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Query: UMLS:C0015695 (fatty liver)
13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oxidative stress in the course of diabetes mellitus can cause disturbance of lipid membranes of cellular organelles. The study is aimed at the determination of oxidative phosphorylation in mitochondria in rats with experimentally induced acute and chronic insulin-dependent diabetes mellitus (IDDM). IDDM was induced by single dose of streptozotocin (45 mg per kg-1). Insulin Interdep (6 U per kg-1) was administered once a day subcutaneously. The authors investigated glycaemia, cholesterol and triacylglycerol concentrations in the blood and liver. Isolation of mitochondria was succeeded by measurement of oxidative phosphorylation indicators after 8 days (acute IDDM) or after 8 weeks (chronic IDDM) from streptozotocin administration. The authors found out that both acute and chronic IDDM were concommited by hyperglycaemia. The group with acute IDDM yielded an increase in cholesterol and triacyglycerols concentrations in the blood, as well as that of cholesterol in the liver. The group with chronic IDDM yields an increase in cholesterol in the blood. Trialcylglycerols in the liver increased in none of the investigated groups. Liver steatosis did not occur. Indicators of oxidative phosphorylation in the liver mitochondria of rats with acute and with chronic IDDM decreased in contrast to healthy controls from NAD substrates glutamate and pyruvate and also form FAD substrate of succinate. Significant decrease in consumption of oxygen in the 3 state occurred, while in acute IDDM the decrease was more significant than in chronic IDDM. Phosphorylation rate significantly decreased in contrast to controls, but there was no difference between IDDM groups. The investigation results imply that in both acute and chronic IDDM there are decreased effectivity of energetic metabolism in liver mitochondria. (Tab. 5, Ref. 29.).
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PMID:[Bioenergetics of liver mitochondria in rats in experimental insulin-dependent diabetes]. 901 45

(1) The chemical properties of thia fatty acids are similar to normal fatty acids, but their metabolism (see below: points 2-6) and metabolic effects (see below: points 7-15) differ greatly from these and are dependent upon the position of the sulfur atom. (2) Long-chain thia fatty acids and alkylthioacrylic acids are activated to their CoA esters in endoplasmatic reticulum. (3) 3-Thia fatty acids cannot be beta-oxidized. They are metabolized by extramitochondrial omega-oxidation and sulfur oxidation in the endoplasmatic reticulum followed by peroxisomal beta-oxidation to short sulfoxy dicarboxylic acids. (4) 4-Thia fatty acids are beta-oxidized mainly in mitochondria to alkylthioacryloyl-CoA esters which accumulate and are slowly converted to 2-hydroxy-4-thia acyl-CoA which splits spontaneously to an alkylthiol and malonic acid semialdehyde-CoA ester. The latter presumably is hydrolyzed and metabolized to acetyl-CoA and CO2. (5) Both 3- and 4-thiastearic acid are desaturated to the corresponding thia oleic acids. (6) Long-chain 3- and 4-thia fatty acids are incorporated into phospholipids in vivo, particularly in heart, and in hepatocytes and other cells in culture. (7) Long-chain 3-thia fatty acids change the fatty acid composition of the phospholipids: in heart, the content of n-3 fatty acids increases and n-6 fatty acids decreases. (8) 3-Thia fatty acids increase fatty acid oxidation in liver through inhibition of malonyl-CoA synthesis, activation of CPT I, and induction of CPT-II and enzymes of peroxisomal beta-oxidation. Activation of fatty acid oxidation is the key to the hypolipidemic effect of 3-thia fatty acids. Also other lipid metabolizing enzymes are induced. (9) Fatty acid- and cholesterol synthesis is inhibited in hepatocytes. (10) The nuclear receptors PPAR alpha and RXR alpha are induced by 3-thia fatty acids. (11) The induction of enzymes and of PPAR alpha and RXR alpha are increased by dexamethasone and counteracted by insulin. (12) 4-Thia fatty acids inhibit fatty acid oxidation and induce fatty liver in vivo. The inhibition presumably is explained by accumulation of alkylthioacryloyl-CoA in the mitochondria. This metabolite is a strong inhibitor of CPT-II. (13) Alkylthioacrylic acids inhibits both fatty acid oxidation and esterification. Inhibition of esterification presumably follows accumulation of extramitochondrial alkylthioacryloyl-CoA, an inhibitor of microsomal glycerophosphate acyltransferase. (14) 9-Thia stearate is a strong inhibitor of the delta 9-desaturase in liver and 10-thia stearate of dihydrosterculic acid synthesis in trypanosomes. (15) Some attempts to develop thia fatty acids as drugs are also reviewed.
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PMID:Thia fatty acids, metabolism and metabolic effects. 903 Jan 89

In this work the mechanism of the hypoglycemic effect of the plant Cleome-Droserifolia (C.d.) was studied in a group of albino rats rendered glucose intolerant by tetracycline (T.) induced fatty liver, and compared with a normal control (C.) rats. The plant extract significantly suppressed the rise in peripheral blood glucose concentrations, both in the basal (fasting) state and after glucose intake. Suppression of basal blood glucose indicated a lowering effect of the plant extract on hepatic glucose output (HGO). The postprandial hypoglycemic effect of the plant extract without increasing insulin secretion was explained by; First: Potentiation of peripheral and hepatic insulin sensitivity. Second: by diminishing intestinal glucose absorption, which was evident by blunting plasma glucose levels throughout the oral glucose challenge. This plant might prove to have a promising therapeutic value in the treatment of diabetes mellitus, for besides its postprandial hypoglycemic effect, its suppression to hepatic glucose output in the fasting state is a beneficial therapeutic finding in favour of the plant as insulin is the most important drug that brings about this effect. The plant has also got a hypocholesterolemic effect more specifically on low density lipoprotein cholesterol (LDL-C) which consequently raised the high density lipoprotein cholesterol/low density lipoprotein cholesterol (HDL-C/LDL-C) ratio. This adds to its value as a protective and antiatherogenic agent.
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PMID:Role of the hypoglycemic plant extract cleome droserifolia in improving glucose and lipid metabolism and its relation to insulin resistance in fatty liver. 903 62

Hyperinsulinemia and insulin resistance are common features seen in most liver diseases. The present study was carried out on an experimental model of fatty liver (tetracycline induced) in albino rats. Significantly elevated levels of both peripheral plasma insulin and plasma glucose concentrations were recorded in both the fasting state and after an oral glucose intake in the tetracycline-treated rats. The presence of hyperinsulinemia accompanying hyperglycemia is considered a sign of insulin resistance. Peripheral insulin resistance has been proved in this work by the reduced "A" value which refer to the peripheral insulin activity (sensitivity) in fatty liver rats compared to normal rats. The hyperinsulinemia recorded here was due to pancreatic hypersecretion and not a result of reduced hepatic degradation. Hypersecretion of insulin was clearly determined by measuring the level of immunoreactive insulin (IRI) in pancreatic vein which exhibited a significant rise in tetracycline-treated rats, and there was a positive correlation between the pancreatic venous and peripheral venous insulin in the basal state and after 30 min. of oral glucose administration. Hepatic degradation of insulin was not a cause as evidenced by First: the amount of insulin secreted and insulin consumed were significantly higher in fatty liver rats than normal controls. Second: the whole body extraction ratio or insulin degradation was not significantly different in the tetracycline-treated rats from the normal rats. The present data suggests that insulin resistance and hyperinsulinemia underlie the observed metabolic disturbances that characterize fatty liver disease.
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PMID:Mechanism of insulin resistance and hyper-insulinemia in fatty liver. 903 63

Abnormal Zinc and Copper metabolism were studied in rats with tetracycline-induced fatty liver and compared with normal rats. The present work recorded decreased serum zinc concentration with increased copper concentration in the tetracycline-injected rats. The results also showed that the liver and heart zinc were significantly decreased; meanwhile it was observed that the concentration of zinc in the kidney tissue of fatty liver rats was significantly raised in comparison with those of normal rats. Histopathological studies of the kidney tissue showed degenerative changes in the tables with areas of focal necrosis. Renal tubular necrosis in such cases is largely caused by the toxic degradation products of tetracycline metabolism. The kidney lesion together with impaired gastrointestinal absorption contributed to the hypozincaemia observed in the present results. Although the present data showed a significant reduction in serum zinc and significant rise in plasma insulin in the fatty liver rats there was nonsignificant correlation between the two variables as compared with the normal rats. The positive correlation between serum zinc concentration and reduced high-density lipoprotein cholesterol (HDL-C) emphasizes the role of zinc deficiency in atherosclerotic disease in fatty liver.
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PMID:Abnormal zinc and copper metabolism in hepatic steatosis. 904 48

Fatty liver has prevailed by 14% in the healthy population of this country. The factors contributing genesis of fatty liver were gender (male), obesity, high alcohol consumption, glucose intolerance and hypertriglyceridemia. And hypertriglyceridemia seems to be the common underlying factor to all other causes. The mechanism for accumulation of triglycerides in the liver can be explained at least by increased HTGL activities and elevated apo A-II levels, a postulated co-factor of HTGL. An hypertriglyceridemic patients with fatty liver had the insulin resistance.
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PMID:Hypertriglyceridemia and fatty liver: clinical diagnosis of fatty liver and lipoprotein profiles in hypertriglyceridemic patients with fatty liver. 922 32

We report the case of a 28-year-old woman attending for hirsutism and diabetes mellitus. Diabetes was a casual finding 2 years before consulting and was treated with diet and antidiabetic drugs. Acromegalic appearance, facial acne, penty, curled and rude hair, hypertrichosis, ade I diffuse goitre, prominent abdomen with umbilical hernia, severe hepatomegaly, prominent muscles and veins with normal genitalia appeared in the physical examination. No other abnormalities were found. Hypophysis, thyroid, suprarenal and ovaric hormonal functional studies were normal. An insulin-resistant diabetes mellitus was found in the metabolic study. Ultrasound and TAC showed severe diffuse hepatomegaly and visceral fat lack. Bone radiographies showed diffuse lesions compatible with polyostotic dysplasia. Subcutaneous, hepatic and bone biopsy revealed lack of fat tissue, hepatic steatosis and osteal fibrosis. Patient s diagnosis was Berardinelli-Seip syndrome, Seip-Lawrence or lipoatrophic diabetes associated with polyostotic fibrotic dysplasia. Case is studies and bibliographic references are reviewed.
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PMID:[Seip-Lawrence syndrome associated with polyostotic fibrous dysplasia. Report of a case]. 923 83

The purpose of this investigation was to study the metabolic situation in clinical cases of bovine ketosis and to diagnose additional diseases. Extensive clinical examination, clinical biochemistry, haematology and fine-needle aspiration biopsy of liver was performed on 17 ketotic and eight control dairy cows in the field, and on seven hospitalized hyperketonaemic fatty liver patients. Additional findings in the ketotic group were heat (n = 7), indigestion (n = 5), endometritis (n = 2), cystic ovaries (n = 1), and mastitis (n = 1), and in the fatty liver group displaced abomasum (n = 4), abomasal ulcers (n = 3), mastitis (n = 2), laminitis (n = 1), bronchopneumonia (n = 1), and hypomagnesaemia (n = 2). There were no additional findings in the control group. Aspartate aminotransferase (AST) and creatine kinase (CK) were elevated in the ketosis and fatty liver groups. Total bilirubin, gamma-glutamyl transferase (GGT) and glutamate dehydrogenase (GD) were elevated in the fatty liver group and in some animals in the ketosis group. Total bile acid was not different between the groups. The free fatty acid/cholesterol ratio was higher in the fatty liver group compared with the control and ketosis groups. There was no or only slight fatty degeneration of the liver cells in the control and ketosis groups. Glucose and insulin preinjection concentrations and changes from basal values after glucagon injection were significantly lower in the ketosis group if compared with the control group. The responses in the fatty liver animals after glucagon injection were more heterogeneous than in the control and ketosis animals, a sign of disturbance in the metabolic adaptation, which together with high free fatty acid (FFA) levels can lead to fatty liver in cows with concurrent diseases.
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PMID:Glucose and insulin responses to glucagon injection in dairy cows with ketosis and fatty liver. 946 72

We report on a 33-year-old male patient with generalized acquired lipodystrophy, insulin resistant diabetes mellitus and acanthosis nigricans (Lawrence Syndrome). First probable symptoms of lipodystrophy (weight loss, shrinkage of subcutaneous fatty tissue, and loss of muscular strength) became evident three years ago, with the onset of diabetes mellitus occurring about six months later. The patient suffered from the following clinical symptoms: IDDM with increasing insulin-requirement, extreme reduction of fatty tissue, fatty liver hepatitis with elevated liver enzymes, glomerulopathy, muscular and neuropathic pains, as well as hypertriglyceridaemia. A basal C-peptide concentration is rather high. Definitely, the endogenous insulin secretion is increased. In other words, insulin resistance is documented. In an effort to identify the pathogenetic mechanisms of lipoatrophic diabetes mellitus in this patient and to develop a therapeutic strategy, antibodies against different tissues and endocrinologic regulation were investigated. It was possible to demonstrate the presence of serum autoantibodies against lipocytes of the subcutis and other tissues, against hepatic stellate cells, together with autoantibodies against different endocrine organs. By studying the basis of diabetic abnormalities relating to the growth hormone (GH), the insulin-like growth factor (IGF) dynamics in this patient, i.e. reductions of GH, IGF-I, IGF-II, IGF-Binding protein (IGF-BP) 2 and IGF-BP 3, were detected. An immunosuppressive treatment strategy was not beneficial.
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PMID:Dysregulation of insulin-like growth factors in a case of generalized acquired lipoatrophic diabetes mellitus (Lawrence Syndrome) connected with autoantibodies against adipocyte membranes. 951 65

The accumulation of triglycerides in the liver has been associated with reduced hepatic function; however, direct evidence that fat accumulation causes decreased liver function is lacking. Hepatocyte monolayers isolated from ruminating calves with an initial low triglyceride concentration were either loaded or not loaded with triglycerides by incubation with 1.5 or 0 mM exogenous nonesterified fatty acids from 12 to 48 h after plating. Basal rates of synthesis of albumin and protein were not affected by triglycerides in the cell. Inclusion of insulin and glucagon from 12 to 72 h after plating increased rates of albumin and protein synthesis. Hepatocytes loaded with triglycerides were less sensitive to the hormonal stimulation of albumin and protein synthesis than were normal hepatocytes. Insulin clearance rates were also lower in hepatocytes loaded with triglycerides than in normal hepatocytes. Decreased insulin clearance and hormonal control of protein synthesis could contribute to the etiology of metabolic disorders that are associated with periparturient fatty liver in dairy cows.
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PMID:Relationship of triglyceride accumulation to insulin clearance and hormonal responsiveness in bovine hepatocytes. 956 77


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