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Article has an altmetric score of 6

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Referenced in 1 patents
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Research Article Free access | 10.1172/JCI113292

Effects of long-chain, saturated fatty acids on membrane microviscosity and adrenocorticotropin responsiveness of human adrenocortical cells in vitro.

R W Whitcomb, W M Linehan, and R A Knazek

Developmental Endocrinology Branch, National Institute of Child Health and Human Development, Bethesda, Maryland 20982.

Find articles by Whitcomb, R. in: PubMed | Google Scholar

Developmental Endocrinology Branch, National Institute of Child Health and Human Development, Bethesda, Maryland 20982.

Find articles by Linehan, W. in: PubMed | Google Scholar

Developmental Endocrinology Branch, National Institute of Child Health and Human Development, Bethesda, Maryland 20982.

Find articles by Knazek, R. in: PubMed | Google Scholar

Published January 1, 1988 - More info

Published in Volume 81, Issue 1 on January 1, 1988
J Clin Invest. 1988;81(1):185–188. https://doi.org/10.1172/JCI113292.
© 1988 The American Society for Clinical Investigation
Published January 1, 1988 - Version history
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Abstract

Adrenoleukodystrophy (ALD) and adrenomyeloneuropathy are inherited disorders in which long-chain, saturated fatty acids (LCFA) accumulate in various tissues. A mechanism by which LCFA cause the endocrine and neurological dysfunction characteristic of these diseases is proposed based on in vitro response of human adrenocortical cells to ACTH in the presence of various fatty acids. Human adrenocortical cells cultured in the presence of 5 microM hexacosanoic (C26:0) or lignoceric (C24:0) acids showed decreased basal and ACTH-stimulated cortisol release compared with cells cultured without exogenous fatty acids or in the presence of linoleic acid (C18:2). Measurement of fluorescence polarization demonstrates a significant increase in the membrane microviscosity of cells cultured in the presence of LCFA. It is hypothesized that cells exposed to LCFA have increased membrane microviscosity with a consequent decrease in their ability to respond to ACTH. This decrease in trophic support may contribute to the adrenal insufficiency and atrophy in patients with ALD.

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Referenced in 1 patents
Referenced in 1 clinical guideline sources
48 readers on Mendeley
1 readers on CiteULike
See more details