Changes in Germinal Tissue and Leydig Cells Correlated with Ethanol Consumption in Males with and without Liver Disease

1984 ◽  
pp. 155-158 ◽  
Author(s):  
P. J. Karhunen ◽  
A. Penttilä ◽  
K. Liesto ◽  
A. Männikkö ◽  
M. Välimäki ◽  
...  
Keyword(s):  
Liver Disease ◽  
Leydig Cells ◽  
Ethanol Consumption ◽  
Germinal Tissue

scholarly journals Light-to-Moderate Ethanol Feeding Augments AMPK-α Phosphorylation and Attenuates SREBP-1 Expression in the Liver of Rats

2013 ◽  
Vol 16 (2) ◽  
pp. 342 ◽  
Author(s):  
Srinivas Nammi ◽  
Basil D Roufogalis
Keyword(s):  
Liver Disease ◽  
Protein Expression ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Metabolic Disorders ◽  
Ethanol Consumption ◽  
Epidemiological Studies ◽  
Ethanol Treatment ◽  
Ethanol Feeding ◽  
Coa Reductase

Purpose: Fatty liver disease, a hepatic manifestation of metabolic syndrome, is one of the major causes of chronic liver diseases. Epidemiological studies suggest that regular light-to-moderate ethanol consumption lowers the risk of developing metabolic disorders including dislipidemia, insulin resistance, type 2 diabetes and fatty liver disease. However, the mechanism(s) of the protective effect of light-to-moderate ethanol consumption on the liver remains unknown. Methods: In the present study, we investigated the effects of light (6%, 0.94 g/kg/day) and moderate (12%, 1.88 g/kg/day) ethanol feeding in rats for 3 weeks on the circulating and hepatic biochemical profiles and on the hepatic protein expression and phosphorylation status of adenosine monophosphate-activated protein kinase-α (AMPK-α) and other down-stream targets of this enzyme including sterol regulatory element-binding protein-1 (SREBP-1), SREBP cleavage-activating protein (SCAP) and 3-hydroxy-3-methyl-glutaryl-CoA reductase (HMG-CoA reductase). Results: Despite no significant difference in food-intake among the groups, light ethanol treatment significantly increased the body weight compared to control rats. Serum glucose, insulin, total cholesterol, triglycerides, phospholipids and hepatic cholesterol and triglycerides were not significantly different among the groups. However, serum free fatty acids were significantly reduced with light ethanol treatment. Both light and moderate ethanol treatment significantly increased the hepatic levels of phosphorylated AMPK-α protein and this was associated with significant reduction of SREBP-1 protein expression, suggesting an enhanced fatty acid oxidation. In addition, light ethanol treatment significantly decreased the SCAP protein expression in the liver. However, liver HMG-CoA protein expression was not significantly different with ethanol consumption. Conclusion: Chronic light-to-moderate ethanol consumption increased AMPK activation which was associated with decreased expression of SREBP-1 and SCAP in the liver. Thus, our studies provide mechanistic evidence for the earlier epidemiological studies that indicate light-to-moderate ethanol intake lowers the risk of development of fatty liver disease and other metabolic disorders. Our studies demonstrate that the protective effects of light-to-moderate ethanol arise at least in part by increased phosphorylation of AMPK-α and decreased SREBP-1 expression in the liver. Further studies are warranted to determine the effects of light-to-moderate ethanol on intracellular up-stream and down-stream targets of AMPK and also on the implications of light-to-moderate ethanol in protecting non-alcoholic fatty liver disease. This article is open to POST-PUBLICATION REVIEW. Registered readers (see “For Readers”) may comment by clicking on ABSTRACT on the issue’s contents page.

199 THE EFFECT OF AN ALCOHOL CONTRACT’ ON ETHANOL CONSUMPTION AFTER TRANSPLANTATION FOR ALCOHOLIC LIVER DISEASE

2012 ◽  
Vol 56 ◽  
pp. S85
Author(s):  
S. Kendrick ◽  
A. Elsharkawy ◽  
S. Latimer ◽  
M. Hudson ◽  
S. Masson
Keyword(s):  
Liver Disease ◽  
Alcoholic Liver Disease ◽  
Ethanol Consumption

Ethanol Consumption, Amino Acid and Glutathione Blood Levels in Patients With and Without Chronic Liver Disease

1999 ◽  
Vol 23 (11) ◽  
pp. 1780-1784 ◽  
Author(s):  
C. Loguercio ◽  
F. Vecchio Blanco ◽  
V. Girolamo ◽  
D. Disalvo ◽  
G. Nardi ◽  
...  
Keyword(s):  
Liver Disease ◽  
Amino Acid ◽  
Chronic Liver Disease ◽  
Ethanol Consumption ◽  
Chronic Liver ◽  
Blood Levels

scholarly journals Nitric oxide in the pathogenesis of alcoholic liver disease

2016 ◽  
Vol 63 (2) ◽  
pp. 118-122
Author(s):  
Ruxandra Deliu ◽  
◽  
Ionuţ Donoiu ◽  
Tudorel Ciurea ◽  
◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Liver Disease ◽  
Endothelial Dysfunction ◽  
Hepatic Steatosis ◽  
Alcoholic Liver Disease ◽  
Alcoholic Hepatitis ◽  
Ethanol Consumption ◽  
Nitric Oxide Synthesis ◽  
Common Condition ◽  
Therapeutic Implications

Alcoholic liver disease is the most common condition associated with ethanol consumption and includes three forms of injury with gradually increasing severity: hepatic steatosis, alcoholic hepatitis and cirrhosis. The complex pathogenesis of this disease includes endothelial dysfunction which comprises as central factor nitric oxide. Synthesis of nitric oxide by the three types of nitric oxide synthases is modulated by many factors with pathogenic and potentially therapeutic implications in alcoholic liver disease.

Crystalloid Inclusions in Hepatocyte Mitochondria and Their Similarity to Cytoplasmic Crystalloids

1974 ◽  
Vol 32 ◽  
pp. 198-199
Author(s):  
Odell T. Minick ◽  
Hidejiro Yokoo
Keyword(s):  
Liver Disease ◽  
Alcoholic Liver Disease ◽  
Special Interest ◽  
Structural Variations ◽  
Mitochondrial Alterations ◽  
The Matrix ◽  
Crystalloid Inclusions ◽  
Liver Biopsies

Mitochondrial alterations were studied in 25 liver biopsies from patients with alcoholic liver disease. Of special interest were the morphologic resemblance of certain fine structural variations in mitochondria and crystalloid inclusions. Four types of alterations within mitochondria were found that seemed to relate to cytoplasmic crystalloids.Type 1 alteration consisted of localized groups of cristae, usually oriented in the long direction of the organelle (Fig. 1A). In this plane they appeared serrated at the periphery with blind endings in the matrix. Other sections revealed a system of equally-spaced diagonal lines lengthwise in the mitochondrion with cristae protruding from both ends (Fig. 1B). Profiles of this inclusion were not unlike tangential cuts of a crystalloid structure frequently seen in enlarged mitochondria described below.

Ultrastructural Study of Human Testicular Biopsies in Infertility

1976 ◽  
Vol 34 ◽  
pp. 156-157
Author(s):  
Shirley Siew ◽  
Philip Troen ◽  
Howard R. Nankin
Keyword(s):  
Electron Microscopy ◽  
Transmission Electron Microscopy ◽  
Basement Membrane ◽  
Leydig Cells ◽  
Clinical Evidence ◽  
Young Male ◽  
Germinal Epithelium ◽  
Transmission Electron ◽  
Age Range ◽  
Male Subjects

Testicular biopsies were obtained from six young male subjects (age range 24-33) who complained of infertility and who had clinical evidence of oligospermia. This was confirmed on histological examination which showed a broad spectrum from profound hypospermatogenesis to relatively normal appearing germinal epithelium. Thickening of the tubular walls was noted in half of the cases and slight peritubular fibrosis in one. The Leydig cells were reported as normal or unremarkable.Transmission electron microscopy showed that the thickening of the supporting tissue of the germinal epithelium was caused more by an increase in the thickness of the layers of the lamina propria than of the tubular wall itself. The changes in the basement membrane of the tubular wall consisted mostly of a greater degree of infolding into the tubule and some reduplication which gave rise to a multilayered appearance.

The structure of the gills of the axolotl, Ambystoma mexicanum

1987 ◽  
Vol 45 ◽  
pp. 824-825
Author(s):  
Mohinder S. Jarial
Keyword(s):  
Leydig Cells ◽  
Secretory Granules ◽  
Light And Electron Microscopy ◽  
Cell Types ◽  
Ambystoma Mexicanum ◽  
Basal Cells ◽  
Granular Cells ◽  
Gill Filaments ◽  
Mitotic Figures ◽  
Apical Membranes

The axolotl is a strictly aquatic salamander in which the larval external gills are retained throughout life. The external gills of the adult axolotl have been studied by light and electron microscopy for ultrastructural evidence of ionic transport. The thin epidermis of the gill filaments and gill stems is composed of 3 cell types: granular cells, the basal cells and a sparce population of intervening Leydig cells. The gill epidermis is devoid of muscles, and no mitotic figures were observed in any of its cells.The granular cells cover the gill surface as a continuous layer (Fig. 1, G) and contain secretory granules of different forms, located apically (Figs.1, 2, SG). Some granules are found intimately associated with the apical membrane while others fuse with it and release their contents onto the external surface (Fig. 3). The apical membranes of the granular cells exhibit microvilli which are covered by a PAS+ fuzzy coat, termed “glycocalyx” (Fig. 2, MV).

Smooth endoplasmic reticulum in perfusion and immersion-fixed Leydig cells

1990 ◽  
Vol 48 (3) ◽  
pp. 82-83
Author(s):  
R.T.F. Bernard ◽  
R.H.M. Cross
Keyword(s):  
Endoplasmic Reticulum ◽  
Electron Microscope ◽  
Steroid Hormones ◽  
Transmission Electron Microscope ◽  
Leydig Cells ◽  
Smooth Endoplasmic Reticulum ◽  
Random Mixture ◽  
Transmission Electron

Smooth endoplasmic reticulum (SER) is involved in the biosynthesis of steroid hormones, and changes in the organisation and abundance of this organelle are regularly used as indicators of changes in the level of steroidogenesis. SER is typically arranged as a meshwork of anastomosing tubules which, with the transmission electron microscope, appear as a random mixture of cross, oblique and longitudinal sections. Less commonly the SER appears as swollen vesicles and it is generally suggested that this is an artefact caused during immersion fixation or during immersion of poorly-perfused tissue.During a previous study of the Leydig cells of a seasonally reproducing bat, in which tissue was fixed by immersion, we noted that tubular SER and vesicular SER often occured in adjacent cells and sometimes in the same cell, and that the abundance of the two types of SER changed seasonally. We came to doubt the widelyheld dogma that vesicular SER was an artefact of immersion fixation and set out to test the hypothesis that the method of fixation does not modify the ultrastructure of the SER.

Healing gone wrong: convergence of hemostatic pathways and liver fibrosis?

2020 ◽  
Vol 134 (16) ◽  
pp. 2189-2201
Author(s):  
Jessica P.E. Davis ◽  
Stephen H. Caldwell
Keyword(s):  
Wound Healing ◽  
Liver Disease ◽  
Hepatic Fibrosis ◽  
Cell Activation ◽  
Stellate Cell ◽  
Factor Xa ◽  
Clinical Trial Data ◽  
Chronic Liver ◽  
Healing Response ◽  
Wound Healing Response

Abstract Fibrosis results from a disordered wound healing response within the liver with activated hepatic stellate cells laying down dense, collagen-rich extracellular matrix that eventually restricts liver hepatic synthetic function and causes increased sinusoidal resistance. The end result of progressive fibrosis, cirrhosis, is associated with significant morbidity and mortality as well as tremendous economic burden. Fibrosis can be conceptualized as an aberrant wound healing response analogous to a chronic ankle sprain that is driven by chronic liver injury commonly over decades. Two unique aspects of hepatic fibrosis – the chronic nature of insult required and the liver’s unique ability to regenerate – give an opportunity for pharmacologic intervention to stop or slow the pace of fibrosis in patients early in the course of their liver disease. Two potential biologic mechanisms link together hemostasis and fibrosis: focal parenchymal extinction and direct stellate cell activation by thrombin and Factor Xa. Available translational research further supports the role of thrombosis in fibrosis. In this review, we will summarize what is known about the convergence of hemostatic changes and hepatic fibrosis in chronic liver disease and present current preclinical and clinical data exploring the relationship between the two. We will also present clinical trial data that underscores the potential use of anticoagulant therapy as an antifibrotic factor in liver disease.

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