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Lecture 13 - Cholesterol Biosynthesis Mechanism …

This flow chart shows how the synthesis of cholesterol occurs in the body, ..

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Cholesterol biosynthesis mechanism Cholesterol, …

In this reaction a carboxyl group is added to acetyl CoA to generate malonyl CoA. This biotin-containing enzyme catalyzes the committed step in fatty acid biosynthesis and is subject to a complex regulation not covered in this activity.

The lanosterol pathway refers to a segment of the cholesterol biosynthesis pathway ..

Background:
The dietary supply of methyl donors such as folate, vitamin B12, betaine, methionine, and choline is essential for normal growth, development, and physiological functions through the life course. Both human and animal studies have shown that vitamin B12 deficiency is associated with altered lipid profile and play an important role in the prediction of metabolic risk, however, as of yet, no direct mechanism has been investigated to confirm this.Results:
Three independent clinical studies of women (i) non-pregnant at child-bearing age, (ii) in early pregnancy, and (iii) at delivery showed that low vitamin B12 status was associated with higher total cholesterol, LDL cholesterol, and cholesterol-to-HDL ratio. These results guided the investigation into the cellular mechanisms of induced cholesterol biosynthesis due to vitamin B12 deficiency, using human adipocytes as a model system. Adipocytes cultured in low or no vitamin B12 conditions had increased cholesterol and homocysteine levels compared to control. The induction of cholesterol biosynthesis was associated with reduced s-adenosylmethionine (AdoMet)-to-s-adenosylhomocysteine (AdoHcy) ratio, also known as methylation potential (MP). We therefore studied whether reduced MP could lead to hypomethylation of genes involved in the regulation of cholesterol biosynthesis. Genome-wide and targeted DNA methylation analysis identified that the promoter regions of SREBF1 and LDLR, two key regulators of cholesterol biosynthesis, were hypomethylated under vitamin B12-deficient conditions, and as a result, their expressions and cholesterol biosynthesis were also significantly increased. This finding was further confirmed by the addition of the methylation inhibitor, 5-aza-2′-deoxycytidine, which resulted in increased SREBF1 and LDLR expressions and cholesterol accumulation in vitamin B12-sufficient conditions. Finally, we observed that the expression of SREBF1, LDLR, and cholesterol biosynthesis genes were increased in adipose tissue of vitamin B12 deficient mothers compared to control group.Conclusions:
Clinical data suggests that vitamin B12 deficiency is an important metabolic risk factor. Regulation of AdoMet-to-AdoHcy levels by vitamin B12 could be an important mechanism by which it can influence cholesterol biosynthesis pathway in human adipocytes.

Mechanism of the inhibition of cholesterol biosynthesis …

demethylation mechanism in cholesterol biosynthesis.

For instance, thisoxysterol repressed the activity of a key rate-controlling enzyme in cholesterolbiosynthesis, hydroxymethylglutaryl (HMG)-CoA reductase.

A combination of factors and mechanisms appears to contribute to the cholesterol lowering action of barley. Soluble fiber is suggested to reduce cholesterol by increased excretion of bile acids or neutral sterols, increased catabolism of LDL cholesterol, and reduced absorption of fat. Soluble fibers were shown to be fermented in the colon and thus to give rise to short-chain fatty acids that can be absorbed and may inhibit hepatic cholesterol synthesis. In addition to the soluble fiber, barley contains a wide range of phytochemicals, some of which are being investigated for their effect on metabolism.

Inhibition of cholesterol biosynthesis

Biosynthesis of cholesterol is directly regulated by the ..

Allicin is the bioactive compound in garlic that inhibits cholesterol synthesis in vitro. However, numerous studies have produced conflicting results regarding garlic's ability to lower blood cholesterol. So, cholesterol lowering potential of garlic remains unproven.

Conclusions:
Clinical data suggests that vitamin B12 deficiency is an important metabolic risk factor. Regulation of AdoMet-to-AdoHcy levels by vitamin B12 could be an important mechanism by which it can influence cholesterol biosynthesis pathway in human adipocytes.

Cholesterol Biosynthesis: A Mechanistic Overview | …
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  • of mammalian cholesterol biosynthesis.

    The results demonstrate that the diol does not originate from known intermediates of cholesterol biosynthesis, ..

  • limiting enzyme of cholesterol biosynthesis, ..

    Free radical oxidation of cholesterol and its precursors: Implications in cholesterol biosynthesis ..

  • cholesterol biosynthesis via an indirect mechanism

    Decreased cholesterol biosynthesis steps up the levels of the LDL-receptor resulting in the positive ..

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Regulation of the cholesterol biosynthetic pathway and …

I’m sorry but your language has changed from unfamiliar to incomprehensible. smile. After trying to understand the above using online dictionaries, the best I can figure this is talking about statin drugs being used to control an enzyme that is found both active and inactive in the body. Glucagon raises sugar in the blood which stimulates inactivation. And it says insulin activates it. It also says HMG-CoA is an intermediate on the pathway for synthesis of ketone bodies (I am familiar with the concept of eating high protein to make ketones) Do I have it basically correct? It is not obvious to me how this relates to carbs being the strongest driver of cholesterol production in the liver. Thank you for your patient attempt to educate me. I do appreciate it.

Inhibition of Cholesterol Biosynthesis in Primary …

“Hormonal control is mediated by covalent modification of HMG-CoA reductase itself. The enzyme exists in phosphorylated (inactive) and dephosphorylated (active) forms. Glucagon stimulates phosphorylation (inactivation), and insulin promotes dephosphorylation, activating the enzyme and favoring cholesterol synthesis.”

Biosynthesis Of Cholesterol Rate Limiting Step

Most evidence supports that omega-3 fatty acids inhibit hepatic triglyceride synthesis, decrease Very low-density lipoproteins (VLDL) production/secretion and increase VLDL metabolism, potentially increasing the conversion of VLDL particles to LDL particles. Overall, despite a potential increase in LDL cholesterol levels, many studies have reported that omega-3 fatty acids reduces non-HDL cholesterol (total cholesterol minus HDL cholesterol), which may be a better predictor of atherosclerotic coronary heart disease risk than LDL cholesterol alone.

Bile Acid Synthesis, Metabolism and Biological Functions

Results:
Three independent clinical studies of women (i) non-pregnant at child-bearing age, (ii) in early pregnancy, and (iii) at delivery showed that low vitamin B12 status was associated with higher total cholesterol, LDL cholesterol, and cholesterol-to-HDL ratio. These results guided the investigation into the cellular mechanisms of induced cholesterol biosynthesis due to vitamin B12 deficiency, using human adipocytes as a model system. Adipocytes cultured in low or no vitamin B12 conditions had increased cholesterol and homocysteine levels compared to control. The induction of cholesterol biosynthesis was associated with reduced s-adenosylmethionine (AdoMet)-to-s-adenosylhomocysteine (AdoHcy) ratio, also known as methylation potential (MP). We therefore studied whether reduced MP could lead to hypomethylation of genes involved in the regulation of cholesterol biosynthesis. Genome-wide and targeted DNA methylation analysis identified that the promoter regions of SREBF1 and LDLR, two key regulators of cholesterol biosynthesis, were hypomethylated under vitamin B12-deficient conditions, and as a result, their expressions and cholesterol biosynthesis were also significantly increased. This finding was further confirmed by the addition of the methylation inhibitor, 5-aza-2′-deoxycytidine, which resulted in increased SREBF1 and LDLR expressions and cholesterol accumulation in vitamin B12-sufficient conditions. Finally, we observed that the expression of SREBF1, LDLR, and cholesterol biosynthesis genes were increased in adipose tissue of vitamin B12 deficient mothers compared to control group.

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