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hepatomegaly/triglyceride
Ο σύνδεσμος αποθηκεύεται στο πρόχειρο
Σελίδα 1 από 293 Αποτελέσματα
CNX-013-B2, a unique pan tissue acting rexinoid, modulates several nuclear receptors and controls multiple risk factors of the metabolic syndrome without risk of hypertriglyceridemia, hepatomegaly and body weight gain in animal models.
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BACKGROUND
In addition to their role in growth, cellular differentiation and homeostasis Retinoid X Receptors (RXR) regulate multiple physiological and metabolic pathways in various organs that have beneficial glucose and lipid (cholesterol) lowering, insulin sensitizing and anti-obesity effects.
The RXR agonist LG100268 causes hepatomegaly, improves glycaemic control and decreases cardiovascular risk and cachexia in diabetic mice suffering from pancreatic beta-cell dysfunction.
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OBJECTIVE
Although retinoid X receptor (RXR) and peroxisome proliferator activated receptor-gamma (PPARgamma) agonists have antidiabetic effects in hyperinsulinaemic animals, little information exists on their effects after pancreatic beta-cell failure. Thus, we examined if RXR and PPARgamma
Biochemical mechanism underlying hypertriglyceridemia and hepatic steatosis/hepatomegaly induced by acute schisandrin B treatment in mice.
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BACKGROUND
It has been demonstrated that acute oral administration of schisandrin B (Sch B), an active dibenzocyclooctadiene isolated from Schisandrae Fructus (a commonly used traditional Chinese herb), increased serum and hepatic triglyceride (TG) levels and hepatic mass in mice. The present study
Alkylthioacetic acids (3-thia fatty acids) as non-beta-oxidizable fatty acid analogues: a new group of hypolipidemic drugs. III. Dissociation of cholesterol- and triglyceride-lowering effects and the induction of peroxisomal beta-oxidation.
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Previous work in this laboratory indicated that sulfur-substituted fatty acid analogues, 1.10-bis(carboxymethylthio)decane and alkylthioacetic acid, both non-beta-oxidizable compounds, and the beta-oxidizable alkylthiopropionic acid (1) caused, to different extents, dose-related hepatomegaly and
Triglyceride storage disease. A report of two affected children associated with neurological abnormalities.
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Two children are described with congenital abnormalities (microcephaly, nystagmus, deafness, hepatomegaly) and the anomalous feature of triglyceride deposits in peripheral adipose tissue associated with severe malnutrition. Peripheral adipose tissue of one of these children displayed: (a) reduced
Multisystem triglyceride storage disorder without ichthyosis in two siblings.
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A four-year-old boy presented with hepatomegaly, vacuolized granulocytes (Jordans' anomaly) and slightly progressive myopathy as signs of multisystem triglyceride storage disease. The nine-year-old sister of the patient also showed Jordans' anomaly and early fatigability, but no overt weakness.
Triglyceride-induced diabetes mellitus in congenital generalized lipodystrophy.
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High levels of triglycerides and free fatty acids have been implicated in the pathogenesis of type 2 diabetes mellitus (DM). Congenital generalized lipodystrophy (CGL) is an autosomal recessive syndrome characterized by intense whole body reduction of subcutaneous fat. Its clinical manifestations
The association between serum triglycerides and gamma glutamyl transpeptidase activity in diabetes mellitus.
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A study conducted on 228 diabetic patients has shown a significant positive association between serum gamma-glutamyl transpeptidase (GGT) and triglyceride levels. Both fall with treatment, the most marked reduction occurring in patients on insulin. We suggest that the association between serum GGT
Multisystem triglyceride storage disorder with impaired long-chain fatty acid oxidation.
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A five-year-old girl presented with congenital ichthyosis, hepatosplenomegaly, vacuolized granulocytes (Jordans' anomaly), and myopathy. Pathological, ultrastructural, and biochemical studies revealed nonlysosomal, multisystemic triglyceride storage. The cultured fibroblasts had increased uptake but
Identification of factors contributing to hepatomegaly in severely burned children.
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Hepatomegaly is a common postmortem observation in severely burned children, with the liver often tripling in size when compared with normal livers for age, weight, and sex. Lesions identified at autopsy include deposition of large and small fat droplets in the hepatocyte, congestion, centrilobular
[Unusual facies and recurrent high triglycerides for more than one year in a girl].
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A girl, aged 1 year and 9 months, was found to have hypertriglyceridemia in the neonatal period, with unusual facies and signs of dark skin all over the body, disappearance of subcutaneous adipose, acanthosis nigricans of the neck, excessive and thick hair, empty cheeks, muscle hypertrophy of the
PPARalpha /gamma ragaglitazar eliminates fatty liver and enhances insulin action in fat-fed rats in the absence of hepatomegaly.
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Peroxisome proliferator-activated receptor (PPAR)alpha and PPARgamma agonists lower lipid accumulation in muscle and liver by different mechanisms. We investigated whether benefits could be achieved on insulin sensitivity and lipid metabolism by the dual PPARalpha/gamma agonist ragaglitazar in high
Fish oil feeding reverses hepatomegaly and disrupted hepatic function due to the lack of FXR signaling.
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Mice lacking farnesoid X receptor (FXR) are used as a model for nonalcoholic fatty liver disease because their livers exhibit hepatomegaly, hepatic steatosis, and hepatic inflammation. The influence of fish oil feeding on hepatomegaly and disrupted hepatic function was investigated using female
Eucaloric substitution of medium chain triglycerides for dietary long chain fatty acids in acquired total lipodystrophy: effects on hyperlipoproteinemia and endogenous insulin resistance.
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Previous studies have suggested that reduction of dietary fat intake, with or without caloric restriction, may lead to improvement in certain of the characteristic abnormalities that accompany total lipodystrophy (TLD). We have studied the effects of eucaloric medium chain triglyceride (MCT)
Gadofullerene inhibits the degradation of apolipoprotein B100 and boosts triglyceride transport for reversing hepatic steatosis
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Hepatic steatosis is a widespread metabolic disease characterized by excessive accumulation of triglyceride (TG) in liver. So far, effective approved drugs for hepatic steatosis are still in development, and removing the unnecessary TG from the hepatocytes is an enormous challenge. Here, we explore
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