The Experts below are selected from a list of 93 Experts worldwide ranked by ideXlab platform
M. Kirchgessner - One of the best experts on this subject based on the ideXlab platform.
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The effect of Dietary fat on activities of lipogenic enzymes in liver and adipose tissue of zinc-adequate and zinc-deficient rats
The Journal of Nutritional Biochemistry, 1996Co-Authors: Klaus Eder, M. KirchgessnerAbstract:Abstract The aim of the present study was to investigate if zinc-deficiency influences the regulation of lipogenic enzymes by Dietary polyunsaturated fatty acids. Therefore, rats were fed a Fat-Free Diet with either adequate or deficient zinc supply for 6 days. After that period the groups were divided; half of the rats were given the Fat-Free zinc-adequate and zinc-deficient Diets for another 3 days, whereas the other half was given the same Diets supplemented with 5% safflower oil. To control food intake, all the rats were force-fed by gastric tube. At the end of the experiment, zinc-deficient rats fed both, the Fat-Free Diet and the 5% safflower oil Diet had largely reduced zinc concentrations and activities of alkaline phosphatase in serum proving their zinc-deficient state. Zinc-deficient rats fed both the Fat-Free and the 5% safflower oil Diet had markedly increased concentrations of triglycerides in liver compared with zinc-adequate rats. Zinc-deficient rats fed both the Fat-Free Diet and the 5% safflower oil Diet had increased activities of glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase compared with their controls. In contrast, activities of fatty acid synthase and malic enzyme were not changed by zinc deficiency. This suggests that fatty liver is not mainly due to increased lipogenesis but to other factors such as impaired exclusion of lipids from liver. The addition of safflower oil to the Fat-Free Diet suppressed activities of hepatic lipogenic enzymes in both, zinc-adequate and zinc-deficient rats. However, the suppression was more pronounced in zinc-adequate rats than in zinc-deficient rats. In adipose tissue, addition of safflower oil elevated activities of lipogenic enzymes in zinc-adequate rats but lowered activities in zinc-deficient rats. Those data suggest that zinc-deficiency affects regulation of lipogenic enzymes in liver and adipose tissue.
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Zinc deficiency and the desaturation of linoleic acid in rats force-fed Fat-Free Diets.
Biological trace element research, 1996Co-Authors: Klaus Eder, M. KirchgessnerAbstract:Recent studies with rats force-fed zinc-deficient Diets containing various types of fat failed to demonstrate a role of zinc in desaturation of linoleic acid. The present study was conducted to investigate the effect of zinc deficiency on desaturation of linoleic acid in rats that were initially force-fed Fat-Free Diets to stimulate activity of desaturases. Therefore, rats were fed zinc-adequate and zinc-deficient Fat-Free Diets for 6 d. After that period, the groups were divided and half of the rats continued feeding the Fat-Free Diet for another 3.5 d whereas the other half was switched to a fat Diet by supplementing the Fat-Free Diet with 5% safflower oil. In order to assess desaturation of linoleic acid, fatty acid compositions of liver phosphatidylcholine, -ethanolamine, and -serine were considered, particularly levels of individual (n-6) polyunsaturated fatty acids (PUFA). Levels of total and individual (n-6) PUFA were similar in zinc-adequate and zinc-deficient rats fed the Fat-Free Diet throughout the experiment. Addition of 5% safflower oil increased levels of total and individual (n-6) PUFA in both zinc-adequate and zinc-deficient rats. However, total (n-6) PUFA in all types of phospholipids were higher in zinc-adequate rats than in zinc-deficient rats. Additionally, in zinc-deficient rats there were changes of (n-6) PUFA levels typical for impaired delta 5 and delta 6 desaturation: linoleic acid and dihomo-gamma-linolenic acid were elevated; arachidonic acid, docosatetraenoic acid, and docosapentaenoic were lowered by zinc deficiency. Therefore, the study shows that zinc deficiency impairs desaturation of linoleic acid in rats force-fed Fat-Free Diets and therefore supports results from former convential zinc deficiency experiments suggesting a role of zinc for desaturation of linoleic acid.
John M. Dietschy - One of the best experts on this subject based on the ideXlab platform.
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Regulation of hepatic cholesterol metabolism in the rat in vivo: Effect of a synthetic Fat-Free Diet on sterol synthesis and low-density lipoprotein transport
Biochimica et biophysica acta, 1995Co-Authors: Marco Bertolotti, David K. Spady, John M. DietschyAbstract:A synthetic Fat-Free Diet, previously shown to decrease hepatic cholesterol synthesis, was utilized to manipulate cholesterol balance in vivo in female Sprague-Dawley rats. A significant 65% decrease of hepatic cholesterol synthesis compared to controls was shown after 1 week of treatment, which remained constant during the following 3 weeks. The inhibitory effect of the Diet was completely abolished by cholestyramine supplementation. At week 3 of the experimental Diet, bile acid synthesis was reduced by 63%, this reduction being correlated with decreased recycling frequency of the bile acid pool. Hepatic clearance of low-density lipoprotein (LDL) was slightly decreased, with no changes in plasma cholesterol, hepatic LDL-cholesterol uptake and whole body LDL-cholesterol production. When cholesterol and saturated fatty acids were supplemented to the Diets in the attempt to disclose alteration in LDL transport, LDL clearance was unaffected; plasma LDL-cholesterol and hepatic LDL-cholesterol uptake were increased, as a consequence of increased LDL-cholesterol production. On the other hand, hepatic cholesterol synthesis was further suppressed; bile acid synthesis was increased by cholesterol supplementation in the Fat-Free group, even if to subnormal levels. These findings suggest that: (1) bile acid synthesis is decreased by feeding a synthetic Fat-Free Diet, probably due to slower recirculation of bile acids along the entero-hepatic axis in conditions of reduced functional need; (2) consequently, a significant reduction of hepatic cholesterol synthesis is observed with no changes in LDL-cholesterol uptake; (3) further supplementation of Dietary cholesterol and saturated fats is compensated for by changes in the rates of cholesterol and bile acid synthesis, but not of LDL transport. The data confirm the existence of independent regulation for hepatic sterol synthesis and LDL transport in this species.
Yoichi Kawashima - One of the best experts on this subject based on the ideXlab platform.
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Inducing Effect of Clofibric Acid on Stearoyl-CoA Desaturase in Intestinal Mucosa of Rats
Lipids, 2014Co-Authors: Tohru Yamazaki, Yoichi Kawashima, Atsushi Mitsumoto, Takeshi Sakamoto, Makiko Kadokura, Yuki Mutoh, Mari Okazaki, Naomi KudoAbstract:Fibrates have been reported to elevate the hepatic proportion of oleic acid (18:1n-9) through inducing stearoyl-CoA desaturase (SCD). Despite abundant studies on the regulation of SCD in the liver, little is known about this issue in the small intestine. The present study aimed to investigate the effect of clofibric acid on the fatty acid profile, particularly monounsaturated fatty acids (MUFA), and the SCD expression in intestinal mucosa. Treatment of rats with a Diet containing 0.5 % (w/w) clofibric acid for 7 days changed the MUFA profile of total lipids in intestinal mucosa; the proportion of 18:1n-9 was significantly increased, whereas those of palmitoleic (16:1n-7) and cis -vaccenic (18:1n-7) acids were not changed. Upon the treatment with clofibric acid, SCD was induced and the gene expression of SCD1, SCD2, and fatty acid elongase (Elovl) 6 was up-regulated, but that of Elovl5 was unaffected. Fat-Free Diet feeding for 28 days increased the proportions of 16:1n-7 and 18:1n-7, but did not effectively change that of 18:1n-9, in intestinal mucosa. Fat-Free Diet feeding up-regulated the gene expression of SCD1, but not that of SCD2, Elovl6, or Elovl5. These results indicate that intestinal mucosa significantly changes its MUFA profile in response to challenges by clofibric acid and a Fat-Free Diet and suggest that up-regulation of the gene expression of SCD along with Elovl6 is indispensable to elevate the proportion of 18:1n-9 in intestinal mucosa.
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Inducing Effect of Clofibric Acid on Stearoyl‐CoA Desaturase in Intestinal Mucosa of Rats
Lipids, 2014Co-Authors: Tohru Yamazaki, Yoichi Kawashima, Atsushi Mitsumoto, Takeshi Sakamoto, Makiko Kadokura, Yuki Mutoh, Mari Okazaki, Naomi KudoAbstract:Fibrates have been reported to elevate the hepatic proportion of oleic acid (18:1n-9) through inducing stearoyl-CoA desaturase (SCD). Despite abundant studies on the regulation of SCD in the liver, little is known about this issue in the small intestine. The present study aimed to investigate the effect of clofibric acid on the fatty acid profile, particularly monounsaturated fatty acids (MUFA), and the SCD expression in intestinal mucosa. Treatment of rats with a Diet containing 0.5% (w/w) clofibric acid for 7 days changed the MUFA profile of total lipids in intestinal mucosa; the proportion of 18:1n-9 was significantly increased, whereas those of palmitoleic (16:1n-7) and cis-vaccenic (18:1n-7) acids were not changed. Upon the treatment with clofibric acid, SCD was induced and the gene expression of SCD1, SCD2, and fatty acid elongase (Elovl) 6 was up-regulated, but that of Elovl5 was unaffected. Fat-Free Diet feeding for 28 days increased the proportions of 16:1n-7 and 18:1n-7, but did not effectively change that of 18:1n-9, in intestinal mucosa. Fat-Free Diet feeding up-regulated the gene expression of SCD1, but not that of SCD2, Elovl6, or Elovl5. These results indicate that intestinal mucosa significantly changes its MUFA profile in response to challenges by clofibric acid and a Fat-Free Diet and suggest that up-regulation of the gene expression of SCD along with Elovl6 is indispensable to elevate the proportion of 18:1n-9 in intestinal mucosa.
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Stearoyl-CoA desaturase activity is elevated by the suppression of its degradation by clofibric acid in the liver of rats.
Journal of pharmacological sciences, 2007Co-Authors: Tomoaki Toyama, Atsushi Mitsumoto, Naomi Kudo, Yasuhide Hibino, Tadashi Tsuda, Yoichi KawashimaAbstract:A mechanism by which fibrates control stearoyl-CoA desaturase (SCD) in the liver was studied. Treatment of rats with 2-(4-chlorophenoxy)-2-methylpropionic acid (clofibric acid) or feeding of a Fat-Free Diet markedly elevated hepatic activity of SCD. Both the treatment with clofibric acid and the feeding of the Fat-Free Diet caused an increase in the steady-state level of SCD1 mRNA and enhanced transcriptional rate. The half-lives of SCD for control rats, rats treated with clofibric acid rats, and rats fed the Fat-Free Diet were estimated to be 2.0, 3.9, and 1.9 h, respectively. Activity of palmitoyl-CoA chain elongase (PCE) was increased by both clofibric acid treatment and feeding of the Fat-Free Diet as was observed with SCD. Steady-state level of rat fatty acid elongase 2 mRNA was increased by the treatment with clofibric acid or feeding of Fat-Free Diet, although the transcriptional rate was not altered. Different from SCD, PCE was highly stable and its half-life was not changed by either clofibric acid or Fat-Free Diet. These results strongly suggest that the decreased degradation of SCD is responsible for the increase in its activity in addition to increased transcription of SCD1 in the rats treated with clofibric acid.
Andrew J. Dannenberg - One of the best experts on this subject based on the ideXlab platform.
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Dietary lipid regulates the amount and functional state of UDP-glucuronosyltransferase in rat liver.
The Journal of nutrition, 1992Co-Authors: Andrew J. Dannenberg, David ZakimAbstract:The effect of a Fat-Free Diet on the amount and functional state of UDP-glucuronosyltransferase was studied in rat liver microsomes. Measurements of enzyme activity showed that activity was approximately 30% lower in untreated microsomes in response to the Fat-Free Diet as compared with the control Diet. Immunoblotting with anti-UDP-glucuronosyltransferase showed approximately 200% less enzyme in rats fed the Fat-Free Diet. A kinetic method for measuring total UDP-glucuronosyltransferase confirmed the result of the immunoblot. Thus, the total amount of enzyme declined to a greater extent than enzyme activity. Responses of the enzyme to activation by palmitoyl-lysophosphatidylcholine or UDP-N-acetyl-glucosamine suggested that rats fed the Fat-Free Diet had a greater activity per molecule of UDP-glucuronosyltransferase than did rats fed the control Diet. This result explained the relatively small decline in enzyme activity as compared with enzyme concentration in microsomes prepared from animals fed the Fat-Free Diet. Fatty acid analysis of microsomal lipids demonstrated that the Fat-Free Diet was associated with lower levels of arachidonic and linoleic acids and greater amounts of palmitoleic, oleic and cis-vaccenic acids.
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Effect of Dietary lipids on levels of UDP-glucuronosyltransferase in liver
Biochemical pharmacology, 1992Co-Authors: Andrew J. Dannenberg, Eun K. YangAbstract:Abstract Others have shown recently that Dietary fish oil protects against acetaminophen-induced liver injury in vivo . Fish oil was protective because it increased the clearance of acetaminophen via glucuronidation. This work left unresolved the basis for increased rates of glucuronidation in animals fed fish oil. We therefore have determined how the amount and type of lipid in the Diet affect the activity of liver microsomal UDP-glucuronosyltransferase activity. Male Wistar rats were fed a Fat-Free Diet or isocaloric Diets containing 5% corn oil, olive oil or fish oil for 4 weeks. The activity of UDP-glucuronosyltransferase was highest in rats fed fish oil and lowest in rats fed the Fat-Free Diet. Treatment with corn oil and olive oil resulted in intermediate levels of activity. Diet-induced differences in amounts of UDP-glucuronosyltransferase were shown by immunoblotting and kinetic measurements. Treatment with fish oil resulted in a 3-fold increase in the amount of UDP-glucuronosyltransferase versus the Fat-Free Diet. Corn oil and olive oil Diets caused 2-fold increases in the amount of UDP-glucuronosyltransferase versus the Fat-Free Diet. Fatty acid analysis of microsomal lipids showed that the Fat-Free Diet was associated with decreased levels of arachidonic acid versus the corn oil or olive oil Diets. The fish oil Diet resulted in increased levels of ω-3 fatty acids versus the other Diets.
Klaus Eder - One of the best experts on this subject based on the ideXlab platform.
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The effect of Dietary fat on activities of lipogenic enzymes in liver and adipose tissue of zinc-adequate and zinc-deficient rats
The Journal of Nutritional Biochemistry, 1996Co-Authors: Klaus Eder, M. KirchgessnerAbstract:Abstract The aim of the present study was to investigate if zinc-deficiency influences the regulation of lipogenic enzymes by Dietary polyunsaturated fatty acids. Therefore, rats were fed a Fat-Free Diet with either adequate or deficient zinc supply for 6 days. After that period the groups were divided; half of the rats were given the Fat-Free zinc-adequate and zinc-deficient Diets for another 3 days, whereas the other half was given the same Diets supplemented with 5% safflower oil. To control food intake, all the rats were force-fed by gastric tube. At the end of the experiment, zinc-deficient rats fed both, the Fat-Free Diet and the 5% safflower oil Diet had largely reduced zinc concentrations and activities of alkaline phosphatase in serum proving their zinc-deficient state. Zinc-deficient rats fed both the Fat-Free and the 5% safflower oil Diet had markedly increased concentrations of triglycerides in liver compared with zinc-adequate rats. Zinc-deficient rats fed both the Fat-Free Diet and the 5% safflower oil Diet had increased activities of glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase compared with their controls. In contrast, activities of fatty acid synthase and malic enzyme were not changed by zinc deficiency. This suggests that fatty liver is not mainly due to increased lipogenesis but to other factors such as impaired exclusion of lipids from liver. The addition of safflower oil to the Fat-Free Diet suppressed activities of hepatic lipogenic enzymes in both, zinc-adequate and zinc-deficient rats. However, the suppression was more pronounced in zinc-adequate rats than in zinc-deficient rats. In adipose tissue, addition of safflower oil elevated activities of lipogenic enzymes in zinc-adequate rats but lowered activities in zinc-deficient rats. Those data suggest that zinc-deficiency affects regulation of lipogenic enzymes in liver and adipose tissue.
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Zinc deficiency and the desaturation of linoleic acid in rats force-fed Fat-Free Diets.
Biological trace element research, 1996Co-Authors: Klaus Eder, M. KirchgessnerAbstract:Recent studies with rats force-fed zinc-deficient Diets containing various types of fat failed to demonstrate a role of zinc in desaturation of linoleic acid. The present study was conducted to investigate the effect of zinc deficiency on desaturation of linoleic acid in rats that were initially force-fed Fat-Free Diets to stimulate activity of desaturases. Therefore, rats were fed zinc-adequate and zinc-deficient Fat-Free Diets for 6 d. After that period, the groups were divided and half of the rats continued feeding the Fat-Free Diet for another 3.5 d whereas the other half was switched to a fat Diet by supplementing the Fat-Free Diet with 5% safflower oil. In order to assess desaturation of linoleic acid, fatty acid compositions of liver phosphatidylcholine, -ethanolamine, and -serine were considered, particularly levels of individual (n-6) polyunsaturated fatty acids (PUFA). Levels of total and individual (n-6) PUFA were similar in zinc-adequate and zinc-deficient rats fed the Fat-Free Diet throughout the experiment. Addition of 5% safflower oil increased levels of total and individual (n-6) PUFA in both zinc-adequate and zinc-deficient rats. However, total (n-6) PUFA in all types of phospholipids were higher in zinc-adequate rats than in zinc-deficient rats. Additionally, in zinc-deficient rats there were changes of (n-6) PUFA levels typical for impaired delta 5 and delta 6 desaturation: linoleic acid and dihomo-gamma-linolenic acid were elevated; arachidonic acid, docosatetraenoic acid, and docosapentaenoic were lowered by zinc deficiency. Therefore, the study shows that zinc deficiency impairs desaturation of linoleic acid in rats force-fed Fat-Free Diets and therefore supports results from former convential zinc deficiency experiments suggesting a role of zinc for desaturation of linoleic acid.