PAF increases hepatic vascular resistance and glycogenolysis in vivo

1991 ◽  
Vol 260 (3) ◽  
pp. G471-G480 ◽  
Author(s):  
K. L. Hines ◽  
A. Braillon ◽  
R. A. Fisher
Keyword(s):  
Blood Flow ◽  
Blood Glucose ◽  
Glucose Concentration ◽  
Glycogen Phosphorylase ◽  
Blood Glucose Concentration ◽  
Portal Pressure ◽  
Hepatic Glycogen ◽  
Hepatic Portal ◽  
Adrenalectomized Rats

Administration of platelet-activating factor (PAF) to portal venous circulation of anesthetized fed rats produced decreases in mean arterial pressure and increases in hepatic portal pressure and blood glucose concentration. These responses to PAF were dose dependent with ED50 values of 0.02-0.05 micrograms/kg and specific as lyso- and enantio-PAF did not reproduce effects of PAF. Specific PAF receptor antagonist SRI 63-675 (75 micrograms/kg) inhibited significantly these PAF (0.1 micrograms/kg)-induced responses in rats. Administration of prazosin (500 micrograms/kg) and propranolol (400 micrograms/kg) to rats abolished phenylephrine (50 micrograms/kg)-induced increases in mean arterial pressure, hepatic portal pressure, and blood glucose concentration but did not prevent PAF (1 microgram/kg)-induced alterations in these parameters. Glycogen phosphorylase alpha levels were increased significantly in livers of rats after administration of PAF (1 microgram/kg) or phenylephrine (50 micrograms/kg). Administration of prazosin and propranolol to rats inhibited phenylephrine- but not PAF-induced activation of hepatic glycogen phosphorylase. Hepatic adenosine 3',5'-cyclic monophosphate (cAMP) concentration was increased slightly by PAF, but these increases were eliminated by adrenergic blockade, suggesting that activation of hepatic glycogen phosphorylase by PAF is not dependent on increases in cAMP. Increases in hepatic portal pressure and blood glucose concentration in response to PAF (0.1 micrograms/kg) were not attenuated in adrenalectomized rats. Moreover, PAF (0.1 micrograms/kg) stimulated increases in hepatic portal pressure after administration of the ganglionic blocking agent chlorisondamine (2.5 mg/kg) to adrenalectomized rats. Administration of PAF (0.05 micrograms/kg) to rats instrumented with pulse Doppler flow probes produced decreases in hepatic arterial and portal vein blood flow and increases in hepatic arterial and portal vascular resistance. These observations provide direct evidence that PAF regulates hepatic hemodynamics and glycogenolysis in vivo. It is suggested that PAF plays an important role in regulating hepatic blood flow and supplying extrahepatic tissues with energy substrates by sympathetic-independent mechanism(s) after its release in acute pathophysiological situations.

scholarly journals Glycogen metabolism in the liver of the neonatal gsd/gsd and control (GSD/GSD) rat

1982 ◽  
Vol 202 (3) ◽  
pp. 623-629 ◽  
Author(s):  
D G Clark ◽  
S D Neville ◽  
M Brinkman ◽  
O H Filsell
Keyword(s):  
Blood Glucose ◽  
Glucose Concentration ◽  
Blood Glucose Concentration ◽  
Glycogen Metabolism ◽  
Hepatic Glycogen ◽  
Living Tissue ◽  
Neonatal Rats ◽  
And Control ◽  
Blood Glucose Concentrations

1. The metabolism of hepatic glycogen, labelled with [6-3H]glucose at day 19.5 of gestation and with 14C from [U-14C]galactose at delivery, was followed for 10 h in food-deprived gsd/gsd and control (GSD/GSD) neonatal rats. 2. In the affected pups glycogen was maintained at 12% (w/w) and there was no loss of incorporated radioactivity. 3. The 3H and 14C in glycogen from the controls were both decreased by 80%, but 14C was removed at 0-5 h and [6-3H]glucose at 5-10 h. 4. Blood glucose concentrations in the unaffected neonatal rats fell from 5.3 mM at 20 min to 1.7 mM after 10 h. In the gsd/gsd pups blood glucose concentration was decreased from 2 mM at birth to 0.3 mM at 2.5 h: it was maintained at 0.8 mM between 5 and 10 h. 5. In neonatal rats that had been dead for 10 h, hepatic glycogen was decreased by 34% in the controls and by 22% in the gsd/gsd pups. These results demonstrate that liver from the affected rats contains glycogenolytic activity, but that it is not expressed in living tissue.

Early hyperglycemia following alloxan administration in vivo is not associated with altered hepatic mitochondrial function: acceptable model for type 1 diabetes?

2011 ◽  
Vol 89 (7) ◽  
pp. 477-484 ◽  
Author(s):  
Dairo A. Rendon ◽  
Jose A. Alvarez-Bustamante
Keyword(s):  
Type 1 Diabetes ◽  
Blood Glucose ◽  
Mitochondrial Dysfunction ◽  
Glucose Concentration ◽  
Alloxan Diabetes ◽  
Blood Glucose Concentration ◽  
Diabetic State ◽  
Acceptable Model

Alloxan and oxidative stress, which have been detected in livers of laboratory animals shortly after in vivo alloxan administration, cause in vitro mitochondrial dysfunction, thus questioning alloxan diabetes as an acceptable model for type 1 diabetes, a model that cannot legitimately be used to investigate mitochondrial metabolism in a diabetic state. In the current study, the blood glucose concentration increased in the drug-treated group of Sprague–Dawley rats (compared with the placebo group) 45 or 60 min after alloxan treatment, whereas at 30 min the blood glucose concentration was unchanged. State 4, state 3, respiratory control, efficiency of oxidative phosphorylation, and mitochondrial ATP synthase activity, assayed using glutamate plus malate, pyruvate plus malate, or succinate as a substrate, were not negatively altered during the entire study. These results indicated that early increases of blood glucose concentration, after in vivo alloxan administration, did not lead to liver mitochondrial dysfunction, suggesting that alloxan diabetes can be used for the study of liver mitochondrial respiration in a diabetic state.

Intraportal glucose infusion and pancreatic islet blood flow in anesthetized rats

2000 ◽  
Vol 279 (4) ◽  
pp. R1224-R1229 ◽  
Author(s):  
Per-Ola Carlsson ◽  
Masanori Iwase ◽  
Leif Jansson
Keyword(s):  
Blood Flow ◽  
Blood Glucose ◽  
Portal Vein ◽  
Insulin Release ◽  
Pancreatic Islet ◽  
Glucose Concentration ◽  
Blood Glucose Concentration ◽  
Islet Blood Flow ◽  
Blood Flow Increase ◽  
Selective Increase

The aim of the study was to evaluate whether a selective increase in portal vein blood glucose concentration can affect pancreatic islet blood flow. Anesthetized rats were infused (0.1 ml/min for 3 min) directly into the portal vein with saline, glucose, or 3- O-methylglucose. The infused dose of glucose (1 mg · kg body wt−1 · min−1) was chosen so that the systemic blood glucose concentration was unaffected. Intraportal infusion of d-glucose increased insulin release and islet blood flow; the osmotic control substance 3- O-methylglucose had no such effect. A bilateral vagotomy performed 20 min before the infusions potentiated the islet blood flow response and also induced an increase in whole pancreatic blood flow, whereas the insulin response was abolished. Administration of atropine to vagotomized animals did not change the blood flow responses to intraportal glucose infusions. When the vagotomy was combined with a denervation of the hepatic artery, there was no stimulation of islet blood flow or insulin release after intraportal glucose infusion. We conclude that a selective increase in portal vein blood glucose concentration may participate in the islet blood flow increase in response to hyperglycemia. This effect is probably mediated via periarterial nerves and not through the vagus nerve. Furthermore, this blood flow increase can be dissociated from changes in insulin release.

scholarly journals In Vitro & In Vivo Anti-Hyperglycemic Potential of Saponins Cake and Argan Oil from Argania spinosa

Foods ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 1078
Author(s):  
Rabie Kamal ◽  
Mourad Kharbach ◽  
Yvan Vander Heyden ◽  
Huiwen Yu ◽  
Abdelaziz Bouklouze ◽  
...  
Keyword(s):  
Body Weight ◽  
Blood Glucose ◽  
Glucose Concentration ◽  
Blood Glucose Concentration ◽  
Chemical Properties ◽  
Diabetic Mice ◽  
Argania Spinosa ◽  
Argan Oil

The Argan tree (Argania spinosa. L) is an evergreen tree endemic of southwestern Morocco. For centuries, various formulations have been used to treat several illnesses including diabetes. However, scientific results supporting these actions are needed. Hence, Argan fruit products (i.e., cake byproducts (saponins extract) and hand pressed Argan oil) were tested for their in-vitro anti-hyperglycemic activity, using α-glucosidase and α-amylase assays. The in-vivo anti-hyperglycemic activity was evaluated in a model of alloxan-induced diabetic mice. The diabetic animals were orally administered 100 mg/kg body weight of aqueous saponins cake extract and 3 mL/kg of Argan oil, respectively, to evaluate the anti-hyperglycemic effect. The blood glucose concentration and body weight of the experimental animals were monitored for 30 days. The chemical properties and composition of the Argan oil were assessed including acidity, peroxides, K232, K270, fatty acids, sterols, tocopherols, total polyphenols, and phenolic compounds. The saponins cake extract produced a significant reduction in blood glucose concentration in diabetic mice, which was better than the Argan oil. This decrease was equivalent to that detected in mice treated with metformin after 2–4 weeks. Moreover, the saponins cake extract showed a strong inhibitory action on α-amylase and α-glucosidase, which is also higher than that of Argan oil.

scholarly journals Noninvasive In Vivo Estimation of Blood-Glucose Concentration by Monte Carlo Simulation

Sensors ◽  
2021 ◽  
Vol 21 (14) ◽  
pp. 4918
Author(s):  
Chowdhury Azimul Haque ◽  
Shifat Hossain ◽  
Tae-Ho Kwon ◽  
Ki-Doo Kim
Keyword(s):  
Monte Carlo ◽  
Blood Glucose ◽  
Glucose Concentration ◽  
Blood Glucose Concentration ◽  
Synthetic Data ◽  
Real Data ◽  
Pearson's R ◽  
Blood Glucose Concentrations ◽  
Finger Model

Continuous monitoring of blood-glucose concentrations is essential for both diabetic and nondiabetic patients to plan a healthy lifestyle. Noninvasive in vivo blood-glucose measurements help reduce the pain of piercing human fingertips to collect blood. To facilitate noninvasive measurements, this work proposes a Monte Carlo photon simulation-based model to estimate blood-glucose concentration via photoplethysmography (PPG) on the fingertip. A heterogeneous finger model was exposed to light at 660 nm and 940 nm in the reflectance mode of PPG via Monte Carlo photon propagation. The bio-optical properties of the finger model were also deduced to design the photon simulation model for the finger layers. The intensities of the detected photons after simulation with the model were used to estimate the blood-glucose concentrations using a supervised machine-learning model, XGBoost. The XGBoost model was trained with synthetic data obtained from the Monte Carlo simulations and tested with both synthetic and real data (n = 35). For testing with synthetic data, the Pearson correlation coefficient (Pearson’s r) of the model was found to be 0.91, and the coefficient of determination (R2) was found to be 0.83. On the other hand, for tests with real data, the Pearson’s r of the model was 0.85, and R2 was 0.68. Error grid analysis and Bland–Altman analysis were also performed to confirm the accuracy. The results presented herein provide the necessary steps for noninvasive in vivo blood-glucose concentration estimation.

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