Let’s start with what cholesterol is and what it does.

In previous investigations, we found high rates of cholesterol synthesis in human fetal liver tissue, second only to rates in fetal adrenal tissue. Previous estimates of the amount of cholesterol in the fetus derived from the maternal compartment are in the range of 20%. Thus, the liver may be the principal source of circulating lipoproteins in the human fetus, as is true in the human adult. Low density lipoprotein is the major source of cholesterol used for fetal adrenal steroidogenesis; therefore, it follows that factors regulating cholesterol synthesis in the human fetal liver may indirectly control the rate of steroid secretion by the adrenal cortex. The purpose of the present investigation was to determine if hormones, particularly those produced by the fetal-placental unit, might serve to stimulate cholesterol synthesis in the human fetal liver. The rate of cholesterol biosynthesis was determined by measuring the rate of incorporation of [3H]water into [3H]cholesterol in hepatocytes maintained in culture or by determination of the specific activity of 3-hydroxy-3-methylglutaryl coenzyme A reductase in microsomal preparations from human fetal liver. The addition of dexamethasone (10-10-10-6 M) stimulated cholesterol synthesis up to 2- to 4-fold between days 2 and 6 of exposure. When human fetal liver cells were maintained in the presence of dexamethasone (10-7 M), the activity of 3-hydroxy-3-methylglutaryl coenzyme A reductase in microsomal fractions was stimulated 4-fold compared to that in control cells. Cortisol also stimulated cholesterol biosynthesis in a concentration-dependent manner. The addition of 17β-estradiol (E2) to the culture medium resulted in stimulation of cholesterol biosynthesis in a concentration-dependent manner from 10-10-10-7 M. The rate of cholesterol synthesis when E2 was present (10-7 M) was 4-fold greater than in untreated cells. Stimulation of cholesterol synthesis by E2 was maintained between 2-7 days of incubation with E2. Estrone, estriol, and E2 (10-6 M) caused similar increases (3- to 4-fold) in the rates of cholesterol synthesis in human fetal hepatocytes. Finally, progesterone in concentrations greater than 10-6 M significantly stimulated cholesterol synthesis in human fetal liver cells. In contrast, other hormones and factors, including insulin, glucagon, PRL, GH, dehydroepiandrosterone and its sulfate, epidermal growth factor, fibroblast growth factor, T3, (Bu)2cAMP, and cholera toxin, had no effect on the rate of cholesterol synthesis in human fetal liver cells. In summary, estrogens, glucocorticoids, and progesterone produced by the fetal-placental unit stimulate the rate of cholesterol synthesis in human fetal liver cells.

Cholesterol synthesis can also be turned off when ..

Cholesterol: Synthesis, Metabolism, Regulation

The process of cholesterol synthesis ..

Thus, feedback inhibition of cholesterol biosynthesis by dietary cholesterol seems to occur primarily at the point of synthesis of mevalonate from hydroxymethylglutarate.

Cholesterol synthesized by the liver, ..

Thus, feedback inhibition of cholesterol biosynthesis by dietary cholesterol seems to occur primarily at the point of synthesis of mevalonate from hydroxymethylglutarate.">

198, 896 (1952)) studied the rate of cholesterol synthesized from labeled acetate by liver slices obtained from normal and diabetic livers.
Consider the vitally important functions of the 6 steroidal hormones, all of which are derived from cholesterol:

04/05/2015 · Cholesterol Synthesis Check Your Liver ..

These studies were undertaken to measure rates of synthesis of digitonin-precipitable sterols in vivo and in vitro in control rabbits (New Zealand (NZ) control) and in homozygous Watanabe heritable hyperlipidemic rabbits (WHHL) that lack receptors for low density lipoproteins (LDL). The plasma cholesterol concentration in NZ control fetuses equaled 79 mg/dl, rose to 315 mg/dl 12 days after birth, and fell to 80 mg/dl in young adult animals. At these same ages, cholesterol concentrations in the WHH animals equal 315, 625, and 715 mg/dl, respectively. The rate of whole animal sterol synthesis in vivo, expressed as the μmol of [3H]water incorporated into sterols per hr per kg of body weight, was lower in the WHHL animals than in the NZ controls both in the fetuses (108 vs 176) and in the adult animals (48 vs 66). In adult NZ controls the content of newly synthesized sterols (rate of sterol synthesis) per g of tissue was highest in the liver (538 nmol/g per hr), adrenal gland (438), small bowel (371), and ovary (225) while lower rates of synthesis were found in 15 other tissues. In the WHHL rabbits a higher content of [3H]sterols was found only in the adrenal gland (2,215) while synthesis was suppressed in the liver (310), colon, lung, and kidney, and was unchanged in the remaining organs. These findings were confirmed by measurements of rates of sterol synthesis in the same tissues in vitro. When whole organ weight was taken into consideration, the tissues that were the major contributors to whole body sterols synthesis in both types of rabbits were liver, small bowel, skin, and carcass. However, it was the lower rate of synthesis in the liver of the WHHL animals that alone accounted for the lower rate of whole animal sterol synthesis seen in these rabbits. These studies demonstrate that in WHHL animals that lack LDL receptors and that have very high levels of circulating LDL cholesterol, the rate of cholesterol synthesis in nearly all tissues is normal but in the liver is significantly suppressed. Only the adrenal gland manifested enhanced synthesis. Such findings suggest that in the WHHL rabbit where LDL receptor activity is reduced and plasma LDL levels rise, mechanisms other than receptor-mediated LDL uptake may act to deliver cholesterol to the cells of the various organs and to the liver.

and are adept at oxidative liver functions such as cholesterol synthesis, ..

and liver — our body revs up its cholesterol synthesis

AB - These studies were undertaken to measure rates of synthesis of digitonin-precipitable sterols in vivo and in vitro in control rabbits (New Zealand (NZ) control) and in homozygous Watanabe heritable hyperlipidemic rabbits (WHHL) that lack receptors for low density lipoproteins (LDL). The plasma cholesterol concentration in NZ control fetuses equaled 79 mg/dl, rose to 315 mg/dl 12 days after birth, and fell to 80 mg/dl in young adult animals. At these same ages, cholesterol concentrations in the WHH animals equal 315, 625, and 715 mg/dl, respectively. The rate of whole animal sterol synthesis in vivo, expressed as the μmol of [3H]water incorporated into sterols per hr per kg of body weight, was lower in the WHHL animals than in the NZ controls both in the fetuses (108 vs 176) and in the adult animals (48 vs 66). In adult NZ controls the content of newly synthesized sterols (rate of sterol synthesis) per g of tissue was highest in the liver (538 nmol/g per hr), adrenal gland (438), small bowel (371), and ovary (225) while lower rates of synthesis were found in 15 other tissues. In the WHHL rabbits a higher content of [3H]sterols was found only in the adrenal gland (2,215) while synthesis was suppressed in the liver (310), colon, lung, and kidney, and was unchanged in the remaining organs. These findings were confirmed by measurements of rates of sterol synthesis in the same tissues in vitro. When whole organ weight was taken into consideration, the tissues that were the major contributors to whole body sterols synthesis in both types of rabbits were liver, small bowel, skin, and carcass. However, it was the lower rate of synthesis in the liver of the WHHL animals that alone accounted for the lower rate of whole animal sterol synthesis seen in these rabbits. These studies demonstrate that in WHHL animals that lack LDL receptors and that have very high levels of circulating LDL cholesterol, the rate of cholesterol synthesis in nearly all tissues is normal but in the liver is significantly suppressed. Only the adrenal gland manifested enhanced synthesis. Such findings suggest that in the WHHL rabbit where LDL receptor activity is reduced and plasma LDL levels rise, mechanisms other than receptor-mediated LDL uptake may act to deliver cholesterol to the cells of the various organs and to the liver.

reductase you not only block synthesis of cholesterol but you may also effect ..

Biosynthesis of Fatty Acid and Cholesterol ..

HDL the so called 'good' cholesterol is the lipo-protein which transports cholesterol from the bloodstream back to the liver. Low levels of HDL reflect a sedentary lifestyle. Doctors and others who push the misinformation about raising HDL as being a good thing, fail to address that HDL levels greater than 75 are actually correlative with autoimmune processes. This is a strong possibility especially if triglyceride levels are low (less than 40). Excess consumption of alcohol, drug use, hypothyroidism, and excess estrogen can also cause HDL levels to become too high.