Effect of ethinyl estradiol treatment on lipoproteins and LCAT activity in aged rats

Sun min Lee, Bhalchandra J. Kudchodkar, Andras G. Lacko

Research output: Contribution to journalArticle

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Abstract

The induction of hepatic lipoprotein (apo B/E) have been investigated in Fischer-344 rats. These studies were aimed to determine the mechanism underlying the previously observed (Lee et al., Mech. Ageing Dev., 61 (1991) 85-98) hypercholesterolemia and the age-related decrease in the fractional rate of endogenous cholesterol esterification. Young (5 months) and aged (22 months) male Fischer-344 rats were treated with pharmacological doses (5 mg/kg per day) of ethinyl estradiol (EE) for 7 days. Reduction of plasma cholesterol (57% in young vs 47% in aged rats) and high density lipoprotein cholesterol (64% in young vs 63% in aged rats) occurred in both groups upon EE treatment. Initial low density lipoprotein levels were very low in the plasma of young rats and consequently were not affected by EE treatment. However, in aged rats, the low density lipoprotein levels were much higher initially and were markedly reduced by EE treatment. (18.0 vs 10.0 mg/dl). Very low density lipoproteins were about the same initially but increased in aged rats and decreased in young rats upon EE treatment. Both the lecithin: cholesterol acyltransferase (LCAT) activity (as determined with a proteoliposome substrate) and the fractional rate (FR) of the endogenous cholesterol esterification decreased in treated animals compared to controls. However, the differences in the FR of the endogenous cholesterol esterification between young and aged rats (observed before treatment) were nearly abolished upon treatment. These data suggest that the previously observed age related decrease in the FR of endogeneous cholesterol esterification is due to the accumulation of apolipoprotein E-rich (apo E) lipoproteins. Furthermore these findings suggest that the decreased removal of the apo E-rich high density lipoprotein (HDL) in aged rats is due to metabolic events other than the decreased ability of aged hepatic cells to express apo B/E receptors.

Original languageEnglish
Pages (from-to)123-131
Number of pages9
JournalMechanisms of Ageing and Development
Volume64
Issue number1-2
DOIs
StatePublished - 1 Jan 1992

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Phosphatidylcholine-Sterol O-Acyltransferase
Ethinyl Estradiol
Esterification
Cholesterol
Apolipoproteins E
Inbred F344 Rats
LDL Lipoproteins
Lipoproteins
lipoprotein cholesterol
VLDL Lipoproteins
Apolipoproteins B
HDL Lipoproteins
Hypercholesterolemia
HDL Cholesterol
Hepatocytes
Pharmacology
Liver

Keywords

  • (CE)
  • (CETP)
  • (EE)
  • (FC)
  • (HDL)
  • (LCAT)
  • (LDL)
  • (TC)
  • (TG)
  • (VLDL)
  • Aging
  • Cholesterol
  • Ethyl estradiol
  • Lecithin cholesterol acyltransferase
  • Lipoproteins
  • Plasma LCAT
  • Rats
  • cholesteryl ester
  • choleteryl ester transfer protein
  • ethinyl estradiol
  • free (unesterified) cholesterol
  • high density lipoproteins(s)
  • low density lipoprotein(s)
  • total cholesterol
  • triglyceride
  • very low density lipoprotein(s)

Cite this

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title = "Effect of ethinyl estradiol treatment on lipoproteins and LCAT activity in aged rats",
abstract = "The induction of hepatic lipoprotein (apo B/E) have been investigated in Fischer-344 rats. These studies were aimed to determine the mechanism underlying the previously observed (Lee et al., Mech. Ageing Dev., 61 (1991) 85-98) hypercholesterolemia and the age-related decrease in the fractional rate of endogenous cholesterol esterification. Young (5 months) and aged (22 months) male Fischer-344 rats were treated with pharmacological doses (5 mg/kg per day) of ethinyl estradiol (EE) for 7 days. Reduction of plasma cholesterol (57{\%} in young vs 47{\%} in aged rats) and high density lipoprotein cholesterol (64{\%} in young vs 63{\%} in aged rats) occurred in both groups upon EE treatment. Initial low density lipoprotein levels were very low in the plasma of young rats and consequently were not affected by EE treatment. However, in aged rats, the low density lipoprotein levels were much higher initially and were markedly reduced by EE treatment. (18.0 vs 10.0 mg/dl). Very low density lipoproteins were about the same initially but increased in aged rats and decreased in young rats upon EE treatment. Both the lecithin: cholesterol acyltransferase (LCAT) activity (as determined with a proteoliposome substrate) and the fractional rate (FR) of the endogenous cholesterol esterification decreased in treated animals compared to controls. However, the differences in the FR of the endogenous cholesterol esterification between young and aged rats (observed before treatment) were nearly abolished upon treatment. These data suggest that the previously observed age related decrease in the FR of endogeneous cholesterol esterification is due to the accumulation of apolipoprotein E-rich (apo E) lipoproteins. Furthermore these findings suggest that the decreased removal of the apo E-rich high density lipoprotein (HDL) in aged rats is due to metabolic events other than the decreased ability of aged hepatic cells to express apo B/E receptors.",
keywords = "(CE), (CETP), (EE), (FC), (HDL), (LCAT), (LDL), (TC), (TG), (VLDL), Aging, Cholesterol, Ethyl estradiol, Lecithin cholesterol acyltransferase, Lipoproteins, Plasma LCAT, Rats, cholesteryl ester, choleteryl ester transfer protein, ethinyl estradiol, free (unesterified) cholesterol, high density lipoproteins(s), low density lipoprotein(s), total cholesterol, triglyceride, very low density lipoprotein(s)",
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year = "1992",
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language = "English",
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Effect of ethinyl estradiol treatment on lipoproteins and LCAT activity in aged rats. / Lee, Sun min; Kudchodkar, Bhalchandra J.; Lacko, Andras G.

In: Mechanisms of Ageing and Development, Vol. 64, No. 1-2, 01.01.1992, p. 123-131.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Effect of ethinyl estradiol treatment on lipoproteins and LCAT activity in aged rats

AU - Lee, Sun min

AU - Kudchodkar, Bhalchandra J.

AU - Lacko, Andras G.

PY - 1992/1/1

Y1 - 1992/1/1

N2 - The induction of hepatic lipoprotein (apo B/E) have been investigated in Fischer-344 rats. These studies were aimed to determine the mechanism underlying the previously observed (Lee et al., Mech. Ageing Dev., 61 (1991) 85-98) hypercholesterolemia and the age-related decrease in the fractional rate of endogenous cholesterol esterification. Young (5 months) and aged (22 months) male Fischer-344 rats were treated with pharmacological doses (5 mg/kg per day) of ethinyl estradiol (EE) for 7 days. Reduction of plasma cholesterol (57% in young vs 47% in aged rats) and high density lipoprotein cholesterol (64% in young vs 63% in aged rats) occurred in both groups upon EE treatment. Initial low density lipoprotein levels were very low in the plasma of young rats and consequently were not affected by EE treatment. However, in aged rats, the low density lipoprotein levels were much higher initially and were markedly reduced by EE treatment. (18.0 vs 10.0 mg/dl). Very low density lipoproteins were about the same initially but increased in aged rats and decreased in young rats upon EE treatment. Both the lecithin: cholesterol acyltransferase (LCAT) activity (as determined with a proteoliposome substrate) and the fractional rate (FR) of the endogenous cholesterol esterification decreased in treated animals compared to controls. However, the differences in the FR of the endogenous cholesterol esterification between young and aged rats (observed before treatment) were nearly abolished upon treatment. These data suggest that the previously observed age related decrease in the FR of endogeneous cholesterol esterification is due to the accumulation of apolipoprotein E-rich (apo E) lipoproteins. Furthermore these findings suggest that the decreased removal of the apo E-rich high density lipoprotein (HDL) in aged rats is due to metabolic events other than the decreased ability of aged hepatic cells to express apo B/E receptors.

AB - The induction of hepatic lipoprotein (apo B/E) have been investigated in Fischer-344 rats. These studies were aimed to determine the mechanism underlying the previously observed (Lee et al., Mech. Ageing Dev., 61 (1991) 85-98) hypercholesterolemia and the age-related decrease in the fractional rate of endogenous cholesterol esterification. Young (5 months) and aged (22 months) male Fischer-344 rats were treated with pharmacological doses (5 mg/kg per day) of ethinyl estradiol (EE) for 7 days. Reduction of plasma cholesterol (57% in young vs 47% in aged rats) and high density lipoprotein cholesterol (64% in young vs 63% in aged rats) occurred in both groups upon EE treatment. Initial low density lipoprotein levels were very low in the plasma of young rats and consequently were not affected by EE treatment. However, in aged rats, the low density lipoprotein levels were much higher initially and were markedly reduced by EE treatment. (18.0 vs 10.0 mg/dl). Very low density lipoproteins were about the same initially but increased in aged rats and decreased in young rats upon EE treatment. Both the lecithin: cholesterol acyltransferase (LCAT) activity (as determined with a proteoliposome substrate) and the fractional rate (FR) of the endogenous cholesterol esterification decreased in treated animals compared to controls. However, the differences in the FR of the endogenous cholesterol esterification between young and aged rats (observed before treatment) were nearly abolished upon treatment. These data suggest that the previously observed age related decrease in the FR of endogeneous cholesterol esterification is due to the accumulation of apolipoprotein E-rich (apo E) lipoproteins. Furthermore these findings suggest that the decreased removal of the apo E-rich high density lipoprotein (HDL) in aged rats is due to metabolic events other than the decreased ability of aged hepatic cells to express apo B/E receptors.

KW - (CE)

KW - (CETP)

KW - (EE)

KW - (FC)

KW - (HDL)

KW - (LCAT)

KW - (LDL)

KW - (TC)

KW - (TG)

KW - (VLDL)

KW - Aging

KW - Cholesterol

KW - Ethyl estradiol

KW - Lecithin cholesterol acyltransferase

KW - Lipoproteins

KW - Plasma LCAT

KW - Rats

KW - cholesteryl ester

KW - choleteryl ester transfer protein

KW - ethinyl estradiol

KW - free (unesterified) cholesterol

KW - high density lipoproteins(s)

KW - low density lipoprotein(s)

KW - total cholesterol

KW - triglyceride

KW - very low density lipoprotein(s)

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U2 - 10.1016/0047-6374(92)90101-I

DO - 10.1016/0047-6374(92)90101-I

M3 - Article

C2 - 1630152

AN - SCOPUS:0026607484

VL - 64

SP - 123

EP - 131

JO - Mechanisms of Ageing and Development

JF - Mechanisms of Ageing and Development

SN - 0047-6374

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