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are used for the synthesis of one cholesterol ..

N2 - Exposure of weanling rats to diet containing the element tellurium results in specific inhibition of squalene epoxidase, an obligate enzyme in cholesterol biosynthesis. Liver responds to the resulting intracellular sterol deficit by up-regulating, in parallel and to the same extent, expression of mRNA for squalene epoxidase and for HMG-CoA reductase, the major rate-limiting enzyme in the pathway. This increased mRNA expression, coupled with additional translational and posttranslational activation of the pathway, allows normal levels of cholesterol synthesis in liver despite tellurium-induced inhibition of squalene epoxidase. The response to tellurium challenge in sciatic nerve is very different. In this tissue, cholesterol synthesis is prominent because of the large amount of cholesterol required for synthesis and maintenance of myelin. Although nerve shows an initial (at 1 day) up-regulation of mRNA expression for both enzymes in response to tellurium exposure, this is followed quickly by parallel down-regulation of both enzymes, in concert with down-regulation of mRNA expression for myelin proteins. We suggest that the tellurium-induced deficit in sterols leads to a coordinate down-regulation of synthesis of myelin components. The initial early up-regulation of cholesterol biosynthesis in sciatic nerve due to the cholesterol deficit is countered by down-regulation which is coordinated with overall control of the program of myelin assembly. This tissue-specific control of cholesterol synthesis in sciatic nerve is a point of vulnerability to toxicants, and may be related to the need for coordinate synthesis of all components by myelin.

The terminal enzymes of cholesterol synthesis, DHCR24 …

AB - Exposure of weanling rats to diet containing the element tellurium results in specific inhibition of squalene epoxidase, an obligate enzyme in cholesterol biosynthesis. Liver responds to the resulting intracellular sterol deficit by up-regulating, in parallel and to the same extent, expression of mRNA for squalene epoxidase and for HMG-CoA reductase, the major rate-limiting enzyme in the pathway. This increased mRNA expression, coupled with additional translational and posttranslational activation of the pathway, allows normal levels of cholesterol synthesis in liver despite tellurium-induced inhibition of squalene epoxidase. The response to tellurium challenge in sciatic nerve is very different. In this tissue, cholesterol synthesis is prominent because of the large amount of cholesterol required for synthesis and maintenance of myelin. Although nerve shows an initial (at 1 day) up-regulation of mRNA expression for both enzymes in response to tellurium exposure, this is followed quickly by parallel down-regulation of both enzymes, in concert with down-regulation of mRNA expression for myelin proteins. We suggest that the tellurium-induced deficit in sterols leads to a coordinate down-regulation of synthesis of myelin components. The initial early up-regulation of cholesterol biosynthesis in sciatic nerve due to the cholesterol deficit is countered by down-regulation which is coordinated with overall control of the program of myelin assembly. This tissue-specific control of cholesterol synthesis in sciatic nerve is a point of vulnerability to toxicants, and may be related to the need for coordinate synthesis of all components by myelin.

lack the enzymes for cholesterol synthesis, ..

The researchers believe silymarin may inhibit HMG-CoA reductase, the enzyme responsible for cholesterol synthesis in the liver.

N2 - We produced transgenic mice that express a dominant-positive truncated form of sterol regulatory element-binding protein-2 (SREBP-2) in liver and adipose tissue. The encoded protein lacks the membrane-binding and COOH- terminal regulatory domains, and it is therefore not susceptible to negative regulation by cholesterol. Livers from the transgenic mice showed increases in mRNAs encoding multiple enzymes of cholesterol biosynthesis, the LDL receptor, and fatty acid biosynthesis. The elevations in mRNA for 3-hydroxy- 3-methylglutaryl coenzyme A (HMG CoA) synthase and HMG CoA reductase were especially marked (13-fold and 75-fold, respectively). As a result, the transgenic livers showed a 28-fold increase in the rate of cholesterol synthesis and a lesser fourfold increase in fatty acid synthesis, as measured by intraperitoneal injection of [3H]water. These results contrast with previously reported effects of dominant-positive SREBP-1a, which activated fatty acid synthesis more than cholesterol synthesis. In adipose tissue of the SREBP-2 transgenics, the mRNAs for cholesterol biosynthetic enzymes were elevated, but the mRNAs for fatty acid biosynthetic enzymes were not. We conclude that SREBP-2 is a relatively selective activator of cholesterol synthesis, as opposed to fatty acid synthesis, in liver and adipose tissue of mice.

Exposure of weanling rats to diet containing the element tellurium results in specific inhibition of squalene epoxidase, an obligate enzyme in cholesterol biosynthesis. Liver responds to the resulting intracellular sterol deficit by up-regulating, in parallel and to the same extent, expression of mRNA for squalene epoxidase and for HMG-CoA reductase, the major rate-limiting enzyme in the pathway. This increased mRNA expression, coupled with additional translational and posttranslational activation of the pathway, allows normal levels of cholesterol synthesis in liver despite tellurium-induced inhibition of squalene epoxidase. The response to tellurium challenge in sciatic nerve is very different. In this tissue, cholesterol synthesis is prominent because of the large amount of cholesterol required for synthesis and maintenance of myelin. Although nerve shows an initial (at 1 day) up-regulation of mRNA expression for both enzymes in response to tellurium exposure, this is followed quickly by parallel down-regulation of both enzymes, in concert with down-regulation of mRNA expression for myelin proteins. We suggest that the tellurium-induced deficit in sterols leads to a coordinate down-regulation of synthesis of myelin components. The initial early up-regulation of cholesterol biosynthesis in sciatic nerve due to the cholesterol deficit is countered by down-regulation which is coordinated with overall control of the program of myelin assembly. This tissue-specific control of cholesterol synthesis in sciatic nerve is a point of vulnerability to toxicants, and may be related to the need for coordinate synthesis of all components by myelin.

Cholesterol: Synthesis, Metabolism, Regulation

in activating transcription of genes encoding enzymes of cholesterol synthesis.

We produced transgenic mice that express a dominant-positive truncated form of sterol regulatory element-binding protein-2 (SREBP-2) in liver and adipose tissue. The encoded protein lacks the membrane-binding and COOH- terminal regulatory domains, and it is therefore not susceptible to negative regulation by cholesterol. Livers from the transgenic mice showed increases in mRNAs encoding multiple enzymes of cholesterol biosynthesis, the LDL receptor, and fatty acid biosynthesis. The elevations in mRNA for 3-hydroxy- 3-methylglutaryl coenzyme A (HMG CoA) synthase and HMG CoA reductase were especially marked (13-fold and 75-fold, respectively). As a result, the transgenic livers showed a 28-fold increase in the rate of cholesterol synthesis and a lesser fourfold increase in fatty acid synthesis, as measured by intraperitoneal injection of [3H]water. These results contrast with previously reported effects of dominant-positive SREBP-1a, which activated fatty acid synthesis more than cholesterol synthesis. In adipose tissue of the SREBP-2 transgenics, the mRNAs for cholesterol biosynthetic enzymes were elevated, but the mRNAs for fatty acid biosynthetic enzymes were not. We conclude that SREBP-2 is a relatively selective activator of cholesterol synthesis, as opposed to fatty acid synthesis, in liver and adipose tissue of mice.

AB - We produced transgenic mice that express a dominant-positive truncated form of sterol regulatory element-binding protein-2 (SREBP-2) in liver and adipose tissue. The encoded protein lacks the membrane-binding and COOH- terminal regulatory domains, and it is therefore not susceptible to negative regulation by cholesterol. Livers from the transgenic mice showed increases in mRNAs encoding multiple enzymes of cholesterol biosynthesis, the LDL receptor, and fatty acid biosynthesis. The elevations in mRNA for 3-hydroxy- 3-methylglutaryl coenzyme A (HMG CoA) synthase and HMG CoA reductase were especially marked (13-fold and 75-fold, respectively). As a result, the transgenic livers showed a 28-fold increase in the rate of cholesterol synthesis and a lesser fourfold increase in fatty acid synthesis, as measured by intraperitoneal injection of [3H]water. These results contrast with previously reported effects of dominant-positive SREBP-1a, which activated fatty acid synthesis more than cholesterol synthesis. In adipose tissue of the SREBP-2 transgenics, the mRNAs for cholesterol biosynthetic enzymes were elevated, but the mRNAs for fatty acid biosynthetic enzymes were not. We conclude that SREBP-2 is a relatively selective activator of cholesterol synthesis, as opposed to fatty acid synthesis, in liver and adipose tissue of mice.

Tissue-specific coordinate regulation of enzymes of cholesterol biosynthesis: Sciatic nerve versus liver
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Introduction to Cholesterol Metabolism

Some of the lipases listed in Table 1 are suitable to be used in the synthesis of various enantiopure molecules such as alcohols, amides, carboxylic acids, and esters. These molecules are used in anti-inflammatory drugs (ibuprofen, naproxen), anticancer drugs an antiviral drug (lobucavir), an antihypertensive drug (captopril), anti-cholesterol drugs (squalene synthase inhibitor), an anti-Alzheimer disease drug ([S]-2-pentanol), and vitamin A.

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