Effects of long-chain, saturated fatty acids on membrane microviscosity and adrenocorticotropin responsiveness of human adrenocortical cells in vitro.
Journal of Clinical InvestigationPublished 1 January 1988Open access
Randall W. Whitcomb, W. Marston Linehan, Richard A. Knazek
Citations165
SJR quartileQ1
SJR score4.72
SNIP2.17
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TL;DR
It is hypothesized that cells exposed to LCFA have increased membrane microviscosity with a consequent decrease in their ability to respond to ACTH and this decrease in trophic support may contribute to the adrenal insufficiency and atrophy in patients with ALD.
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.
Keywords
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