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.

Effects of Epinephrine on Carbohydrate Metabolism in Underfed and ad Libitum-Fed Rats

1957 ◽  
Vol 190 (2) ◽  
pp. 239-242
Author(s):  
B. N. Spirtos ◽  
R. G. Stuelke ◽  
N. S. Halmi
Keyword(s):  
Carbohydrate Metabolism ◽  
Blood Sugar ◽  
Blood Lactate ◽  
Liver Glycogen ◽  
Hepatic Glycogen ◽  
Commercial Diet ◽  
Ad Libitum ◽  
Sugar Levels ◽  
Fasted Rats

Rats fed 10 gm of a commercial diet for 4–5 weeks and fasted for 24 hours showed less rise in liver glycogen and blood sugar levels in response to the injection of epinephrine than did ad libitum-fed-fasted rats. Gastrocnemius glycogen levels were found to be higher in underfed-fasted animals and fell to the same extent as in ad libitum fed-fasted animals when epinephrine was given. Blood lactate concentrations, however, rose less markedly in the underfed-fasted group. This may have been at least partly responsible for the diminished rise in hepatic glycogen and blood sugar.

Hyperlipemia and ketosis in the pregnant rat

1964 ◽  
Vol 206 (4) ◽  
pp. 796-804 ◽  
Author(s):  
Robert O. Scow ◽  
Sidney S. Chernick ◽  
Marlene S. Brinley
Keyword(s):  
Blood Glucose Concentration ◽  
Late Pregnancy ◽  
Maternal Blood ◽  
Insulin Administration ◽  
Pregnant Rats ◽  
Pregnant Rat ◽  
Fat Mobilization ◽  
Fractional Clearance ◽  
Ad Libitum ◽  
Fasted Rats

Pregnant rats fasted on the 18th or 19th day of gestation developed hypoglycemia, severe ketosis, and hyperlipemia. The latter, which consisted primarily of triglycerides, was accompanied by increased plasma free fatty acids and accumulation of fat in the liver and kidneys. The effects of fasting were diminished by starting the fast earlier in pregnancy or by hysterectomy. Both ketosis and hyperlipemia were corrected by administration of insulin, tolbutamide, or glucose. The findings indicate that increased fat mobilization and ketosis in fasting pregnant rats are the result of insulin lack. It is suggested that the high priority of the fetuses for glucose reduced the maternal blood glucose concentration to a level too low to stimulate insulin secretion during fasting. Fasting did not alter the rapid growth of the fetuses. Pregnant rats fed ad libitum also developed hypertriglyceridemia if the diet contained fat. This hyperlipemia, unlike that in the fasted rats, was not due to increased fat mobilization and was unaffected by insulin administration. It is concluded that the fractional clearance of blood triglycerides is greatly reduced during late pregnancy.

scholarly journals Assessment of Cytotoxicity, Fetotoxicity, and Teratogenicity ofPlathymenia reticulataBenth Barks Aqueous Extract

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Lia de Barros Leite Albuquerque ◽  
Cháriston André Dal Belo ◽  
Marcio Galdino dos Santos ◽  
Patricia Santos Lopes ◽  
Marli Gerenutti ◽  
...  
Keyword(s):  
Aqueous Extract ◽  
Reproductive Toxicity ◽  
Late Pregnancy ◽  
Control Group ◽  
Corpora Lutea ◽  
Experimental Conditions ◽  
Pregnant Rats ◽  
Skeletal Analysis ◽  
Ld50 Test

Scientific assessment of harmful interactions of chemicals over the entire reproductive cycle are divided into three segments based on the period: from premating and mating to implantation (I), from implantation to major organogenesis (II), and late pregnancy and postnatal development (III). We combined the segments I and II to assessPlathymenia reticulataaqueous extract safety. In order to investigate reproductive toxicity (segment I), pregnant rats received orally 0.5 or 1.0 g/kg of extract, daily, during 18 days. These concentrations were determined by a preliminaryin vitroLD50 test in CHO-k1 cells. A control group received deionized water. The offspring was removed at the 19th day, by caesarean, and a teratology study (segment II) was carried out. The corpora lutea, implants, resorptions, live, and dead fetuses were then counted. Placenta and fetuses were weighted. External and visceral morphology were provided by the fixation of fetuses in Bouin, whereas skeletal analysis was carried out on the diaphanizated ones. The increase in the weights of placenta and fetuses was the only abnormality observed. Since there was no sign of alteration on reproduction parameters at our experimental conditions, we conclude thatP. reticulataaqueous extract is safe at 0.5 to 1.0 g/kg and is not considered teratogenic.

The Effects of Dimethylsulfoxide on Experimental Hepatic Ischemia

Swiss Surgery ◽  
2000 ◽  
Vol 6 (1) ◽  
pp. 23-27 ◽  
Author(s):  
Akyürek ◽  
Kafali ◽  
Muhtaroglu
Keyword(s):  
Blood Glucose ◽  
Vena Cava ◽  
Liver Glycogen ◽  
Hepatic Tissue ◽  
Control Group ◽  
Hepatic Glycogen ◽  
Free Oxygen Radical ◽  
Hepatic Ischemia ◽  
Portal Triad ◽  
Ischemic Period

Aims: The aim of the study is to investigate the effects of dimethylsulfoxide (DMSO), a non-enzymatic free oxygen radical detoxifier, on the alterations observed during hepatic ischemia. Methods: Twenty four albino rabbits were entered into the study. DMSO (500mg/kg) was administered through inferior vena cava following dissection of the portal triad and immediately prior to clamping. The alterations on liver glycogen, blood glucose, ALT, AST, LDH, intracellular ATP, GSH-px, SOD, MDA within the erythrocyte and hepatic tissue MDA were investigated. Results: In the control group, following ischemia, a reduction in blood glucose, hepatic glycogen and ATP levels within the cell and an increase in AST and LDH levels, MDA, GSH-px and SOD levels within the erythrocyte and hepatic tissue MDA level were observed (p < 0.01). In the study group, the blood glucose values increased at 30th minute following ischemia. The increase in LDH level was not statistically significant (p < 0.05). The increase in AST level was significantly lower when compared to the control group (p < 0.05). No effect was observed on ALT and ALP levels. DMSO lowered the reduction in hepatic glycogen level (p < 0.05), GSH-px (p <0.01), MDA (p < 0.05) and ATP (p < 0.05) levels within the erythrocyte and hepatic tissue MDA level (p < 0.01) that were increased following ischemia. The increase in blood SOD level was not statistically significant (p >0.05). Conclusion: DMSO can be administered in attempt to prolong the duration of ischemia or to reduce the adverse effects of ischemia on the hepatic tissue during the existing ischemic period.

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.

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.

Formation of gluconeogenic precursors in rat skeletal muscle during fasted-refed transition

1990 ◽  
Vol 259 (4) ◽  
pp. E513-E516
Author(s):  
M. N. Goodman ◽  
R. Dietrich ◽  
P. Luu
Keyword(s):  
Skeletal Muscle ◽  
Blood Lactate ◽  
Muscle Metabolism ◽  
Liver Glycogen ◽  
Hepatic Glycogen ◽  
Indirect Pathway ◽  
Rat Skeletal Muscle ◽  
Fasted State ◽  
Glycogen Repletion ◽  
Fasted Rats

During the fasted-refed transition, hepatic glycogen repletion from glucose can occur by the direct and indirect pathway. In the indirect pathway, glucose is first metabolized to 3-carbon intermediates that then are converted in the liver to glucose 6-phosphate via the gluconeogenic pathway before conversion to glycogen. The present study evaluated whether skeletal muscle is a major source of 3-carbon intermediates (i.e., lactate, pyruvate, and alanine) during refeeding of 1-day fasted rats. Arteriovenous differences for lactate, pyruvate, and alanine across the anesthetized rat hindlimbs were used to evaluate muscle metabolism in the fed, fasted, and refed state. In the fasted state, liver glycogen was depleted, and muscle released 3-carbon intermediates. One hour after refeeding, hepatic glycogen was 30% repleted, and blood lactate, pyruvate, and alanine increased. Despite this, the release of alanine by muscle diminished at this time and lactate was removed. At 4 h after refeeding, 3-carbon intermediates were all released by hindlimb tissue but in an amount not greater than in the fasted state. Overall, these results suggest that skeletal muscle in the rat is not a major source of 3-carbon precursors for early postprandial hepatic glycogen repletion via the indirect pathway, nor is the rise in 3-carbon intermediates in blood during refeeding caused by their increased output by muscle.

Effect of interferon-γ treatment on the expression of interleukin-1β at the maternal - fetal interface of pregnant rats

2007 ◽  
Vol 19 (3) ◽  
pp. 510 ◽  
Author(s):  
Hong-Fei Xia ◽  
Quan-Hong Sun ◽  
Jing-Pian Peng
Keyword(s):  
Late Pregnancy ◽  
Interferon Γ ◽  
Control Group ◽  
Cytokine Network ◽  
Pregnant Rats ◽  
Endometrial Stromal Cells ◽  
Protein Levels ◽  
Decidua Basalis ◽  
Ifn Γ

In the present study, the possible mechanisms by which interferon (IFN)-γ affects pregnancy were investigated using the cytokine network model. The IFN-γ-induced expression of interleukin (IL)-1β was examined using western blotting, immunohistochemistry and immunofluorescence. The results showed that IFN-γ treatment significantly decreased the expression of uterine IL-1β protein during the preimplantation, post-implantation and mid-gestation periods. The expression of IL-1β protein was increased after IFN-γ treatment compared with the control group in late pregnancy. In the placenta, IL-1β protein levels were significantly increased after IFN-γ treatment in early and mid-pregnancy. In late pregnancy, IFN-γ treatment significantly decreased placental IL-1β protein levels. IL-1β was mainly expressed in the myometrium, uterine arteries, decidua basalis, trophospongium of the junctional layer and trophoblastic epithelium of the labyrinthine layers. IL-1β was mainly located in the cytoplasm of in vitro cultured endometrial stromal cells (ESCs). IFN-γ treatment did not affect the distribution of IL-1β, only the expression of IL-1β. The effects of IFN-γ on the proliferation of ESCs were determined using an MTS (a novel tetrazolium compound) assay. IFN-γ treatment inhibited the proliferation of ESCs and decreased the weight of the fetus and placenta. These results indicate that exogenous IFN-γ affects the expression of IL-1β and inhibits ESC proliferation.

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.

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