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Results for “fatty liver”

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At least 19 recordsLinked to original sources
PubMed1977

Fatty liver induced in Zucker "fatty" (ff) rats by a semisynthetic diet rich in sucrose.

A new fatty liver model is described in which heredity plays a major role. A marked fatty liver develops when the homozygous mutant Zucker rat (ff or "fatty") is fed a semi-synthetic diet enriched in sucrose. Lean littermates do not develop fatty livers on this experimental diet. Even old ff rats do not develop fatty livers on chow; the experimental diet is required. The fatty liver is described, including light microscopic and preliminary electron microscopic observations.

Animals↗
PubMed1977

Fatty liver induced in Zucker "fatty" (ff) rats by a semisynthetic diet rich in sucrose.

A new fatty liver model is described in which heredity plays a major role. A marked fatty liver develops when the homozygous mutant Zucker rat (ff or "fatty") is fed a semisynthetic diet enriched in sucrose. Lean littermates do not develop fatty liver on this experimental diet. Even old ff rats do not develop fatty livers on chow; the experimental diet is required. The fatty liver is described, including light microscopic and preliminary electron microscopic observations.

Animals↗
PubMed1978

Biotin deficiency and liver metabolism in relation to fatty liver and kidney syndrome.

Varying degrees of biotin deficiency were induced by adding freeze-dried, raw egg white to the diet of broiler chicks. Aspects of liver metabolism were studied with reference to fatty liver and kidney syndrome. Mortality was low with 11.8 g egg white/kg diet, or less, but with 17.7 g/kg or more, mortality was very high. High mortality was observed with less than 0.33 microgram biotin/g liver. Associated with low concentrations of liver biotin were substantial increases in liver weight and lipid content in starved birds. The increased liver lipid content was not observed in birds fed ad libitum. The increased liver lipid content in biotin-deficient, starved birds was not reflected in the specific activities of hepatic lipogenic enzymes or hepatic lipogenesis in vivo measured by the incorporation of tritium from 3H-labelled water into liver lipid. Biotin deficiency affected the specific activities of the biotin-requiring enzymes, pyruvate carboxylase and acetyl CoA carboxylase, differently; the latter was unaffected whereas the former decreased concomitantly with liver biotin concentration.

Animals↗
PubMed2026

Ovarian H3K27ac remodeling is associated with impaired follicular development in laying hens with fatty liver hemorrhagic syndrome.

Fatty liver hemorrhagic syndrome (FLHS) is a metabolic disease of laying hens that reduces egg production and is accompanied by reproductive impairment, but the ovarian regulatory mechanisms that connect nutritional stress to follicular dysfunction remain unclear. This study examined whether active chromatin remodeling in the ovary is associated with FLHS induced by a high-energy, low-protein (HELP) diet. Hy-Line Brown hens were assigned to a basal diet or HELP diet, and ovarian tissue was collected for histone H3 lysine 27 acetylation (H3K27ac) chromatin immunoprecipitation sequencing and RNA sequencing. The HELP diet reduced laying performance and the numbers of small yellow and hierarchical follicles, indicating compromised follicular development. Genome-wide H3K27ac profiling identified 2,111 regions with lower acetylation and 1,707 regions with higher acetylation in FLHS ovaries. Genes linked to differential H3K27ac regions were enriched in pathways related to oocyte meiosis, cell cycle control, FoxO signaling, gonadotropin-releasing hormone signaling, and steroid hormone biosynthesis. RNA sequencing identified 341 differentially expressed genes, with a predominance of downregulated genes. Integration of chromatin and transcriptome data highlighted folliculogenesis-related genes, including FGF1, FGF9, and MMP10, that showed reduced H3K27ac enrichment together with decreased expression. Super-enhancer analysis further identified 131 regions with reduced H3K27ac signal in FLHS ovaries, including regions located near PCNA and RAP1A, two genes involved in cellular proliferation and survival signaling. Motif enrichment of differential H3K27ac regions implicated Fos, SF-1/NR5A1, and GATA-4 as candidate transcriptional regulators. These findings indicate that HELP diet-induced FLHS is associated with broad attenuation of active ovarian regulatory elements and reduced expression of genes required for follicle growth, tissue remodeling, and steroidogenic function. The study provides an ovarian epigenomic framework for understanding reproductive decline in FLHS-affected laying hens.

Fatty liver hemorrhagic syndrome↗
PubMed1979

Fatty liver hepatitis and cirrhosis in obese patients.

Liver function and liver biopsy findings were studied in a selected group of 29 overweight patients. Fatty liver, fatty hepatitis, fatty fibrosis and fatty cirrhosis were seen with equal frequency. Diabetes was also present with an equal incidence in each of these four pathologic groups. Lipoprotein abnormalities, particularly type IV hyperlipoproteinemia, were found mostly in the two groups with the lesions with less fibrosis (fatty liver and fatty hepatitis). The pathologic picture resembled that of alcohol and postjejunoileal bypass-induced liver diseases suggesting a common denominator in these three conditions.

Adolescent↗
PubMed1976

An ultrastructural study of the liver, kidney and myocardium in the fatty liver and kidney syndrome in the fowl.

In birds with the fatty liver and kidney syndrome large lipid droplets measuring up to 4 mum in diameter were observed in increased numbers in liver, kidney and heart muscle, particularly in the livers and the proximal convoluted tubules (PCT) of the kidneys. In the hepatocytes and the PCT a much smaller type of lipid particle (LP) was also observed, both intracellularly within the cisternae of the Golgi-ER system and outside the plasma membranes in the space between neighbouring parenchymal cells, within the space of Disse and among the basal processes of the PCT. The origin of these LP is discussed.

Animals↗
PubMed1979

Ultrastructure of lipogranulomas in human fatty liver.

Lipogranulomas from severe fatty livers due to alcoholism, diabetes or overweight were examined in the electron microscope. When a fat droplet protrudes through the cell membranes of a liver cell histiocytes and lymphyocytes settle around it, and a lipogranuloma is formed. Remnants of the liver cell may be seen between the fat droplet and the histiocytes. It is confirmed that the fat droplets are situated extracellularly in the fully developed lipogranulomas.

Cell Nucleus↗
PubMed1977

Abnormal mitochondria in hepatocytes in human fatty liver.

Liver biopsies from fatty livers in thirty patients whose daily alcohol consumption was excessive, or they were in a diabetic state or overweight, and liver biopsies from seven control patients not presenting the above disorders, were studied by light microscopy 0.75 micronm EPON embedded, toluidine blue stained sections, and electron microscopy. Abnormal mitochondria were rarely found in normal liver tissue and, if present, they were found only in periportal hepatocytes. The frequency of hepatocytes containing abnormal mitochondria was significantly higher in fatty liver than in normal liver (p less than 0.01). These cells were usually localized periportally, practically never in the centre of the lobule (p less than 0.01). The occurrence of abnormal mitochondria was not correlated with the degree of steatosis, and the increase in number of abnormal mitochondria was equally high in alcoholists, diabetics, and overweight subjects. The ultrastructural appearance and the periportal localization suggest a hyperfunction of the mitochondria, which may prevent a development of steatosis in these areas.

Alcoholism↗
PubMed1979

The radiographic signs of fatty liver.

Ninteen cases of radiographically visible fatty liver are presented. The four radiographic signs are muscle-fat interface, fat-water interface, a visible hollow viscus wall, and blurring of the medial margin of the right properitoneal fat stripe. The last sign, the authors believe, is the earliest radiographic change in developing fatty liver. In one case, isolated glycogen synthetase deficiency was the cause of fatty liver; this finding, to the authors' knowledge, has not previously been described. The value of the chest radiograph in diagnosing fatty liver is stressed.

Adolescent↗
PubMed1977

Role and mechanism of peripheral fatty acid mobilization in 2-mercaptoethanol-induced fatty liver.

2-Mercaptoethanol-induced fatty liver involves an increased free fatty acid mobilization which is primarily due to an inhibition of free fatty acid reesterification in adipose tissue. Furthermore, increased free fatty acid mobilization as well as fatty liver induction are not induced by 2-mercaptoethanol per se but result most probably from 2-mercaptoacetate through oxidation of 2-mercaptoethanol.

Adenosine Triphosphate↗
PubMed1979

Follow-up study on patients with non-alcoholic and non-diabetic fatty liver.

From a group of 424 patients with histologically verified fatty liver 92 patients without diabetes mellitus and alcohol abuse were subjected to follow-up examination for 3 1/2 years. 56 patients underwent second liver biopsy at this time; 20 of these patients had shown marked fatty liver at the initial liver biopsy examination. These 20 patients with marked fatty liver and 25 further patients with moderarte fatty liver could be followed up 5 and 7 1/2 years later; the clinical examination, the various liver function tests, liver scan and blind liver biopsy did not show any evidence of progression of fatty liver towards chronic inflammatory liver disorders or precirrhotic states. This clinical study therefore suggests the harmlessness of non-alcoholic fatty liver.

Adult↗
PubMed1978

[Clinical and experimental studies on changes in lysosomal enzyme activity in fatty livers (author's transl)].

In order to examine a role of lysosomes in the pathogenesis of fatty livers, analysis was made on possible etiologic factors, clinical signs and symptoms as well as laboratory data of routine liver function tests in 32 subjects with fatty livers. Of 18 cases, enzyme activities of serum acid phosphatase (Acp), beta-glucuronidase (betaG) and n-acetyl-beta-glucosaminidase (nbetaG) were measured and compared with those obtained in 20 normal subjects. Subjective symptoms were observed in 75% of the cases examined, liver swelling in 56%, positive GOT, GPT and BSP retention were in 59, 75 and 68%, respectively. The activity of serum lysosomal enzymes such as Acp, betaG and nbetaG were significantly increased and their incidence was 28, 89 and 78%, respectively. In animal experiments, activities of these enzymes in both serum and liver homogenate were examined in rats with choline-deficient, ethionine-treated, and alcoholic fatty livers. Results obtained were as follows: 1) Lysosomal enzyme activity in sera and livers of choline-deficient rats showed a significant decrease in lysosome-rich fraction and a significant increase in supernatant fraction and sera. 2) The enzyme activity in ethionine-treated rats decreased significantly in lysosome-rich fraction and tended to increase in supernatant fraction. The activity of betaG in sera increased markedly. 3) In rats given ethanol for 4 weeks, the enzyme activity of sera and liver homogenates significantly increased in lysosome-rich fraction. These results indicate that the analysis of serum lysosomal enzyme activity, in the light of clinical features and laboratory data of routine liver function tests, is useful for the diagnosis of the fatty liver. A discussion is given of a possible mode of variation of lysosomal enzymes in rats with fatty livers.

Acid Phosphatase↗
PubMed1977

Role of estrogen as a cause of fatty liver hemorrhagic syndrome.

Fatty liver-hemorrhagic syndrome (FLHS), a nutritional disorder previously reported only in laying chickens was induced in immature male and female chickens, 11 weeks of age, of broiler and egg-laying breeds. Force-feeding three times a day for 21 days, amounts of feed equal to 125% and 150% of ad libitum intake, produced a gradient response in hepatic steatosis (measured by percentage of fat in the liver, and the ratio of fat to the fat-free dry weight), but not FLHS. Intramuscular injection of beta-estradiol-17-dipropionate at 2 mg/kg body weight, three times weekly for 21 days, produced a gradient response in hemorrhagic score and an increase in ad libitum feed intake. There was no significant difference between sex or breed in the score values used to evaluate FLHS, but females of both breeds accumulated significantly more fat in the liver than males. Testosterone dipropionate at 25 mg/kg of body weight, injected three times per week in immature females force-fed at the 150% level, produced increases in food intake and liver fat as did estrogen, but no hepatic hemorrhaging. The data implicate estrogen as a factor in the production of FLHS along with the necessity for the chicken to be in a positive energy balance creating sufficient hepatic fat for FLHS to occur.

Animals↗
PubMed1978

Lipid metabolism in laying hens. The relationship of plasma lipids and liver fatty acid synthetase activity to changes in liver composition.

Plasma and liver samples were taken from a random sample of caged commercial hybrid layer hens which had been in egg production for fifteen months. The concentration of plasma and liver lipids and the activity of liver fatty acid synthetase (FAS) were measured in laying hens with liver weight of 20 to 53 g. Liver total lipid, water, non-lipid, and cytosolic fractions, which are the four major liver components, increased linearly with respect to wet liver weight. FAS activity increased with all liver components. Accumulation of lipid in the liver did not inhibit FAS activity. Total cholesterol, free cholesterol, esterified cholesterol, triglycerides, and phosphorous were measured on each plasma sample. Multiple regression analysis showed that all plasma lipids, except cholesterol esters, were related cubically with increasing wet liver weight and cytosolic protein.

Animals↗
PubMed1977

Fatty liver in patients with moderate alcohol consumption, diabetes mellitus and overweight.

A relationship between the occurrence of fatty liver and moderate alcohol intake, maturity onset diabetes, overweight--and combinations of these three factors--was searched for in 112 patients. Fifty-three of 59 patients with moderate alcohol consumption, 49 of 57 overweight patients, and 42 of 51 diabetic patients had fatty liver. Patients who had a moderate alcohol consumption or suffered from a combination of diabetes and overweight were found to have a significantly higher frequency and degree of fatty liver than patients in the control group. Diabetes alone, and overweight alone were not significantly related to fatty liver. Whether the diabetic state was overt of latent, there was no influence on the frequency or degree of fatty liver. A correlation between the degree of overweight and the degree of fatty liver was found only in the group of overweight patients with moderate alcohol consumption. The degree of fatty liver produced by the combination of overweight and diabetes was not significantly increased by moderate alcohol consumption.

Alcoholism↗