Turnover of plasma cholesterol in man

Goodman, DeWitt S.; Noble, Robert P.

doi:10.1172/jci105719

Cited by 284 publications

(129 citation statements)

References 23 publications

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“…Sitosterol turnover was calculated from the plasma sitosterol specific activity-decay curve (Table 1) by use of the two-pool model. 19 The half-lives of the two exponentials varied between 5 and 12 days for t A l/2 (mean±SD, 9.2±3.3 days) and between 78 and 280 days for t B l/2 (mean±SD, 156±109 days). The size of the rapidly exchangeable pool (M A ) ranged between 1,354 and 2,664 mg (mean±SD, l,962±660 mg), and that of the total exchangeable pool was between 4,704 and 6,284 mg (mean±SD, 5,437±796 mg).…”

Section: Sitosterol and Cholesterol Turnoversmentioning

confidence: 95%

“…Sitosterol and cholesterol turnovers were calculated according to the two-pool model. 19 As stated above, whenever required in the study feces were collected daily for 7 consecutive days. Also KAA, rate constant for total removal from pool A; KAB, rate constant for the transfer from pool A to pool B; K A , rate constant for the removal from pool A and the whole system; K B B, rate constant for total removal from pool B; K BA , rate constant for transfer from pool B to pool A.…”

Section: Sitosterol and Cholesterol Turnovermentioning

confidence: 99%

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Sluggish sitosterol turnover and hepatic failure to excrete sitosterol into bile cause expansion of body pool of sitosterol in patients with sitosterolemia and xanthomatosis.

Bhattacharyya

Connor

Lin

et al. 1991

Arterioscler Thromb

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Sitosterolemia and xanthomatosis are characterized by the development of tendon and tuberous xanthomas at an early age and premature atherosclerosis despite normal plasma cholesterol concentrations. The reason(s) for the xanthoma formation and premature atherosclerosis are not clearly understood. The accumulation of sitosterol in the tissues of these patients could be due to increased uptake of low density lipoprotein (LDL) via LDL receptors because of an expanded sitosterol pool caused by sluggish turnover and decreased excretion of sitosterol into bile and feces coupled with the hyperabsorption of sitosterol. We have studied sitosterol and cholesterol turnovers, the biliary and fecal excretion of neutral and acidic steroids, and the response of plasma sterol (sitosterol and cholesterol) levels to either a sterol-free formula or low plant sterol diet in three patients. The average half-life of the first exponential (t A l/2) for sitosterol was 9.2 ±3.3 (mean±SD) days, which was more than twice that in normal humans. The second exponential (t B l/2) was 156±108 days, which was nearly 10 times longer than that for normal humans. The average cholesterol production rate in pool A was 0.87 g/day, which is about 40% of that in normal humans. Cholesterol synthesis measured by the sterol balance technique was also found to be about 70% lower than that for normal humans. In two patients fed a sterol-free formula diet, by 25 days their plasma sitosterol and cholesterol levels had decreased by 42% and 36%, respectively. However, in one patient plasma sitosterol and cholesterol concentrations remained unchanged while on the low plant sterolmixed food diet. The sitosterol to cholesterol ratio in bile (0.05) was extremely low compared with that found in plasma (0.14), indicating low excretion of sitosterol into the bile. Thus, patients with sitosterolemia have a slow turnover of sitosterol, low excretion of sitosterol into the duodenal bile and feces, and low cholesterol synthesis. These metabolic defects have implications in the formation of xanthomas and the development of premature atherosclerosis in these patients. (Arteriosclerosis and Thrombosis 1991;11:1287-1294)

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Section: Sitosterol and Cholesterol Turnoversmentioning

confidence: 95%

Section: Sitosterol and Cholesterol Turnovermentioning

confidence: 99%

Sluggish sitosterol turnover and hepatic failure to excrete sitosterol into bile cause expansion of body pool of sitosterol in patients with sitosterolemia and xanthomatosis.

Bhattacharyya

Connor

Lin

et al. 1991

Arterioscler Thromb

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“…The maximum incorporation into free cholesterol was less than 0.01 #g cholesterol/flask in 6 hr, or less than 1/~0 of 1% of the cell cholesterol/hr. This influx would have no effect on the cholesterol kinetics (13).…”

Section: Effect Of Serum Concentration On the Kinetics Of Exchange--mentioning

confidence: 98%

Cholesterol Metabolism in the Macrophage

Werb

Cohn

1971

The Journal of Experimental Medicine

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Cholesterol is a constituent of all mammalian cells and serves as a structural unit of membranes. Cytomembranes of the "thick" variety (80-100 A) which have potential access to the extracellular milieu are rich in cholesterol and include plasma membrane, lysosomal membrane, and secretion granules (1-10). In contrast, "thin" membranes (40-70 A) such as endoplasmic reticulum, mitochondria, and nuclear envelope are poor in cholesterol, whereas Golgi membranes are intermediate in size and cholesterol content (5,11,12).Although there is an extensive literature on cholesterol metabolism of the whole organism (13-16), our knowledge of the cellular level is fragmentary. Exceptions are the well-documented studies first described by Hagerman and Gould (17) demonstrating cholesterol exchange from plasma lipoproteins to the membrane of erythrocytes. No net change in cholesterol content of red cell takes place and cholesterol ester (CE) 1 exchange is very limited. Recently, the de novo biosynthesis of cholesterol by cultured eukaryotic cells has been shown (18-20) although its conversion to metabolites other than its esters has not been demonstrated (19,21,22).We have chosen to examine the metabolism of cholesterol in homogeneous populations of macrophages. This was prompted by the physiological role of this cell in the processing of chylomicrons and effete erythrocytes (23)(24)(25) and its association with a number of pathological events in which lipid storage takes place (26)(27)(28)(29)(30). In addition, macrophages exhibit striking endocytic activity in which the flow and turnover of cholesterol-rich membranes might be examined.In this article we will describe the content and subcellular distribution of macrophage cholesterol, the factors controlling exchange, and its biosynthesis under defined cultural conditions.

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“…For both patients, the plasma cholesterol-specific radioactivity decay curve could be resolved precisely into the sum of two exponentials. The various parameters of cholesterol turnover were calculated on the basis of the kinetic analysis of the two-pool model (15). However, the semilogarithmic plots of the plasma cholestanol-specific radioactivity were widely scattered in both patients.…”

Section: Cholesterol and Cholestanol Turnovermentioning

confidence: 99%

Cholestanol metabolism in patients with cerebrotendinous xanthomatosis: absorption, turnover, and tissue deposition

Bhattacharyya

Lin

Connor

2007

Journal of Lipid Research

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To study the metabolism of cholestanol in patients with cerebrotendinous xanthomatosis (CTX), we measured the cholestanol absorption, the cholesterol and cholestanol turnover, and the tissue content of sterols in two patients. Cholestanol absorption was z5.0%. The rapid exchangeable pool of cholestanol was 233 mg, and the total exchangeable pool was 752 mg. The production rate of cholestanol in pool A was 39 mg/day. [4-14

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Turnover of plasma cholesterol in man

Cited by 284 publications

References 23 publications

Sluggish sitosterol turnover and hepatic failure to excrete sitosterol into bile cause expansion of body pool of sitosterol in patients with sitosterolemia and xanthomatosis.

Sluggish sitosterol turnover and hepatic failure to excrete sitosterol into bile cause expansion of body pool of sitosterol in patients with sitosterolemia and xanthomatosis.

Cholesterol Metabolism in the Macrophage

Cholestanol metabolism in patients with cerebrotendinous xanthomatosis: absorption, turnover, and tissue deposition

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