin (melatonin precursor).No ultrastructural differences were evident between the control, and the pregnancy and melatonin groups. However, the estradiol injected animals exhibited a marked increase in the amount and size of rough endoplasmic reticulum within the pineal cells.

Effect of Matricaria chamomilla L. extract on fetal absorption, placenta structure and liver of diabetic pregnant rats.

Planta Medica ◽  
2011 ◽  
Vol 77 (12) ◽  
Author(s):  
F Namjooyan ◽  
M Panahi ◽  
F Ahmadpour ◽  
A Darvish ◽  
M Azemi ◽  
...  
Keyword(s):  
Matricaria Chamomilla ◽  
Pregnant Rats
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