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.

scholarly journals Preconditioning with L-alanyl-glutamine reduces hepatic ischemia-reperfusion injury in rats

2011 ◽  
Vol 26 (suppl 1) ◽  
pp. 8-13 ◽  
Author(s):  
Raimundo José Cunha Araújo Júnior ◽  
Raimundo Gerônimo da Silva Júnior ◽  
Marcelo Pinho Pessoa de Vasconcelos ◽  
Sérgio Botelho Guimarães ◽  
Paulo Roberto Leitão de Vasconcelos ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Control Group ◽  
Average Weight ◽  
Sham Operation ◽  
Hepatic Ischemia ◽  
Portal Triad ◽  
Hepatic Ischemia Reperfusion ◽  
Control Sham

PURPOSE: To evaluate the effects of pre-conditioning with L-alanyl- glutamine (L-Ala-Gln) in rats subjected to total hepatic ischemia. METHODS: Thirty Wistar rats, average weight 300g, were randomly assigned to 3 groups (n=10): G-1 - Saline, G-2- L-Ala-Gln, G-3-control (Sham). G-1 and G-3 groups were treated with saline 2.0 ml or L-Ala-Gln (0.75mg/Kg) intraperitoneally (ip) respectively, 2 hours before laparotomy. Anesthetized rats were subjected to laparotomy and total hepatic ischemia (30 minutes) induced by by clamping of portal triad. Control group underwent peritoneal puncture, two hours before the sham operation (laparotomy only). At the end of ischemia (G1 and G2), the liver was reperfused for 60 minutes. Following reperfusion blood samples were collected for evaluation of alanine aminotransferase (ALT) and lactate dehydrogenase (LDH) levels. Liver (medium lobe) was removed for immunohistochemistry study with antibody for Caspase-3. RESULTS: It was found a significant decrease (p<0.05) of ALT levels (270.6 +40.8 vs 83.3 +5.5 - p <0.05), LDH (2079.0 +262.4 vs. 206.6 +16.2 - p <0.05) and Caspase-3 expression (6.72 +1.35 vs. 2.19 +1.14, p <0.05) in rats subjected to I / R, comparing the group treated with L-Ala -Gln with G-2. Also, the ALT level was significantly lower (P<0.05) in G-1 and G-2 groups than in G-3 (control group). CONCLUSION: L-Ala-Gln preconditioning in rats submitted to hepatic I/R significantly reduces ALT, LDH and Caspase-3 expression, suggesting hepatic protection.

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.

Inclusion of low amounts of fructose with an intraportal glucose load increases net hepatic glucose uptake in the presence of relative insulin deficiency in dog

2005 ◽  
Vol 288 (6) ◽  
pp. E1160-E1167 ◽  
Author(s):  
Masakazu Shiota ◽  
Pietro Galassetti ◽  
Kayano Igawa ◽  
Doss W. Neal ◽  
Alan D. Cherrington
Keyword(s):  
Blood Glucose ◽  
Glucose Uptake ◽  
Control Period ◽  
Glucose Infusion ◽  
Control Group ◽  
Hepatic Glycogen ◽  
Arterial Blood ◽  
Hepatic Glucose ◽  
Arterial Blood Glucose ◽  
Hepatic Glucose Uptake

The effect of small amounts of fructose on net hepatic glucose uptake (NHGU) during hyperglycemia was examined in the presence of insulinopenia in conscious 42-h fasted dogs. During the study, somatostatin (0.8 μg·kg−1·min−1) was given along with basal insulin (1.8 pmol·kg−1·min−1) and glucagon (0.5 ng·kg−1·min−1). After a control period, glucose (36.1 μmol·kg−1·min−1) was continuously given intraportally for 4 h with (2.2 μmol·kg−1·min−1) or without fructose. In the fructose group, the sinusoidal blood fructose level (nmol/ml) rose from <16 to 176 ± 11. The infusion of glucose alone (the control group) elevated arterial blood glucose (μmol/ml) from 4.3 ± 0.3 to 11.2 ± 0.6 during the first 2 h after which it remained at 11.6 ± 0.8. In the presence of fructose, glucose infusion elevated arterial blood glucose (μmol/ml) from 4.3 ± 0.2 to 7.4 ± 0.6 during the first 1 h after which it decreased to 6.1 ± 0.4 by 180 min. With glucose infusion, net hepatic glucose balance (μmol·kg−1·min−1) switched from output (8.9 ± 1.7 and 13.3 ± 2.8) to uptake (12.2 ± 4.4 and 29.4 ± 6.7) in the control and fructose groups, respectively. Average NHGU (μmol·kg−1·min−1) and fractional glucose extraction (%) during last 3 h of the test period were higher in the fructose group (30.6 ± 3.3 and 14.5 ± 1.4) than in the control group (15.0 ± 4.4 and 5.9 ± 1.8). Glucose 6-phosphate and glycogen content (μmol glucose/g) in the liver and glucose incorporation into hepatic glycogen (μmol glucose/g) were higher in the fructose (218 ± 2, 283 ± 25, and 109 ± 26, respectively) than in the control group (80 ± 8, 220 ± 31, and 41 ± 5, respectively). In conclusion, small amounts of fructose can markedly reduce hyperglycemia during intraportal glucose infusion by increasing NHGU even when insulin secretion is compromised.

scholarly journals The Role of Hormones in the Regulation of Glycogen Metabolism in the Clawed Toad Xenopus Laevis (Daudin)

2019 ◽  
pp. 17-24
Author(s):  
Daphna Atar-Zwillenberg ◽  
Michael Atar ◽  
Gianni Morson ◽  
Udo Spornitz
Keyword(s):  
Blood Glucose ◽  
Xenopus Laevis ◽  
Muscle Glycogen ◽  
Hormonal Regulation ◽  
Glycogen Content ◽  
Glycogen Metabolism ◽  
Liver Glycogen ◽  
Hepatic Glycogen ◽  
Lipid Levels ◽  
Liver Glycogen Content

The hormonal regulation of amphibian glycogen metabolism was studied in Xenopus laevis as a typical member of the anurans (tailless amphibians).The main focus of this study was given to the effects of various hormones on the glycogen/glucose balance in adult toads. We determined biochemically the liver and muscle glycogen contents as well as the blood glucose and lipid levels for a number of hormones and also diabetes inducing substances. Additionally, we examined ultrastructure changes in hepatocytes induced by the various treatments, and also investigated the activity of carbohydrate-relevant enzymes by histochemistry. With one exception, the liver glycogen content of Xenopus remained basically unchanged by the treatments or was even slightly enhanced. Only human chorionic gonadotropin, through which the vitellogenic response is triggered, prompts a significant decrease of liver glycogen in females. Under the same conditions the male liver glycogen content remained stable. Muscle glycogen contents were not affected by any of the treatments. Blood glucose and lipid levels on the other hand were elevated considerably in both sexes after application of either epinephrine or cortisol. The ultrastructural examination revealed a proliferation of Rough Endoplasmic Reticulum (RER) in hepatocytes from epinephrine treated toads of both sexes as well as from HCG treated females. By histochemistry, we detected an elevated glucose-6-phosphatase activity in the hepatocytes from toads treated with either epinephrine or cortisol. These treatments also led to enhanced glycogen phosphorylase activity in males, and to a slightly elevated glyceraldehyde-3-phosphate dehydrogenase activity in females. Our results show that the hepatic glycogen is extremely stable in adult Xenopus. Only vitellogenesis causes a marked utilization of glycogen. Since the blood glucose levels are elevated in epinephrine or cortisol treated toads without the liver glycogen being affected, we conclude that either protein and/or lipid metabolism are involved in carbohydrate metabolism in Xenopus laevis.

scholarly journals Essential Oils From Cymbopogon Citratus and Lippia Sidoides in the Anesthetic Induction and Transport of Ornamental Fish Pterophyllum Scalare

2021 ◽  
Author(s):  
Iara Cruz de Oliveira ◽  
Rebeca Santos Matos Oliveira ◽  
Carlos Henrique da Paixão Lemos ◽  
Crislaine Palmeira Barbosa de Oliveira ◽  
Altiery Felix e Silva ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Essential Oils ◽  
Ornamental Fish ◽  
Control Group ◽  
Hepatic Glycogen ◽  
Cymbopogon Citratus ◽  
Lippia Sidoides ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Pterophyllum Scalare

Abstract This study verified the effects of essential oils from Lippia sidoides (EOLS) and Cymbopogon citratus (EOCC) on the anesthesia of freshwater angelfish (Pterophyllum scalare) of two different sizes (juveniles I (0.82 g) and II (2.40 g)) and on the transport (8 h) of juveniles II. Fish were exposed to different concentrations of EOLS and EOCC: 0, 10, 25, 50, 75, 100, 150, 200, and 250 mg L−1. Ventilatory rate (VR) and transport for 8 h with 0, 10, and 15 mg L−1 of each essential oil were evaluated in juveniles II. The major components found in EOLS and EOCC were carvacrol (44.50%) and a-citral (73.56%), respectively. The best sedation and anesthesia times for both essential oils were obtained with 10 and 25 mg L−1 and 200 and 250 mg L−1 for juveniles I and II, respectively. Fish sedated with EOLS had lower VR values than the other treatments. For transported fish, blood glucose levels were higher in ornamental fish transported with 10 and 15 mg EOLS L−1 and 15 mg EOCC L−1. Hepatic glycogen values were higher in the control group. In general, fish transported with 10 mg EOLS L−1 showed fewer gill histological alterations than other transported fish. When the type of lesion was evaluated, the highest gill alterations occurred in fish transported with EOCC. In conclusion, for the transport of juveniles II, 10 mg EOLS L−1 could be used because although this concentration increased blood glucose, it decreased the VR and caused only mild alterations to the gills.

scholarly journals Alteration of connexins gene expression by silibinin during hepatic warm ischemia-reperfusion injury in the rat model

2021 ◽  
Keyword(s):  
Gene Expression ◽  
Reperfusion Injury ◽  
Mrna Expression ◽  
Normal Saline ◽  
Connexin 43 ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Hepatic Tissue ◽  
Control Group ◽  
Hepatic Ischemia

Background: Ischemia-reperfusion injury (IRI) is an injurious phenomenon that is the primary determinant of liver dysfunction after surgery and transplantation. The present evidence demonstrated that connexin 43 (Cx43), Cx32, and Cx26 are the essential gap junction proteins involved in the liver IRI. This study aimed to characterize the beneficial effects of silibinin on Cx43, Cx32, and Cx26 gene expression during warm hepatic ischemia-reperfusion (IR). Materials and Methods: A total of 32 male Wistar rats weighing 250-300 g were randomly divided into four equal groups of eight animals in each group as follows: 1) control group (laparotomy+normal saline), 2) laparotomy+silibinin (30 mg/kg) (SILI), 3) liver IR procedure+normal saline (IR), and 4) liver IR procedure+silibinin (30 mg/kg) (IR+SILI). After 1 h of ischemia followed by 3 h of reperfusion, blood samples and tissue sections were gathered to assess the serum liver markers and evaluate the liver histological changes as well as gene expression, respectively. Results: The obtained data proved no considerable differences between control and SILI groups in all experiments. Furthermore, the gene expression of Cx26, Cx32, and Cx43 was significantly induced in the IR group, compared to the control group. Silibinin markedly reduced Cx26 and Cx32 mRNA expression, whereas increased Cx43 mRNA expression. Moreover, serum alanine aminotransferase and aspartate aminotransferase levels were markedly elevated in the IR group (P<0.001), compared to the control group. However, in the IR+SILI group, silibinin could significantly decline these elevations, compared to the IR group. In addition, silibinin diminished hepatic tissue damages during IR. Conclusion: Silibinin could attenuate liver injury through better cell-to-cell communication via lowering Cx32 and Cx26, as well as increasing Cx43 gene expression, respectively.

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.

Some effects of fasting on rats fed a choline-deficient diet

1960 ◽  
Vol 198 (2) ◽  
pp. 371-374 ◽  
Author(s):  
E. Douglas Rees ◽  
William W. Winternitz ◽  
William F. Lattanzi
Keyword(s):  
Blood Glucose ◽  
Ketone Bodies ◽  
Blood Glucose Concentration ◽  
Liver Glycogen ◽  
Control Group ◽  
Deficient Diet ◽  
Hepatic Fat ◽  
Blood Ketone Bodies ◽  
Deficient Group

The blood ketone body concentrations of fasted and nonfasted rats fed a diet deficient in choline were determined and found to be similar to the concentrations obtained from a control group fed the same diet supplemented with choline. However, the animals on the choline-deficient diet had an 18–20% greater mean liver mass, and this could account for the failure to demonstrate the depressed level of blood ketone bodies which was anticipated on the basis of previous in vitro studies. Other possible explanations of this discrepancy are discussed. Despite a high hepatic fat content, the choline-deficient group had a normal concentration of liver glycogen. The nonfasting blood glucose concentration of the choline-deficient group (91.5 ± 5 mg %) was lower than that of the control group (102 ± 3 mg %). After 24 hours of fasting, the values were 52 ± 3 mg % and 61 ± 5 mg % for the choline-deficient and control group, respectively. The 72-hour fasting values were 43 ± 2 mg %, and 49 ± 2 mg %, respectively. Data showing the effect of diet composition on ketonemia, liver glycogen and blood glucose are presented and are in accord with previous studies.

scholarly journals GGsTop, a novel and specific γ-glutamyl transpeptidase inhibitor, protects hepatic ischemia-reperfusion injury in rats

2016 ◽  
Vol 311 (2) ◽  
pp. G305-G312 ◽  
Author(s):  
Kaneto Tamura ◽  
Nobuhiko Hayashi ◽  
Joseph George ◽  
Nobuyuki Toshikuni ◽  
Tomiyasu Arisawa ◽  
...  
Keyword(s):  
Blood Flow ◽  
Liver Injury ◽  
Group Treatment ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Vena Cava ◽  
Hepatic Tissue ◽  
Protective Effects ◽  
Hepatic Ischemia ◽  
Glutamyl Transpeptidase

Ischemia-reperfusion (IR) injury is a major clinical problem and is associated with numerous adverse effects. GGsTop [2-amino-4{[3-(carboxymethyl)phenyl](methyl)phosphono}butanoic acid] is a highly specific and irreversible γ-glutamyl transpeptidase (γ-GT) inhibitor. We studied the protective effects of GGsTop on IR-induced hepatic injury in rats. Ischemia was induced by clamping the portal vein and hepatic artery of left lateral and median lobes of the liver. Before clamping, saline (IR group) or saline containing 1 mg/kg body wt of GGsTop (IR-GGsTop group) was injected into the liver through the inferior vena cava. At 90 min of ischemia, blood flow was restored. Blood was collected before induction of ischemia and prior to restoration of blood flow and at 12, 24, and 48 h after reperfusion. All the animals were euthanized at 48 h after reperfusion and the livers were harvested. Serum levels of alanine transaminase, aspartate transaminase, and γ-GT were significantly lower after reperfusion in the IR-GGsTop group compared with the IR group. Massive hepatic necrosis was present in the IR group, while only few necroses were present in the IR-GGsTop group. Treatment with GGsTop increased hepatic GSH content, which was significantly reduced in the IR group. Furthermore, GGsTop prevented increase of hepatic γ-GT, malondialdehyde, 4-hydroxynonenal, and TNF-α while all these molecules significantly increased in the IR group. In conclusion, treatment with GGsTop increased glutathione levels and prevented formation of free radicals in the hepatic tissue that led to decreased IR-induced liver injury. GGsTop could be used as a pharmacological agent to prevent IR-induced liver injury and the related adverse events.

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