TY - JOUR
T1 - Non-esterified fatty acids are not relate'l to plasma apoB levels in familial combined hyperlipidemia
AU - Shamir, R.
AU - Williams, K. J.
AU - Hudgins, L.
AU - Levine, L.
AU - Conner, J. A.
AU - Fisher, E. A.
PY - 1996
Y1 - 1996
N2 - Recently, insulin resistance, elev; lions in plasma levels of apoB and non-esterified fatty acids (NEFA) wer: reported in adults with familial combined hyperlipidemia (FCHL), ihe leading cause of familial hyperlipidemia. Since saturated fatty acids (lauric, myristic, and palmitic) are generally associated with elevations of LDL, we hypothesized that in FCHL patients, elevated NEFA would b<; disproportionately saturated. In 5 families containing 12 FCHL subjects (; adults, 7 children) and 8 normals (5 adults), dietary assessments, anthropametric and plasma measurements (glucose, insulin, lipoproteins, apopro eins, NEF A-total and type) were made. In FCHL patients vs unaffected family members, elevated (p<0.01) were TG (199 ±27 mg/dL vs. 97-12 ). VLDL-TG (40 ±5 mg/dL vs 19 ± 2 ), apoB ( 134 ±9 mg/dl vs. 96 ±8) anc insulin (11 t l units vs 7 ±1 ). In contrast, the dietary intake of total and saturated fat was equivalent in the 2 groups, as were plasma levels of total-NEFA and the individual saturated species. We conclude that in both FCHL and normals, circulating total or particular fatty acids are not important c eterminants of plasma apoB levels and that other metabolic factors underlie the disease phenotype.
AB - Recently, insulin resistance, elev; lions in plasma levels of apoB and non-esterified fatty acids (NEFA) wer: reported in adults with familial combined hyperlipidemia (FCHL), ihe leading cause of familial hyperlipidemia. Since saturated fatty acids (lauric, myristic, and palmitic) are generally associated with elevations of LDL, we hypothesized that in FCHL patients, elevated NEFA would b<; disproportionately saturated. In 5 families containing 12 FCHL subjects (; adults, 7 children) and 8 normals (5 adults), dietary assessments, anthropametric and plasma measurements (glucose, insulin, lipoproteins, apopro eins, NEF A-total and type) were made. In FCHL patients vs unaffected family members, elevated (p<0.01) were TG (199 ±27 mg/dL vs. 97-12 ). VLDL-TG (40 ±5 mg/dL vs 19 ± 2 ), apoB ( 134 ±9 mg/dl vs. 96 ±8) anc insulin (11 t l units vs 7 ±1 ). In contrast, the dietary intake of total and saturated fat was equivalent in the 2 groups, as were plasma levels of total-NEFA and the individual saturated species. We conclude that in both FCHL and normals, circulating total or particular fatty acids are not important c eterminants of plasma apoB levels and that other metabolic factors underlie the disease phenotype.
UR - http://www.scopus.com/inward/record.url?scp=33749185555&partnerID=8YFLogxK
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AN - SCOPUS:33749185555
SN - 0892-6638
VL - 10
SP - A521
JO - FASEB Journal
JF - FASEB Journal
IS - 3
ER -