Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In non-obese but diabetic 15-week-old KK mice which showed fatty liver histopathologically, the content of liver lipids and the levels of blood glucose and plasma IRI were greater than those in the control ICR mice of the same age and were quite similar to those in GTG-obese mice. In 6-week-old KK mice which excreted no glycosuria and showed normal hepatic tissues, only plasma IRI level was slightly elevated as compared with that in the control mice. The cyclic 3',5'-AMP stimulators like epinephrine and theophylline exerted far less potent stimulatory effects on lipolytic activity in 6-week-old KK mice than in the control mice, as in diabetic 15-week-old KK mice and GTG-obese mice. Theophylline potentiated the lipolytic effect of epinephrine lineraly in KK mice, the tendency being different from that in the control mice, and only the submaximal rate was obtained. Furthermore, the inhibitory effect of theophylline on PDE from the epididymal adipose tissue was less potent in 6-week-old KK mice than in healthy ICR mice of the same age.
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PMID:Effects of epinephrine and theophylline on lipolytic response in hereditary diabetic mice. 18 66

Perfluorodecanoic acid (PFDA) is a peroxisome proliferator that causes a dose-dependent (20-80 mg/kg) increase in hepatic triacylglycerol and cholesteryl ester levels in the rat. We hypothesized that PFDA may cause an increase in the de novo synthesis of fatty acids and cholesterol in this species, which would explain observed effects. The incorporation of 3H2O into tissue lipids was examined 7 days after rats received vehicle or 20 or 80 mg/kg of PFDA. PFDA treatment decreased the rate of synthesis of cholesterol and fatty acids in the live and in epididymal fat pad. At a PFDA dose (20 mg/kg) that decreased de novo synthesis of fatty acids and cholesterol, there was no effect on the concentration of fatty acids and cholesterol in the liver, epididymal fat pads, and plasma. We conclude that PFDA induced fatty liver is due to either a decrease in the oxidation of fatty acids in the liver, or an impairment of triacylglycerol catabolism and/or export from the liver, and is not the result of an increase in de novo synthesis of fatty acids and cholesterol.
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PMID:Effects of perfluorodecanoic acid on de novo fatty acid and cholesterol synthesis in the rat. 179 7

In order to test whether or not overeating of a nutritionally adequate diet with reasonable fat content could result in significant fat accumulation in the liver, male Sprague-Dawley rats were provided with free access to either a nutritionally adequate liquid diet with 35 per cent of calories as fat or a regular diet (controls) for 3 months. After the feeding period, body weight, Lee index, and epididymal adipose tissue weight, were significantly greater in rats fed with the liquid diet than in the controls. Liver weight, hepatic triglyceride levels were also greater in the liquid diet group. Histologically, remarkable fatty infiltration was observed predominantly in periportal areas in rats fed with the liquid diet ad libitum for 3 months. Compared to a large body of the literature concerning diet-induced obesity in experimental animals, information on animal models of fatty liver by dietary manipulations is insufficient. The results of this study clearly indicate that the overeating of a nutritionally adequate diet with reasonable fat content could result in remarkable fat accumulation in the liver in rats.
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PMID:Fatty liver in rats induced by excessive intake of a nutritionally adequate liquid diet. 344 Jun 81

The growth pattern of visceral organs was investigated in monosodium L-glutamate (MSG)-treated obese mice with hypothalamic lesions. Male Jcl-ICR strain mice were subcutaneously injected with MSG, 2 mg/g of body weight daily, for five days after birth. The MSG-treated mice became obese after 4 weeks of age. According to patterns of weight gain compared with those in the control mice, the visceral organs in the MSG-treated mice were classified into three groups as follows: The first group of organs (heart, lungs, spleen, pancreas, kidneys, testes, brain and submandibular glands) remained absolutely lower in weight throughout their growth. The second group of organs (liver and stomach) was low in weight until 12 weeks of age, but became identical to that of the control mice after 16 weeks of age. The third group of organs (epididymal fat, small intestine and colon) showed lower weight until 4 weeks of age and were significantly heavier than those in the control mice after 8 weeks of age. The heart in the first group of organs apparently had hypertrophic muscle cells after 8 weeks of age and became significantly hypoplastic due to decreased cell production as was revealed by the continuous suppression of mitotic activity and DNA synthesis by [3H]thymidine autoradiography. The liver in the second group of organs became significantly hypoplastic due to decreased cell production and showed the same weight with the control mice due to the development of fatty liver. The small intestine in the third group of organs became hypoplastic due to decreased cell production in the crypts until 4 weeks of age, and became hypertrophic and hyperplastic by the acceleration of cell production in the crypts from 4 to 8 weeks of age. From these findings, in the MSG-treated mice with specific growth patterns of visceral organs, it is suggested that low energy expenditure results in a relatively excessive energy supply and leads to obesity, because most of the important organs with major physiological functions became hypoplastic. Moreover, it seems that hypertrophy and hyperplasia of the intestine suggest a possible acceleration of the absorptive function.
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PMID:Morphological and cell proliferative study on the growth of visceral organs in monosodium L-glutamate-treated obese mice. 380 54

The effect of ingestion of saline, glucose, and ethanol (isocaloric with the glucose) on the mobilization of radiopalmitate from epididymal fat prelabeled in vivo and the incorporation of the mobilized label into liver lipids was investigated in rats. The mobilization of radiopalmitate from epididymal fat and the incorporation of the mobilized label into liver triglyceride were most markedly elevated by ingestion of ethanol. Increased mobilization and diversion of epididymal adipose tissue fatty acids to liver lipids of ethanol-treated rats were shown also by the close resemblance of the fatty acids of liver triglyceride to the fatty acids of epididymal fat. The amount of radiopalmitate mobilized by the saline-treated rats, comprising approximately a third of that mobilized by the ethanol-treated animals, was larger than the amount mobilized by the rats treated with glucose; most of it was oxidized rather than incorporated into the liver fats. In glucose-treated rats a larger fraction of radiopalmitate mobilized from one prelabeled epididymal pad was diverted to and incorporated into the lipids of the contralateral pad of the same animal. The specific activity of hepatic triglyceride of ethanol- and saline-treated rats was similar and significantly higher than that of animals treated with glucose. These data indicate that the ethanol-induced fatty liver can be attributed to an increased mobilization and incorporation of adipose tissue fatty acids into liver lipid and to an altered hepatic metabolism of fatty acids and triglyceride.
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PMID:Effect of ingestion of saline, glucose, and ethanol on mobilization and hepatic incorporation of epididymal pad palmitate-1-14C in rats. 597 73

A six-months out-patient study of chronic alcoholics with undecompensated liver disease has shown a statistically significant inverse correlation between the change in mean corpuscular volume and the change in body weight (r = -0.4, P less than 0.01). A fall in body weight over this period was the best clinical indicator of apparently continuing alcohol abuse. Previous anthropometric studies have indicated that reduced adipose tissue is one cause of lower body weights in such patients. To determine whether this is due to the effects of alcohol or of poor nutrition, the epididymal fat pad weights of rats following 28 days administration of alcohol (36% of total calories) as part of a nutritionally adequate liquid diet were compared with those of pair-fed controls initially matched for body weight. At the end of the experiment, body weight gain was the same in both groups but the mean weight of the fat pads of alcohol-fed animals (371.7 mg +/- 60.0 mg SD) all of which developed hepatic steatosis was 29% greater than that of pair-fed controls (288.7 mg +/- 42.4 mg). This difference was statistically significant (P less than 0.025). This study shows that alcohol intake per se does not prevent an increase in body weight or fat even if hepatic steatosis is induced and that loss of adipose tissue in chronic alcoholics who continue to drink is probably due to simultaneous inadequate nutritional intake.
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PMID:Differential effect of chronic alcohol intake and poor nutrition on body weight and fat stores. 653 64

An attempt was made to mobilize adipose tissue cholesterol independently of triacylglycerol by feeding cholesterol to intact Fischer 344 rats to 'load' adipocytes followed by hypolipidemic drug treatment in order to lower plasma cholesterol and, hence, adipocyte cholesterol. In this strain of rat, body weight and adipocyte sizes remain relatively constant after 1 year of age. Therefore, alterations in adipocyte cholesterol can be ascribed to factors other than cell size. Both oxandrolone and combined cholestyramine/clofibrate treatment caused significant reductions in plasma cholesterol in cholesterol-fed rats, but cholesterol concentrations in liver were reduced only by cholestyramine/clofibrate treatment. Oxandrolone enhanced the development of liver fatty liver in the cholesterol-fed rats, but cholestyramine/clofibrate significantly reduced liver triacylglycerol concentrations. Adipocyte cholesterol in the epididymal depot was significantly elevated, not lowered, in both concentrations. Adipocyte cholesterol in the epididymal depot was significantly elevated, not lowered, in both groups of drug-treated animals. Subcutaneous adipocytes from rats receiving drug treatment also contained more cholesterol, especially in rats given oxandrolone. Increments in adipocyte cholesterol were associated with decreases in the absolute amounts of apolipoproteins, A-I and A-IV, as measured by densitometric scanning of electrophoretic gels. Under the present experimental conditions, changes in plasma cholesterol scanning of electrophoretic gels. Under the present experimental conditions, changes in plasma cholesterol concentration did not adequately reflect the cholesterol content of either liver or adipose tissue.
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PMID:Accumulation of adipocyte cholesterol during hypolipidemic drug treatment in cholesterol-fed rats. 715 Jun 24

Our preceding paper reported that mepanipyrim, a new fungicide, induced fatty liver in the rat. This study was undertaken to examine this phenomenon further on hepatic triglyceride (TG) synthesis, on liver and serum lipid concentrations, and on concentration of serum very-low-density lipoprotein (VLDL) in rats fed for 3 weeks on the drug at 4,000 ppm. Mepanipyrim decreased the incorporation of 14C-acetate into hepatic TG, total cholesterol (TC) and total lipids. In addition, mepanipyrim treatment induced a drastic increase in hepatic TG accompanying a decrease in serum TG. Esterified cholesterol (CE), phospholipid (PL) and non-esterified fatty acid (NEFA) also increased in the liver with a concomitant decrease in the serum. The decrease of serum VLDL by mepanipyrim was comparable to the decrease in serum TG. Because hepatic TG is secreted into the blood by forming VLDL, which consists of TG, TC, PL, and apoprotein, the decrease in serum TG would be mainly ascribable to that in serum VLDL. Mepanipyrim also decreased serum concentrations of low-density lipoprotein (LDL) and high-density lipoprotein (HDL), and the relative weights of the epididymal adipose tissue, indicating that a reduction in serum VLDL does not reflect acceleration of serum VLDL dissimulation. These results suggest that the fatty liver induced by mepanipyrim would be due to the inhibition of hepatic VLDL synthesis or its secretion into the blood.
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PMID:Effects of mepanipyrim on lipid metabolism in rats. 977 16

We studied the influence of oligofructose (OFS), a nondigestible fructan, on lipid metabolism in obese fa/fa Zucker rats. The addition of 10 g/100 g OFS to the diet slowed the increase in body weight without modifying serum triglycerides or glucose concentrations after 7 wk of treatment. However, an oral load of 2 g glucose and 5 g corn oil/kg body weight increased triglyceridemia more in OFS-fed rats than in control rats. After 10 wk, OFS decreased the hepatic concentration of triglycerides 57% relative to controls. The less severe steatosis was confirmed by histologic analysis. Among the key enzymes involved in fatty acid synthesis and esterification, only malic enzyme activity was significantly lower in OFS-fed rats than in controls. The epididymal fat mass was significantly lower in OFS-fed rats. In conclusion, dietary enrichment with OFS can counteract both the fat mass development and the hepatic steatosis that occur in obese Zucker rats. Future studies will be designed to clarify in obese animals the influence of dietary OFS on postprandial triglyceridemia, which is an important variable associated with the development of atherosclerosis in humans, and to analyze the biochemical mechanism underlying the "hepatoprotective" effect of OFS.
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PMID:Dietary oligofructose lessens hepatic steatosis, but does not prevent hypertriglyceridemia in obese zucker rats. 1080 36

The Nagoya-Shibata-Yasuda (NSY) mouse is an inbred strain with spontaneous development of type 2 (non-insulin-dependent) diabetes mellitus. The purpose of this study was to determine the mode of inheritance of various phenotypes related to diabetes in this strain. Two reciprocal outcrosses, female C3H/He x male NSY F1 (C3NF1) and female NSY x male C3H/He F1 (NC3F1) mice, were performed. The phenotypic characteristics in both F1 mice were investigated. The cumulative incidence of diabetes was 100% (25 of 25) in male C3NF1 mice and 97% (29 of 30) in male NC3F1 mice at 48 weeks of age, indicating that diabetes in NSY mice was transmitted to male F1 hybrids in an autosomal dominant manner. Fatty liver also showed an autosomal dominant mode of inheritance. In contrast, epididymal fat accumulation and impaired insulin secretion showed an autosomal recessive mode of inheritance. The body mass index (BMI) showed a codominant mode of inheritance. Paternal-maternal effects associated with the severity of diabetes were observed. Insulin resistance was much more severe in male F1 mice than in the parental NSY strain. These data indicate different modes of inheritance among phenotypes related to type 2 diabetes. The presence of more severe insulin resistance in F1 mice versus the parental strains suggests the interaction of both parental genomes in the development of insulin resistance. The F1 mouse is expected to be useful for studies of the pathogenesis and genetic synergism of the insulin resistance syndrome.
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PMID:Paternal-maternal effects on phenotypic characteristics in spontaneously diabetic Nagoya-Shibata-Yasuda mice. 1083 Nov 78


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