Intestinal Synthesis, Secretion, and Transport of Lipoproteins

Bisgaier, Charles L.; Glickman, Robert M.

doi:10.1146/annurev.ph.45.030183.003205

Cited by 142 publications

(66 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The jejunum is the principal site of active absorption of most nutrients, including lipids and is the most active site of lipoprotein formation (28). Staining of this tissue with nonimmune IgG was confined to cells of the lamina propria which are probably leukocytes with high levels of endogenous peroxidase.…”

Section: Resultsmentioning

confidence: 99%

Immunohistochemical localization of low density lipoprotein receptors in adrenal gland, liver, and intestine.

Fong¹,

Bonney²,

Kosek³

et al. 1989

J. Clin. Invest.

View full text Add to dashboard Cite

The localization of LDL receptors in adrenal gland, liver, and intestine was studied using immunohistochemistry. The anti-LDL receptor antibody used was shown to be monospecific and did not react with striated muscle, a tissue which has a very low level of LDL receptors. Similarly, cerebral cortex showed only faint reactivity and that was to an area previously demonstrated to have LDL receptors. Adrenal gland was intensely reactive with the zona fasciculata, having a greater density of receptors than the zona reticularis. In normal liver, LDL receptors were present on the sinusoidal membranes and were sparse in the areas of hepatocyte-to-hepatocyte contact without an obvious portal to central gradient. LDL receptors were present throughout the intestine. In jejunum, staining was most intense at the base of the villus and extended up toward the villus tip. At the base of the villus, the receptor was primarily at the basal lateral membrane, but toward the villus tip, there was appreciable intracellular staining. Staining in crypts was more faint; in duodenum, staining in crypts equaled that in the villus region in intensity. In colon, there was intense staining throughout the epithelial cells.These results provide new information about the cellular and subcellular localization of LDL receptors and raise the interesting possibility that there is a role for LDL-derived cholesterol in new lipoprotein formation.

show abstract

Section: Resultsmentioning

confidence: 99%

Immunohistochemical localization of low density lipoprotein receptors in adrenal gland, liver, and intestine.

Fong¹,

Bonney²,

Kosek³

et al. 1989

J. Clin. Invest.

View full text Add to dashboard Cite

show abstract

“…Future studies will determine whether the effects of 4F on the intestine, which was proposed to be their major site of action by Navab et al, also involve the removal of oxidized lipids via lipoproteins similar to those in the circulation. It should be noted that the intestine is the second major site of lipoprotein synthesis ( ‫ف‬ 30%) (53)(54)(55).…”

Section: Discussionmentioning

confidence: 99%

Enhancement by LDL of transfer of L-4F and oxidized lipids to HDL in C57BL/6J mice and human plasma

Meriwether

Imaizumi

Grijalva

et al. 2011

Journal of Lipid Research

View full text Add to dashboard Cite

“…The plateau tracer/tracee ratio of VLDL apoB-100, a primarily liver-derived protein, has been used as an estimate for the apoA-I precursor tracer/tracee ratio (40,41). However, because apoA-I is known to be synthesized in the small intestine as well as the liver (48,49), and since evidence suggests that the precursor pool tracer/tracee ratio may not be the same in these two organs (45,50), theoretical concerns have been raised that the VLDL apoB-100 plateau may not serve as a reliable estimate for apoA-I precursor tracer/tracee ratio. We have investi- gated apoA-I kinetics by simultaneous endogenous and exogenous labeling in several subjects with a wide range of plasma apoA-I levels and have found that the use of the VLDL apoB-100 plateau tracer/tracee ratio resulted in apoA-I kinetic parameters by endogenous labeling that were highly comparable (only 4% difference) with those obtained by exogenous radiotracer techniques (Ikewaki, unpublished data).…”

Section: Discussionmentioning

confidence: 99%

Delayed catabolism of high density lipoprotein apolipoproteins A-I and A-II in human cholesteryl ester transfer protein deficiency.

Ikewaki¹,

Rader²,

Sakamoto³

et al. 1993

J. Clin. Invest.

145

View full text Add to dashboard Cite

Deficiency of the cholesteryl ester transfer protein (CETP) in humans is characterized by markedly elevated plasma concentrations of HDL cholesterol and apoA-I. To assess the metabolism of HDL apolipoproteins in CETP deficiency, in vivo apolipoprotein kinetic studies were performed using endogenous and exogenous labeling techniques in two unrelated homozygotes with CETP deficiency, one heterozygote, and four control subjects. All study subjects were administered '3C6-labeled phenylalanine by primed constant infusion for up to 16 h. The fractional synthetic rates (FSRs) of apoA-I in two homozygotes with CETP deficiency (0.135, 0.134 /d) were found to be significantly lower than those in controls (0.196±0.041 /d, P < 0.01).Delayed apoA-I catabolism was confirmed by an exogenous radiotracer study in one CETP-deficient homozygote, in whom the fractional catabolic rate of 125I-apoA-I was 0.139/d (normal 0.216±0.018/d). The FSRs of apoA-II were also significantly lower in the homozygous CETP-deficient subjects (0.104, 0.112/d) than in the controls (0.170±0.023/d, P < 0.01). The production rates of apoA-I and apoA-II were normal in both homozygous CETP-deficient subjects. The turnover of apoA-I and apoA-II was substantially slower in both HDL2 and HDL3 in the CETP-deficient homozygotes than in controls. The kinetics of apoA-I and apoA-II in the CETP-deficient heterozygote were not different from those in controls.These data establish that homozygous CETP deficiency causes markedly delayed catabolism of apoA-I and apoA-II without affecting the production rates of these apolipoproteins. (J.

show abstract

Intestinal Synthesis, Secretion, and Transport of Lipoproteins

Cited by 142 publications

References 0 publications

Immunohistochemical localization of low density lipoprotein receptors in adrenal gland, liver, and intestine.

Immunohistochemical localization of low density lipoprotein receptors in adrenal gland, liver, and intestine.

Enhancement by LDL of transfer of L-4F and oxidized lipids to HDL in C57BL/6J mice and human plasma

Delayed catabolism of high density lipoprotein apolipoproteins A-I and A-II in human cholesteryl ester transfer protein deficiency.

Contact Info

Product

Resources

About