Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P56851 (epididymal)
 11,273 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine whether resistance to insulin or to thyroid hormones rather than an inherent defect in enzyme activity expression account for the age-related changes in lipogenic enzymes, the activities of malic enzymes (ME), fatty acid synthase (FAS), glucose-6-phosphate dehydrogenase (G-6PD) and 6-phosphogluconate dehydrogenase (6-PGD) were assayed in hepatic, retroperitoneal fat and epididymal fat cytosol of male Fischer 344 rats at 3.5, 12 and 25 months of age. The rats were maintained on either regular rat chow with 62% of calories as complex carbohydrates or were given either high glucose or fructose diet with 65.7% of calories provided by glucose or fructose respectively. Additional groups of young and aged rats were treated with L-triiodothyronine (T3) (15 microg/100 g body weight) for 10 days. Treatment with T3 resulted in higher levels of hepatic ME activity regardless of the diet consumed or the age of the rats. T3 had no consistent effect on FAS, G-6PD or 6-PGD activities. ME response to T3 in young rats was significantly greater than that found in aged rats regardless of diet. The age-related decrease in basal hepatic ME activity was not apparent in rats maintained on the high glucose or the high fructose diets, yet the T3 responsiveness of ME in rats maintained on these diets was not normalized. In adipose tissue, with the exception of the age-related changes in basal activity of the lipogenic enzymes, neither T3 nor the feeding of the test diets had any consistent effects. Since insulin resistance induced by high fructose feeding did not reduce hepatic lipogenic enzymes, it is unlikely that the age-related increase in insulin resistance explains the reduced lipogenic enzyme activity in aged rats. However, resistance to thyroid hormone action found in aged rats may partly account for the reduced hepatic lipogenic enzyme activity.
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PMID:The age-related changes in lipogenic enzymes: the role of dietary factors and thyroid hormone responsiveness. 1040 Mar 7

Lipid disorders are one of the known metabolic changes associated with chronic renal failure (CRF) [1, 2]. They are present as: hypertriglyceridemia--existed in 60% of CRF patients and hypercholesterolemia observed in 20-30% of people with this syndrome. These disorders, what was shown also in our own studies, are existing in different intensity in patients treated with maintenance haemodialysis [3], peritoneal dialysis [4] and after renal transplantation as well [5]. Mechanism of hypertriglyceridemia, despite over thirty years of studies, is still not finally elucidated. The opinion that it is a result of impaired triglyceride removal (due to decreased activities of both lipoprotein and hepatic lipases) is well documented, however the role of lipogenesis in its development is obscure [6, 7]. The reports concerning this problem contain contradictory data. In our studies performed several years ago we have shown that lipogenesis rate in white adipose tissue of uremic rats is significantly augmented [8, 9, 10] due to activation of free fatty acid synthase. Therefore, recently we paid once again our attention on the activity of this lipogenesis rate limiting enzyme responsible for the long term regulation. We measured its activity, protein abundance and mRNA level in liver and epididymal white adipose tissue of rats with surgically induced renal failure (two-stage subtotal nephrectomy). The results support the thesis that lipogenesis takes a part in a hypertriglyceridemia found in renal failure. There have been observed a significant increase in plasma triglyceride and VLDL concentrations in uremic animals and it was associated with the increase of FAS activity, FAS protein abundance and FAS mRNA. The results were similar in both studied tissues. Moreover, there have been also observed the increased activities of malic enzyme, glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase. All these enzymes participate in NADPH production, which is a necessary substrate for fatty acid biosynthesis [11, 12, 13]. Concluding, it appears that the rise in plasma triglyceride and VLDL concentrations observed in CRF rats is not only the result of increased liver and white adipose tissue lipogenesis rate. One has to remember, that these date are strictly original and enabling to elucidation further pathogenesis of hyperlipidemia in CRF. In the second set of experiments performed also in rats with experimentally induced CRF we have found that hypercholesterolemia observed in those animals is dependent on the significant activation of cholesterol synthase, induced by increased production of this enzyme (increment of protein abundance and synthase mRNA [14, 15]. Simultaneously, we have performed original studies on the diurnal rhythm of cholesterologenesis, showing that activity of this process is significantly augmented during whole twenty four hours [15]. Summarizing, one have to underline that our observations have important impact to the elucidation of lipid disturbances pathomechanism. Nevertheless further studies are necessary to establish how experimental data are corresponding with human pathology.
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PMID:[Pathomechanism of hyperlipoproteinemia in chronic renal failure]. 1497 58


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