Movement Of Cholesterol Research Articles

Movement of sodium and cholesterol across porcine aortic intima.

1. A method for measuring the movement of substances across porcine aortic intima in vitro is described. 2. The rates of movement of sodium and cholesterol were decreased by adding dinitrophenol to the bathing solutions and increased by adding adrenaline. 3. The relevance of these results to hypertension and atheroma is mentioned. 4. The possibility of active transport of sodium and cholesterol is suggested.

The economy of cholesterol in man: drug effects.

A partial list of the factors controlling the movement and storage of cholesterol in man must include: intake; absorption; lipoprotein synthesis and transport capacity; tissue equilibria with plasma cholesterol; endogenous synthesis; conversion to bile acids; pool sizes; excretion rates and pathways. All of these can now be defined with directness and exactitude except for measurement of pool sizes and of tissue-plasma equilibria, utilizing sterol balance and isotope kinetic techniques. Although pool sizes can be estimated by isotope kinetics, as yet we have no independent means by which to verify these estimates.

Atheroma and arterial wall shear. Observation, correlation and proposal of a shear dependent mass transfer mechanism for atherogenesis.

On the basis of various observations, we argue that there is spatial variation of the time averaged wall shear rate in arteries, both overall and locally. From our own observations, and those of others, we show that the distribution of early atheroma in man is coincident with those regions in which arterial wall shear rate is expected to be relatively low, while the development of lesions is inhibited or retarded in those regions in which wall shear rate is expected to be relatively high. Such a correlation is inconsistent with a proposal, made by several workers, that there is a causative relation between arterial blood mechanics and the development of atheroma, i. e. that atheroma is associated with wall damage due to the motion of blood. Instead it immediately suggests that the process is associated with shear dependent mass transport phenomena. It has been demonstrated by others that mass transport, in the inner part of the arterial wall, is dominantly to and from blood flowing within the lumen. We review theory relevant to diffusional mass transport across such a sheared interface, and examine available experimental evidence, relating to normally occurring (quasi-steady state) and experimentally induced (transient-type) atheroma, as well as the distribution of cholesterol in arteries. These results are considered in the light of simple theoretical schemes which we develop for the movement of cholesterol, in particular, although the arguments may also be relevant to other diffusing species. Shear enhances mass transport by means of a steepening effect on the concentration gradient, thus diffusion of material from a wall is promoted when material which has already diffused is swept rapidly away, so that the concentration gradient leading to further diffusion remains steep. However, the influence of shear on the diffusion of a species, say, from just within the wall of an artery to fluid in the main stream, depends upon the relative resistances to its diffusion from within the wall to surface fluid (wall phase) and from surface fluid to fluid in the main stream (blood phase); diffusion is not appreciably shear dependent if the latter resistance is small compared with the former. Assuming simplified flow conditions and that as suggested by others cholesterol is transported in blood in association with plasma protein, we can estimate resistance for diffusion of this species in the blood phase, for different stations in the arterial system. However, we possess no definite comparable information for the wall phase; we conjecture that this resistance is relatively small, and assume shear dependence of diffusional transport of cholesterol between arterial walls and intraluminal blood. We find that a net flux of cholesterol from blood to wall, as has been suggested by others, cannot account, in terms of the proposed schemes, for the observed normally occurring (quasi-steady state) distribution of atheromatous lesions in man and in animals; mass transport is inhibited in low shear regions by the thick diffusional boundary layer. Instead it appears that cholesterol, which has been shown by others to be synthesized in arterial walls, accumulates in low shear regions because its local diffusional efflux from wall to blood is inhibited by the reduced concentration gradient. Given suitable values for relevant parameters, the theoretical schemes are also able to account for adequacy of supply of precursor to the wall for cholesterol synthesis, for the preferential occurrence that we now recognize of lesions in high shear regions in response to sudden natural or experimental elevation of blood cholesterol, and for the responses to administration of labelled cholesterol (transient type phenomena); it appears therefore possible, in terms of these schemes, to unify naturally occurring and experimentally induced atheroma. It is reported by others that platelets are associated only with advanced lesions; the correlation of naturally occurring atheroma with low shear regions, and transient type lesions with high shear regions, with the fluid mechanics being unaltered in the two situations, provides no support for the implication of platelets in the development of early atheroma. It appears that wall shear rate may be a major controlling factor in the development of atheroma, i.e. that high shear, such as is associated for example with increased cardiac output in exercise, will retard progression of the process. Its progression will also be retarded by any means which reduces the accumulation of atheromatous material, by influencing its rate of net production or diffusion.

Cholesterol turnover in the American cockroach, Periplaneta americana (L.)

Turnover of cholesterol in the American cockroach, Periplaneta americana (L.), was investigated by feeding cholesterol-4-C14 in the diet and examining periodically the specific radioactivity of the total carcass cholesterol. It was found that the movement of cholesterol into and out of the roach tissues was much slower than has been reported for mammals. The ester cholesterol pool was found to equilibrate slowly with the free cholesterol pool. At least 40% of the carcass cholesterol was found to be exchangeable with the dietary cholesterol.

Movement of Serum Cholesterol on the Employee in a Tire Company

Movement of Serum Cholesterol on the Employee in a Tire Company

Passage of labeled cholesterol into the aortic wall of the normal dog.

In the normal dog the rate of movement of cholesterol from the serum into the inner layer of the aortic wall is greatest at the proximal end of the aorta and decreases progressively along the length of the aorta until in the terminal aorta the rate is only about one sixth that in the proximal aorta. A similar gradient of rates was previously demonstrated for albumin which enters the aortic wall about three times as fast as cholesterol. The similarity of the gradients and the relative magnitude of the rates for cholesterol and albumin support the concept that cholesterol is carried into the aortic wall of the normal dog by the passage of the lipoproteins of which it is a part.

The Menne-oxygen melting process: Iron Age, lxxxvi, 8.

Steroidogenic acute regulatory protein (StAR) facilitates the movement of cholesterol from the outer to inner mitochondrial membrane for steroidogenesis. Here, we investigated the effect of cigarette smoke (CS) on steroidogenesis using adrenal mitochondria isolated from mice chronically exposed to CS. Steroidogenesis was decreased approximately 78% in CS-exposed mitochondria, as measured by synthesis of the steroid hormone precursor pregnenolone. This effect was accompanied by decreased mitochondrial import of 35S-StAR. Further characterization of the imported 35S-StAR by native gradient PAGE revealed the presence of a high molecular weight complex in both control and CS-exposed groups. Following density gradient fractionation of 35S-StAR that had been extracted from control mitochondria, precursor StAR could be found in fractions 2–6 and smaller-sized StAR complexes in fractions 6–13. In the CS-exposed group, the appearance of precursor shifted from fraction 1–6 and the smaller complexes in fractions 6–9 disappeared. Mass spectrometric analysis revealed that the 35S-StAR-associated protein complex was composed of several resident matrix proteins as well as the OMM resident, VDAC. VDAC expression was greatly reduced by CS, and blockage of VDAC with Koenig's polyanion decreased pregnenolone synthesis in isolated mitochondria. Taken together, these results suggest that VDAC may participate in steroidogenesis by promoting StAR interaction with the OMM and that CS may inhibit steroidogenesis by reducing VDAC–StAR interactions.