Electron microscopic study of liver fibrosis associated with diabetes mellitus

Balázs, M; Halmos, T

doi:10.1016/s0232-1513(85)80037-2

Cited by 16 publications

(15 citation statements)

References 24 publications

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“…Similar conditions were reported by other studies [22,33,41]. On the other hand, Guven et al, [29] did not observe marked peri-sinusoidal fibrosis or increase in doi: 10.7243/2055-091X-4-1 collagen fibers in the diabetic liver.…”

Section: Discussionsupporting

confidence: 88%

Study on morphological changes induced by aspartame on liver of normal and diabetic male albino rats

Khidr¹,

El‐Sokkary²,

Saleh³

2017

J Histol Histopathol

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Background: This work was designed to study the histological and ultrastructure abnormalities in the liver induced by high dose of aspartame (ASP) in normal and diabetic rats. Methods: Forty adult male rats were used in this study and divided into four groups with ten animals for each. Rats of group one served as controls and administered vehicle. Rats of group two were administered aspartame (ASP) at 200 mg/Kg bwt once daily for 4 weeks. Rats of group three (D) were given streptozotocin (STZ) one time at a dose of 70 mg/Kg bwt. The fourth group (D+ASP) was represented by diabetic rats administered with aspartame at 200 mg/Kg bwt. Results: The most obvious changes that occurred in the liver treated rats were destruction of hepatocytes which led to necrosis, the appearance of large areas of rarified cytoplasm separating dense areas of cellular organelles, disorganization of cellular organelles, increase in collagenous fibers and depletion of polysaccharides (carbohydrate content of hepatocytes). Conclusions: Our results indicated that ASP administration may be responsible for the morphological alternations of liver in both normal and diabetic animals.

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Section: Discussionsupporting

confidence: 88%

Study on morphological changes induced by aspartame on liver of normal and diabetic male albino rats

Khidr¹,

El‐Sokkary²,

Saleh³

2017

J Histol Histopathol

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“…The hepatocyte nuclei are usually enlarged and sometimes showed irregular contours and intranuclear inclusions [6]. Cytoplasmic changes observed in the STZ-induced diabetes included markedly depressed glycogen granules and poorly developed rough endoplasmic reticulum [38].…”

Section: Discussionmentioning

confidence: 99%

“…Hepatobiliary disorders, such as inflammation, necrosis or fibrosis of non-alcoholic fatty liver disease, cirrhosis, hepatocellular carcinoma, hepatitis C, acute liver failure, and cholelithiasis are complications of diabetes [6,7].Therefore combating diabetes mellitus goes far beyond mere glycaemic control.…”

Section: Introductionmentioning

confidence: 99%

<i>Ocimum Gratissimum</i> Linn Causes Dose Dependent Hepatotoxicity in Streptozotocin-Induced Diabetic Wistar Rats

Onaolapo

2012

Macedonian Journal of Medical Sciences

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Aim: Hepatoprotective effects of Ethanolic extract Ocimum gratissimum leaves (O. gratissimum) in streptozotocin-induced diabetic rats was studied. Material and Methods:Thirty-six adult rats were assigned into six groups (A, B, C, D, E and F) of six rats each. Group A was the control, while diabetes was induced in groups B, C, D, E and F. Fasting blood glucose was determined and rats with blood glucose concentration >18.0 mmol/L were considered diabetic. Group A (non diabetic control) and F (diabetic control) received normal saline orally, group B received a Metformin at 25 mg/kg while groups C, D and E had O. gratissimum at 400, 600 and 800 mg/ kg. Treatment was daily for a period of 28 days for all groups. Fasting blood glucose was monitored weekly, serum levels of Alanine transaminase (ALT) and Aspartate transaminase (AST) were measured on day twenty eight. Animals were sacrificed, liver sections processed for histological study. Statistical analysis was carried out using a one way ANOVA followed by a post-hoc test.Results: Results showed reduction in blood sugar and increase in biochemical and histologic markers of hepatic injury. Conclusion:Ethanolic extract of O. gratissimum causes dose dependent hepatic injury despite its glucose lowering ability.

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“…"Skinner et al, 1966Pfeifer and Alterman, 1979;Johannessen, 1979;Pfeifer et al, 1983. "Droz et al, 1984Phillips et al, 198713. Extensive perisinusoidal fibrosis: Impairment of exchanges 'Popper and Acs, 1985;Lough et al, 1987;Brouwer et al, 1988;Jones and Summerfield, 1988. (Bernuau et al, 1982;Balazs, 1985;Latry, 1987), malignant liver diseases3 (in nontumoral tissue during hepatocellular carcinoma and liver metastases) (Bioulac-Sage et al, 1988b), non-Hodgkin's malignant lymphoma (Bioulac-Sage et al, 1988;Zafrani, 19881, miscellaneous4 (Bioulac-Sage et al, 1988) (intestinal and biliary fistulae, alcohol, hepatocellular damage etc.). -In primary biliary cirrhosis, decreased serum retinol binding protein (s-RBP) and serum vitamin A levels with normal or elevated liver vitamin A level are associated with normal s-RBP and cellular retinol binding protein (CRBP) immunostaining of hepatocytes and increased CRBP of PS whose relative number is increased (Nyberg et al, 1988).…”

Section: Alcoholic Liver Disease (Except Cirrhosis)mentioning

confidence: 99%

Fine structure of hepatic sinusoids and sinusoidal cells in disease

Bail

Bioulac‐Sage

Senuita

et al. 1990

J. Elec. Microsc. Tech.

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Liver sinusoids are special capillaries that are limited by fenestrated endothelial cells, without a genuine basement membrane, surrounded by perisinusoidal cells storing vitamin A, and harbouring Kupffer cells and pit cells, resident macrophages, and large granular lymphocytes, respectively. Each nonparenchymal cell and parenchymal cell of the liver interacts with all others and with the extracellular matrix. Therefore, the functional ability of each cell is constantly being modified by the metabolic activity of the others. Human liver biopsies (132), needle or surgical, perfusion-fixed with glutaraldehyde and processed for transmission electron microscopy (TEM), and occasionally for scanning electron microscopy (SEM), were examined. The study included liver diseases (such as alcoholic liver diseases, benign and malignant liver tumors, cholestasis of various origins, fulminant hepatitis, acute rejection after orthotopic liver transplantation, Budd-Chiari syndrome), as well as general or extrahepatic diseases (such as diabetes, hemochromatosis, hypervitaminosis A, various hematological disorders), and normal controls. Ultrastructural abnormalities are described and illustrated under two different headings: 1) elementary lesions of sinusoidal cells (endothelial, Kupffer, perisinusoidal and pit cells), nonsinusoidal cells (in the space of Disse and/or in the lumen), the extracellular matrix; and 2) the major pathological entities including perisinusoidal fibrosis, capillarization of sinusoids, sinusoidal dilatation, and peliosis. In the discussion, an overview of the major abnormalities reported in the literature is presented, and some specific questions regarding 1) perisinusoidal fibrosis in liver with normal histology, 2) the overload of perisinusoidal cells with lipids in non-hypervitaminosis A intoxication and 3) the etiological relationship of sinusoidal dilatation, peliosis, perisinusoidal fibrosis, or sinusoidal tumors with drugs and toxic compounds are discussed. In the event that lesions are not specific to any diagnosis, the knowledge of the ultrastructure of sinusoids is extremely useful from the perspective of the liver as an ecosystem.

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Electron microscopic study of liver fibrosis associated with diabetes mellitus

Cited by 16 publications

References 24 publications

Study on morphological changes induced by aspartame on liver of normal and diabetic male albino rats

Study on morphological changes induced by aspartame on liver of normal and diabetic male albino rats

<i>Ocimum Gratissimum</i> Linn Causes Dose Dependent Hepatotoxicity in Streptozotocin-Induced Diabetic Wistar Rats

Fine structure of hepatic sinusoids and sinusoidal cells in disease

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