Influence of the Blood Ethanol Concentration on the Acute Ethanol-Induced Liver Triglyceride Accumulation in Rats

1974 ◽  
Vol 33 (3) ◽  
pp. 207-213 ◽  
Author(s):  
O. Johnson
Keyword(s):  
Ethanol Concentration ◽  
Liver Triglyceride ◽  
Blood Ethanol Concentration ◽  
Triglyceride Accumulation ◽  
Acute Ethanol

scholarly journals Effect of acute postexercise ethanol intoxication on the neuroendocrine response to resistance exercise

2000 ◽  
Vol 88 (1) ◽  
pp. 165-172 ◽  
Author(s):  
L. Perry Koziris ◽  
William J. Kraemer ◽  
Scott E. Gordon ◽  
Thomas Incledon ◽  
Howard G. Knuttgen
Keyword(s):  
Resistance Exercise ◽  
Ethanol Concentration ◽  
Pooled Analysis ◽  
Cortisol Concentration ◽  
Neuroendocrine System ◽  
Sympathoadrenal System ◽  
Ethanol Intoxication ◽  
Blood Ethanol Concentration ◽  
Neuroendocrine Response ◽  
Prolonged Effect

This investigation was conducted to determine the effect of postexercise ethanol intoxication (21.97 ± 1.09 mmol/l blood) on the response of selected aspects of the neuroendocrine system to a resistance exercise (Ex) session. Nine resistance-trained men (25.0 ± 1.4 yr, 179.4 ± 3.4 cm, 79.7 ± 3.3 kg) were used to compare three 3-day treatments: control, Ex, and ethanol after exercise (ExEt). Blood was collected serially from an antecubital vein before exercise, immediately after exercise, and for pooled analysis at 20–40 (2 samples), 60–120 (4 samples), and 140–300 (9 samples) min after exercise on day 1 and in the morning (2 samples each) on days 2 and 3. Ethanol did not increase circulating epinephrine, norepinephrine, or cortisol concentration (Cort) above Ex elevations. At 60–120 min, only ExEt Cort was greater than control Cort. Concentrations of testosterone, luteinizing hormone, and corticotropin were not affected by either treatment. It is concluded that, although this blood ethanol concentration is insufficient to acutely increase Cort above that caused by Ex alone, it appears that ethanol may have a prolonged effect beyond the Ex response. This blood ethanol concentration does not further stimulate the sympathoadrenal system during the postexercise response.

The impact of blood ethanol concentration on the classification of head injury severity in traumatic brain injury

Brain Injury ◽  
2015 ◽  
Vol 29 (13-14) ◽  
pp. 1648-1653 ◽  
Author(s):  
Pål Rønning ◽  
Per Ole Gunstad ◽  
Nils-Oddvar Skaga ◽  
Iver Arne Langmoen ◽  
Knut Stavem ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Head Injury ◽  
Injury Severity ◽  
Ethanol Concentration ◽  
Blood Ethanol Concentration ◽  
The Impact ◽  
Head Injury Severity

Inhibition of matrix metalloproteinases increases PPAR-α and IL-6 and prevents dietary-induced hepatic steatosis and injury in a murine model

2006 ◽  
Vol 291 (6) ◽  
pp. G1011-G1019 ◽  
Author(s):  
Ian P. J. Alwayn ◽  
Charlotte Andersson ◽  
Sang Lee ◽  
Danielle A. Arsenault ◽  
Bruce R. Bistrian ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Liver ◽  
Hepatic Steatosis ◽  
Essential Fatty Acid ◽  
De Novo ◽  
De Novo Lipogenesis ◽  
Resonance Spectroscopy ◽  
Liver Triglyceride ◽  
Triglyceride Accumulation ◽  
Tnf Α

Steatosis is a prominent feature of nonalcoholic fatty liver disease and a potential promoter of inflammation. Injury leading to cirrhosis is partly mediated by dysregulation of matrix protein turnover. Matrix metalloproteinase (MMP) inhibitors protect mice from lethal TNF-α induced liver injury. We hypothesized that Marimastat, a broad-spectrum MMP and TNF-α converting enzyme (TACE) inhibitor, might modulate this injury through interruption of inflammatory pathways. Triglyceride and phospholipid levels (liver, serum) and fatty acid profiles were used to assess essential fatty acid status and de novo lipogenesis as mechanisms for hepatic steatosis. Mice receiving a fat-free, high-carbohydrate diet (HCD) for 19 days developed severe fatty liver infiltration, demonstrated by histology, magnetic resonance spectroscopy, and elevated liver function tests. Animals receiving HCD plus Marimastat (HCD+MAR) were comparable to control animals. Increased tissue levels of peroxisome proliferator activated receptor-α (PPAR-α), higher levels of serum IL-6, and decreased levels of serum TNF-α receptor II were also seen in the HCD+MAR group compared with HCD-only. In addition, there was increased phosphorylation, and likely activation, of PPAR-α in the HCD+MAR group. PPAR-α is a transcription factor involved in β-oxidation of fatty acids, and IL-6 is a hepatoprotective cytokine. Liver triglyceride levels were higher and serum triglyceride and phospholipid levels lower with HCD-only but improved with Marimastat treatment. HCD-only and HCD+MAR groups were essential fatty acid deficient and had elevated rates of de novo lipogenesis. We therefore conclude that Marimastat reduces liver triglyceride accumulation by increasing fat oxidation and/or liver clearance of triglycerides. This may be related to increased expression and activation of PPAR-α or IL-6, respectively.

scholarly journals Metformin Ameliorates Ethanol-Induced Liver Triglyceride Accumulation by LKB1/AMPK/ACC Pathway

2021 ◽  
Author(s):  
Fotian Xie ◽  
Dongmei Wang ◽  
Kwok Fai So ◽  
Jia Xiao ◽  
Yi Lv
Keyword(s):  
Lipid Accumulation ◽  
Therapeutic Potential ◽  
Lipid Lowering ◽  
Liver Triglyceride ◽  
Hepatic Lipid Accumulation ◽  
Triglyceride Accumulation ◽  
Lipid Formation

Abstract Background: Hepatic lipid accumulation is one of the main pathological features of alcoholic liver disease. Metformin is an AMPK activator that has been shown to have lipid lowering effects. The purpose of this study was to investigate whether metformin had a beneficial effect on lipid accumulation in the pathogenesis of ALD.Methods: AML12 cells and male C57BL/6 mice were used to establish ALD models in vitro and in vivo, respectively. The effects of metformin on hepatocyte lipid accumulation and ALD progression in mice were detected. The role of LKB1/AMPK/ACC axis in metformin against ethanol-induced lipid accumulation was evaluated by siRNA and AAV-shRNA interference.Results: Metformin reduced the ethanol-induced lipid accumulation in AML12 cells through activating AMPK/ACC and SREBP1c and inhibiting PPARα. In addition, compared with control mice, metformin treatment inhibited ethanol-induced liver adipose accumulation and the increase of ALT and AST in serum. Interference with LKB1 attenuated the effect of metformin on ethanol-induced lipid accumulation both in vitro and in vivo.Conclusion: Metformin protects against lipid formation in ALD by activating LKB1/AMPK/ACC axis. Thus, metformin has therapeutic potential for the prevention of ALD.

Numerical treatment for studying the blood ethanol concentration systems with different forms of fractional derivatives

2020 ◽  
Vol 31 (03) ◽  
pp. 2050044 ◽  
Author(s):  
M. M. Khader ◽  
Khaled. M. Saad
Keyword(s):  
Fractional Derivatives ◽  
Ethanol Concentration ◽  
Algebraic Equations ◽  
Efficient Tool ◽  
Blood Ethanol Concentration ◽  
Fractional Models ◽  
Fractional Differential ◽  
Relative Errors ◽  
The Given ◽  
First Time

The purpose of this paper is to implement an approximate method for obtaining the solution of a physical model called the blood ethanol concentration system. This model can be expressed by a system of fractional differential equations (FDEs). Here, we will consider two forms of the fractional derivative namely, Caputo (with singular kernel) and Atangana–Baleanu–Caputo (ABC) (with nonsingular kernel). In this work, we use the spectral collocation method based on Chebyshev approximations of the third-kind. This procedure converts the given model to a system of algebraic equations. The implementation of the proposed method to solve fractional models in ABC-sense is the first time. We satisfy the efficiency and the accuracy of the given procedure by evaluating the relative errors. The results show that the implemented technique is an easy and efficient tool to simulate the solution of such models.

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