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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↗
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↗
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↗
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↗
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↗
PubMed1979

[Experimental and clinical studies on the mechanism of alcoholic fatty liver (author's transl)].

In order to clarify the mechanism of alcoholic fatty liver, rats were reared with alcohol diet from adult, foetal or weanling periods. When rats were fed with the diet from adult for 4 weeks, these livers showed apparent fatty deposition histologically and biochemically. Low density lipoprotein (LDL) in serums of these rats lowered in level significantly than control, which indicate decreased production of secretion of very low density lipoprotein (VLDL) in the liver from which converted to LDL in peripheral tissues. When rats were reared with the diet from their foetal life, their livers deposited little of fat at any time examined after birth up to 13 weeks in spite of good diet uptake. The same phenomenon was observed in rats reared from their weanling period with the diet. In situ liver perfusion was performed to clarify the anti-fatty liver mechanism. Ketone body (KB) production rates from palmitate infused constantly at physiological concentration and bile production rates were not different among control, weanling and foetal groups. Oxygen consumption rate in control decreased after infusion of palmitate-albumin complex solution. However the rates in weanling and foetal alcohol rats increased significantly after infusion of the solution. The latter group showed more increase in rate than the former. When theoretical oxygen consumption for production of KB was compared with actual one, livers from control rats seemed to use the whole oxygen for KB production. On the other hand only 59.7% of whole oxygen in foetal alcohol group and 85.9% in weanling group used for KB production respectively. It is surmized that the increased non ketone oxygen in these groups, especially in foetal alcohol group, indicate the anti-fatty liver mechanism in these groups, probably augmented FFA oxidation. Electrophoretic analysis of lipoproteins in chronic alcoholisms showed decreased beta and pre-beta band and increased alpha band. These changes returned to normal after 1 week of admission. These experimental and clinical data indicate that impaired oxidation of FFA is an important factor for the formation of alcoholic fatty liver and impaired transport of fat from liver might enhance the change in the liver.

Adult↗
PubMed1975

Effects of nutritional factors on the development of ethanol-induced fatty liver in KK and KK-Ay mice.

KK and KK-Ay mice developed a steady and reproducible fatty liver when they were given free access to an ethanol solution as a drinking fluid for 10 to 20 days. The present studies were undertaken to elucidate effects of nutritional factors on liver fat contents of the mice given water or ethanol solution. In contrast to cornstarch, sucrose tended to increase the liver fat of control mice. A higher concentration of dietary casein lowered the liver fat of control mice, whereas the dietary concentration of cottonseed oil did not significantly affect the liver rat levels either in control or ethanol groups. Thus the standard basal diets favorable for the development of the alcoholic fatty liver have been established, for example, 10% cottonseed oil, 25 and 30% casein, 58.4 and 53.4% cornstarch for KK (12-15 weeds old) and KK-Ay (5-10 weeks old), respectively. Neither choline, myoinositol, nor any lipotropic agent tested prevented the development of the alcoholic fatty liver. Unlike in rats, orotic acid did not induce a fatty liver but rather alleviated the ethanol-induced fatty liver in these mice.

Age Factors↗
PubMed1979

Abnormalities of hepatic mitochondrial urea-cycle enzyme activities and hepatic ultrastructure in acute fatty liver of pregnancy.

Two patients presenting with acute fatty liver of pregnancy were studied. Because of similarities between acute fatty liver of pregnancy and Reye's syndrome, we investigated hepatic ultrastructure, urea-cycle enzyme activities, and plasma amino acids. Initial liver biopsies obtained 12 and 21 days after the onset of illness demonstrated microvesicular fat deposition and mitochondrial ultrastructural changes, including pleomorphism and abundant crystalline inclusions. In both biopsies, activity of the mitochondrial urea-cycle enzyme OTC was markedly below normal limits. Activity of the other mitochondrial urea-cycle enzyme, CPS, was low in one patient. Abnormalities of these enzymes persisted in second biopsies obtained at 9 and 28 weeks, respectively. By 44 weeks all urea-cycle enzyme activities had returned to normal in one patient. However, in the other patient OTC activity was still reduced at 52 weeks, although it had doubled in comparison to previous biopsies. Morphological changes of the mitochondria generally improved in parallel with the urea-cycle enzymes. Plasma amino acids, obtained at the time of the initial biopsies, demonstrated a generalized hypoaminoacidemia with the exception of glutamate. Serial observations in patients with this rare disease indicate that there are similarities with Reye's syndrome, in particular, reduced activity of the mitochondrial urea-cycle enzymes. But there are important differences. (1) Enzymatic and ultrastructural abnormalities of mitochondria persist for a longer period of time than in Reye's syndrome. (2) Mitochondrial ultrastructure is different. (3) Plasma amino acid profiles are different.

Acute Disease↗
PubMed1978

[Attenuation values of normal and pathological liver tissue as a basis for computer tomographic densitometry of fatty livers (author's transl)].

Measurements of the density of normal and diffusely disease liver parenchyma show a significant difference only in the presence of fatty livers. A linear relationship between the fat content and density (g/cm3) has been demonstrated. Computer tomographic densitometry of liver tissue correlates well with physical in vitro measurements and permits measurements of fat content which are sufficiently accurate for clinical use. Other types of liver disease cannot be differentiated by densitometry.

Absorptiometry, Photon↗
PubMed1979

Nutritional and metabolic aspects of fatty liver disease in poultry.

There are two metabolic disorders of major commercial importance in poultry that involve the occurrence of fatty deposits in the liver. Fatty Liver and Kidney Syndrome (FLKS) affects young birds and the main manifestations, lipid infiltrations into liver and many other organs, are apparently secondary effects of the primary lesion that lies in carbohydrate metabolism. Although several nutritional and environmental factors influence FLKS, the main factor is the vitamin, biotin. In the absence of an adequate supply of biotin, the hepatic activity of pyruvate carboxylase, a biotin-dependent enzyme, becomes so low that gluconeogenesis in the liver via pyruvate becomes negligible. When the bird is then subject to a mild stress and/or short term fasting, liver glycogen reserves become rapidly depleted and a progressive hypoglycaemia develops that ultimatley proves fatal. Supplementing diets with adequate amounts of biotin can prevent the syndrome. Fatty Liver Haemorrhagic Syndrome (FLHS) is brought about by an excessive accumulation of fat in the livers of adult hens which weakens the cellular structure of the liver and allows fatal haemorrhaging to occur. The aetiology of the syndrome is not clear, but a major factor is an excessive intake of dietary energy. However, the involvement of hormonal and toxicological factors, as well as other nutritional factors, is also possible.

Animal Nutritional Physiological Phenomena↗
PubMed1979

Accentuation of white phosphorus induced fatty liver by phenobarbitone in male rats compared to female rats.

The possible influence of a potent enzyme inducer, phenobarbitone, on white phosphorus fatty liver, was studied. Pretreatment by phenobarbitone for four days in white phosphorus poisoned rats provoked a decrease in mortality and an increase in hepatic triglycerides (fatty liver) in male rats. The activity of uridine diphosphoglucuronyl transferase (UDPGT), an inducible enzyme, is not modified by this pretreatment in white phosphorus poisoned rats. The accentuation of white phosphorus fatty liver by phenobarbitone in male rats could be explained by an increased hydroxylation of testosterone, thus counteracting the protective effect of this hormone on fatty liver.

Animals↗
PubMed1975

Factors affecting the reassociation and reactivation of the half-molecular weight nonidentical subunits of pigeon liver fatty acid synthetase.

The pigeon liver fatty acid synthetase complex (14 S) is dissociated in low ionic strength buffer containing dithiothreitol to form a half-molecular weight subunits (9 S) which are completely inactive for the synthesis of saturated fatty acids. The dithiothreitol-protected (reduced) subunits are rapidly reassociated and reactivated to form the active enzyme complex, not only by an increase in salt concentration but also by micromolar concentrations of NADP+ or NADPH. Increases in KCl or NADPH concentration result in an increase in the extent of reactivation (equilibrium) with no change in the over-all rate of the reaction or the half-life ofreactivation of the enzyme. The extent (equilibrium) of reactivation of the enzyme is the same in 0.2 M potassium phosphate buffer, pH 7.0; 0.2 M KCl in 5 mM Tris-35 mM glycine buffer, PH 8.3; and 50 muM NADP+ or NADPH in the Tris-glycine buffer. The extent and rate of reactivation of the enzyme is dependent not only on ionic strength and NADPH concentration, but also on pH and temperature. Reactivation with 0.2 M KCl is optimal between pH 7.3 and 8.5. At higher and lower pH values the rate and extent of reactivation are lowered. The rate and extent of reactivation are also decreased as the temperature is lowered below 10 degrees. At 0 degrees there is little reactivation of enzyme activity. However, in the presence of 0.2 M KCl containing 15 to 40% glycerol at 0 degrees, reactivation of the enzyme is about 50% complete. The rate of reactivation of enzyme in the presence of KCl or NADPH conforms to first order kinetics. This result suggests that the subunits first combine to form an inactive complex which is subsequently transformed to an enzymatically active complex. Evidence for the presence of inactive complex was obtained in experiments carried out in 0.2 M KCl at pH 6.0, and in 0.2 M KCl at pH 8.3, at both 6 and 3 degrees. Under these conditions the amount of complex observed upon ultracentrifugation was greater than expected from determinations of enzyme activity. The above findings suggest that ionic and hydrophobic interactions, and possibly the water structure surrounding the interacting sites, are of prime importance in reassociation and reactivation of enzyme. In addition, NADP+ and NADPH have very specific effects in bringing about reassociation and in maintaining the structural integrity of the multienzyme complex.

Animals↗