Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to elucidate the mechanism(s) of hyperlipidemia following glucocorticoid administration, dexamethasone (0.125 mg/Kg) was administered daily intramuscularly for 2 wk to male Sprague-Dawley rats and the effects on plasma triglyceride (TG) and cholesterol (Chol), lipoprotein neutral lipids, hepatic triglyceride secretion rates (TGSR; Triton), and epididymal fat lipoprotein lipase (LPL) were determined. Special measures were taken to maintain positive caloric balance and keep the weights of control and dexamethasone-treated animals comparable. Significant increases (p less than 0.001) in TG and very-low density lipoprotein (VLDL) triglyceride associated with no change in Chol and actual reduction in both triglyceride and cholesterol in low density lipoprotein (ldl) were observed in the steroid-treated animals. Dexamethasone treatment was associated with increased basal insulin and glucose levels, an insignificant increment in TGSR, and a highly significant reduction (p less than 0.001) in LPL. These findings suggest that glucocorticoid treatment increases splanchnic triglyceride production rates, but the resulting hypertriglyceridemia is primarily a consequence of impaired VLDL removal due to low adipose tissue LPL activity.
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PMID:Glucocorticoids and triglyceride transport: effects on triglyceride secretion rates, lipoprotein lipase, and plasma lipoproteins in the rat. 17 40

Ehrlich ascites carcinoma growth in mice induces hypertriglyceridemia. The degree of hypertriglyceridemia found in one laboratory (Spector's) was much greater than we observed in our laboratory. Moreover, major differences were reported with respect to fasting (no effect on tumor extracellular fluid triglyceride levels in Spector's tumor-bearing mice; marked decrease in ours). We have obtained tumorous CBA mice from Spector's laboratory and have studied them simultaneously with our Swiss-Webster mice. Triglyceride levels of the above two groups and from two controlled crossover groups, included to evaluate the influence of mouse and tumor strains on hypertriglyceridemia, were determined. The CBA mice had intense hypertriglyceridemia and high triglyceride levels in tumor extracellular fluid regardless of the subline source of ascites tumor. On the other hand, only mild hyperlipidemia was induced with both strains of tumor in Swiss-Webster mice. Thus, the variations in plasma and tumor extracellular fluid triglyceride levels probably arise from the mouse strains and not from variations in the tumor subline. Fasting caused a decrease in both plasma and tumor extracellular fluid triglyceride concentrations in CBA, as well as in Swiss-Webster mice. A mouse strain difference was also evident from a significant decrease in wet weights of adipose tissues like epididymal fat, inguinal fat, and intermuscular fat with tumor growth in the CBA strain which was not observed in the Swiss-Webster strain at the corresponding stage of tumor growth. Study of these strain diffeences may lead to an understanding of factors that regulate hyperlipidemia.
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PMID:Hypertriglyceridemia in Ehrlich ascites carcinomatous mice: tumor and mouse strain differences. 84 97

The effects of long-term moderate food restriction were assessed in lean and obese male Zucker rats. A 30% reduction in food intake from 5 to 68 wk of age resulted in parallel lowering of body weight in both lean and obese rats compared to their respective ad libitum-fed control groups. In lean rats, epididymal and retroperitoneal fat pad weights and cell size were lowered by food restriction. In obese rats there was an effect of food restriction on growth of the epididymal pad but not the retroperitoneal pad. Hyperinsulinemia, hyperlipidemia and elevated serum albumin levels, as well as higher activity of lipogenic enzymes, were also not affected by food restriction in the obese rat. In a second experiment, long-term food restriction resulted in greater glucose conversion to CO2 in response to insulin in adipocytes from lean rats but not obese rats compared to their respective control groups. These results indicate that food restriction throughout the first year of life in the obese Zucker rat does not alter the development of hyperplastic obesity and insulin resistance.
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PMID:Effects of long-term moderate food restriction on growth, serum factors, lipogenic enzymes and adipocyte glucose metabolism in lean and obese Zucker rats. 355 7

The effects of 2-aminoethanesulfonic acid (taurine) and its structural analogs, 3-aminopropanesulfonic acid (homotaurine) and 4-aminobutanesulfonic acid (ABSA), on lipid metabolism were investigated in rats with dietary hyperlipidemia. The serum cholesterol levels increased approximately five-fold in rats fed a diet containing 0.5% cholesterol and 1% cholic acid for 10 d. omega-Aminosulfonic acids dissolved in water were orally administered for 10 d concurrently with the 0.5% cholesterol diet. Taurine suppressed elevation in serum cholesterol levels by 46.9 and 63.9% at doses of 250 and 500 mg/kg, respectively. Serum triglycerides levels, however, were not significantly altered by taurine. Both homotaurine and ABSA, 500 mg/kg each, inhibited the elevation in serum cholesterol levels to an extent, namely, 32.0 and 22.3% lower than that of the controls, respectively. Treatment with homotaurine in doses of 250 and 500 mg/kg significantly increased serum triglycerides levels by 37.6 and 35.9%, respectively, and ABSA (500 mg/kg) also revealed a tendency to raise these levels. All the sulfonic acids (500n mg/kg each) reduced cholesterol levels in the liver similarly, while changes in triglycerides levels in the liver were insignificant. Both taurine and homotaurine (t00 mg/kg each) inhibited intestinal absorption of cholesterol. The inhibitory effect of homotaurine was as great as 31.5% and greater than that of taurine. No influence of taurine (500 mg/kg) was observed in lipoprotein lipase activity in the epididymal fat tissue, but the activity did appear to be inhibited by homotaurine (500 mg/kg).
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PMID:Effects of omega-aminosulfonic acids on lipid metabolism in dietary hyperlipidemic rats. 663 58

Expression of the obese (ob) gene is augmented in the adipose tissue in several rodent models of genetic obesity. In the present study, we examined the ob gene expression in a rodent model of acquired obesity obtained by pure overfeeding of normal rats. Male Sprague-Dawley rats at 8 weeks of age were fed standard diet or high-fat diet. Rats fed high-fat diet developed moderate degree of obesity, hyperglycemia, and hyperlipidemia as compared with rats fed standard diet. Northern blot analysis revealed that the ob gene is expressed abundantly in the adipose tissue obtained from the epididymal, mesenteric, subcutaneous, retroperitoneal, and interscapular fat pads in rats fed standard diet. Expression of the ob gene was augmented in all the adipose tissue examined in rats fed high-fat diet. The present study demonstrates that the ob gene expression is augmented in the adipose tissue in diet-induced obesity, thereby suggesting the pathophysiologic roles of the ob gene in acquired obesity.
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PMID:Augmented expression of the obese gene in the adipose tissue from rats fed high-fat diet. 748 12

To elucidate the regulation of obese (ob) gene expression in obesity and diabetes, we examined ob gene expression in KK mice and congenic lethal yellow obese KKAy mice. Northern blot analysis revealed that the ob mRNA levels are roughly equivalent in each of the epididymal, mesenteric, and subcutaneous white adipose tissue (WAT) from KK and KKAy mice at 4 wk of age, when the obese phenotype of KKAy mice was not apparent. Expression of the ob gene was augmented in the mesenteric and subcutaneous WAT but was unchanged in the epididymal WAT in KKAy mice at 12 wk of age, when KKAy mice developed marked obesity with hyperglycemia, hyperlipidemia, and hyperinsulinemia. The ob gene expression was also examined during fasting in 12-wk-old KK and KKAy mice. After 24 or 72 h of fasting in both mouse strains, ob gene expression was downregulated in the epididymal and mesenteric WAT but was unchanged in the subcutaneous WAT. The present study demonstrates that adipose tissue expression of the ob gene is regulated depending on the nutritional status in KK and KKAy mice.
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PMID:Regulation of obese gene expression in KK mice and congenic lethal yellow obese KKAy mice. 877 28

Experimental rat models (5-week-old Sprague-Dawley rats) with hyperlipemia were prepared by feeding high-cholesterol feed containing sodium cholate and casein as a protein source. Dried maitake (Grifola frondosa) powder was mixed with the basic high-cholesterol feed and the serum lipids were periodically measured. Values of cholesterol, triglyceride and phospholipid in serum of rats in the maitake-feed group were suppressed by 0.3-0.8 times those in animals fed the basic feed, the latter values being close to those in rats given normal feed. The value of high density lipoprotein (HDL)-cholesterol in serum which is generally reduced by the ingestion of high-cholesterol feed remained the level it was at the beginning of the experiment. Weights of extirpated liver and epididymal fat-pads were significantly less (0.6-0.7 times) than those in the basic feed group, indicating that maitake inhibits lipid accumulation in the body. Liver lipids were also measured and the values were found to be decreased by maitake administration as true of serum lipid, suggesting maitake has an anti-liver lipid activity. Measurement of the amount of total cholesterol and bile acid in feces showed, the ratio of cholesterol-excretion had increased 1.8 times and bile acid-excretion 3 fold by maitake treatment. From these results, it is believed that maitake helps to improve the lipid metabolism as it inhibits both liver lipid and serum lipid which are increased by the ingestion of high-fat feed.
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PMID:Anti-hyperliposis effect of maitake fruit body (Grifola frondosa). I. 925 20

A line of transgenic rats (heterozygotes) carrying a chimeric gene comprising a regulatory portion of murine whey acidic protein and a structural portion of human GH (hGH) genes developed severe obesity with age. To characterize physiological mechanisms that lead to fat accumulation, an array of parameters related to obesity were studied. Blood hGH levels were continuously low, endogenous rat GH secretion was suppressed, and the pulsatility in peripheral GH levels was absent. Plasma glucose, insulin, triglyceride, and FFA levels in the male transgenic rats significantly exceeded those in nontransgenic littermates at 12 and 17 weeks, but not at 7 weeks, of age. All symptoms except hyperlipidemia were restored to normal by treatment with an antidiabetic agent, thiazolidinedione (troglitazone), for 1 week from 17 weeks of age. As phenotypic expression of obesity was already evident before aberration of physiological parameters, it was assumed that animals had a condition in which obesity or hyperlipidemia caused hyperinsulinemia. Gene expression and enzymatic activity of lipoprotein lipase in the adipose tissue in the transgenic rats were not different from those in normal rats. In contrast, the gene expression level of glycerol-3-phosphodehydrogenase was markedly elevated, suggesting that glycerol synthesis was much enhanced in the adipocytes of the transgenic rats. In an i.p. glucose tolerance test, the transgenic rats were not hyperglycemic at 7 weeks of age; however, the animal became hyperglycemic at 15-17 weeks of age. Finally, treatment with recombinant hGH for 1 week to produce pulsatile secretion reduced the size of epididymal and kidney fat pads and restored normal weight gain. These observations suggest that continuously low peripheral GH levels with the lack of pulsatile secretion resulted in obesity and noninsulin-dependent diabetes mellitus.
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PMID:Obesity and insulin resistance in human growth hormone transgenic rats. 964 76

Abnormal lipid metabolism and its restoration by dietary methionine (Met) and cystine (Cys) were studied in Donryu rats subcutaneously implanted with an ascites hepatoma cell line of AH109A. The hepatoma-bearing rats exhibited hyperlipidemia characterized by rises in serum triglyceride and cholesterol levels. Decreased lipoprotein lipase (LPL) activities in epididymal adipose tissue, cardiac muscle, and gastrocnemius as well as increased fatty acid mobilization from adipose tissue were considered to be responsible for the hepatoma-induced hypertriglyceridemia, while increased hepatic cholesterogenesis and decreased steroid excretion into feces were thought to be responsible for the hepatoma-induced hypercholesterolemia. Dietary-supplemented Met or Cys reduced the AH109A-induced hypertriglyceridemia with suppression of fatty acid synthesis in the host liver. Met restored the fall of LPL activities, while Cys did not. Dietary Met or Cys also reduced the hypercholesterolemia with restoration of decreased bile acid excretion into feces. These results suggest that dietary Met or Cys is hypolipidemic in the hepatoma-bearing rats with slight differences in their modes of action.
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PMID:Effects of dietary methionine and cystine on lipid metabolism in hepatoma-bearing rats with hyperlipidemia. 977 38

HQL-975 (3-{4-12-(5-methyl-2-phenyl-oxazol-4-yl)-ethoxyl-phenyl}-2S- propylamino-propionic acid) is a new oral antidiabetic agent which has been shown to be effective in insulin-resistant diabetic animals. In the present study, we examined the effects of HQL-975 on glucose utilization and insulin action in KK-Ay mice with genetically obese non-insulin diabetes. (1) Dietary administration of HQL-975 (19 mg/kg/d for 7 d) improved hyperglycemia, hyperlipidemia and hyperinsulinemia in the mice. (2) The HQL-975-treated mice showed enhanced net glucose utilization, that is, glucose was significantly incorporated into total lipids in the white adipose tissue (WAT) and liver, and into glycogen in the diaphragm for the last 24 h of the drug administration period. (3) Treatment improved the decreased stimulative action of insulin in the epididymal WAT and the agent increased insulin-stimulated lipogenesis from both glucose and acetate. (4) Treatment also increased the activity of lipogenic enzymes such as glycerol-3-phosphate dehydrogenase and fatty acid synthetase. (5) In vitro exposure of WAT to HQL-975 enhanced lipogenesis in the presence of insulin. From these findings, we conclude that HQL-975 improves glucose utilization of KK-Ay mice through the enhancement of insulin action, which is associated with its lipogenic effects.
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PMID:Lipogenic action of the novel oral antidiabetic agent HQL-975 in genetically obese diabetic KK-Ay mice. 1040 28


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