Reduced hepatic sterol carrier protein-2 expression in the streptozotocin treated diabetic rat

M. P. McLean, K. Nanjo, R. B. Irby, K. J. Warden, J. T. Billheimer

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

While a strong relationship between the hypercholesterolemia of diabetes and premature atherosclerosis is established, the etiology for the elevation in serum cholesterol in this disease is unknown. To determine whether diabetic hypercholesterolemia may be related to alterations in hepatic cholesterol transport capacity, sterol carrier protein-2 (SCP2) expression was examined in rats treated with streptozotocin (SZT). Furthermore, this study examined whether 17β-estradiol and insulin confer a protective effect on liver cholesterol homeostasis by maintaining hepatic SCP2 levels. SCP2 protein and mRNA expression were examined 13 days following SZT-induced diabetes onset and in diabetic rats treated with estradiol (1 cm silastic implant) or insulin (12 units/day). Data indicate that SCP2 protein levels were significantly reduced in the diabetic animals and that SCP2 protein expression in the liver was inversely related to the level of serum cholesterol in the diabetic animals. In contrast, SCP2 mRNA levels examined by slot blot, ribonuclease protection assay, and Northern blot analysis were significantly elevated. Both insulin and estradiol were able to enhance the expression of SCP2 protein in the liver following SZT treatment. The results of this investigation clearly indicate that hepatic SCP2 protein levels are significantly altered in the diabetic state suggesting that cholesterol transport capacity is reduced in the SZT-treated diabetic rat. The inverse relationship between serum cholesterol and hepatic SCP2 protein content suggests that the reduction in this protein may be a contributing factor in diabetic hypercholesterolemia.

Original languageEnglish (US)
Pages (from-to)563-571
Number of pages9
JournalEndocrine
Volume3
Issue number8
DOIs
StatePublished - Aug 1 1995

Fingerprint

Streptozocin
Liver
Cholesterol
Hypercholesterolemia
Proteins
Estradiol
Insulin
Serum
sterol carrier proteins
Messenger RNA
Experimental Diabetes Mellitus
Ribonucleases
Northern Blotting
Atherosclerosis
Homeostasis

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

Cite this

McLean, M. P. ; Nanjo, K. ; Irby, R. B. ; Warden, K. J. ; Billheimer, J. T. / Reduced hepatic sterol carrier protein-2 expression in the streptozotocin treated diabetic rat. In: Endocrine. 1995 ; Vol. 3, No. 8. pp. 563-571.
@article{c9c6ba72504c48a9b73e8c8179f7b46d,
title = "Reduced hepatic sterol carrier protein-2 expression in the streptozotocin treated diabetic rat",
abstract = "While a strong relationship between the hypercholesterolemia of diabetes and premature atherosclerosis is established, the etiology for the elevation in serum cholesterol in this disease is unknown. To determine whether diabetic hypercholesterolemia may be related to alterations in hepatic cholesterol transport capacity, sterol carrier protein-2 (SCP2) expression was examined in rats treated with streptozotocin (SZT). Furthermore, this study examined whether 17β-estradiol and insulin confer a protective effect on liver cholesterol homeostasis by maintaining hepatic SCP2 levels. SCP2 protein and mRNA expression were examined 13 days following SZT-induced diabetes onset and in diabetic rats treated with estradiol (1 cm silastic implant) or insulin (12 units/day). Data indicate that SCP2 protein levels were significantly reduced in the diabetic animals and that SCP2 protein expression in the liver was inversely related to the level of serum cholesterol in the diabetic animals. In contrast, SCP2 mRNA levels examined by slot blot, ribonuclease protection assay, and Northern blot analysis were significantly elevated. Both insulin and estradiol were able to enhance the expression of SCP2 protein in the liver following SZT treatment. The results of this investigation clearly indicate that hepatic SCP2 protein levels are significantly altered in the diabetic state suggesting that cholesterol transport capacity is reduced in the SZT-treated diabetic rat. The inverse relationship between serum cholesterol and hepatic SCP2 protein content suggests that the reduction in this protein may be a contributing factor in diabetic hypercholesterolemia.",
author = "McLean, {M. P.} and K. Nanjo and Irby, {R. B.} and Warden, {K. J.} and Billheimer, {J. T.}",
year = "1995",
month = "8",
day = "1",
doi = "10.1007/BF02953020",
language = "English (US)",
volume = "3",
pages = "563--571",
journal = "Endocrine",
issn = "0969-711X",
publisher = "Humana Press",
number = "8",

}

Reduced hepatic sterol carrier protein-2 expression in the streptozotocin treated diabetic rat. / McLean, M. P.; Nanjo, K.; Irby, R. B.; Warden, K. J.; Billheimer, J. T.

In: Endocrine, Vol. 3, No. 8, 01.08.1995, p. 563-571.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Reduced hepatic sterol carrier protein-2 expression in the streptozotocin treated diabetic rat

AU - McLean, M. P.

AU - Nanjo, K.

AU - Irby, R. B.

AU - Warden, K. J.

AU - Billheimer, J. T.

PY - 1995/8/1

Y1 - 1995/8/1

N2 - While a strong relationship between the hypercholesterolemia of diabetes and premature atherosclerosis is established, the etiology for the elevation in serum cholesterol in this disease is unknown. To determine whether diabetic hypercholesterolemia may be related to alterations in hepatic cholesterol transport capacity, sterol carrier protein-2 (SCP2) expression was examined in rats treated with streptozotocin (SZT). Furthermore, this study examined whether 17β-estradiol and insulin confer a protective effect on liver cholesterol homeostasis by maintaining hepatic SCP2 levels. SCP2 protein and mRNA expression were examined 13 days following SZT-induced diabetes onset and in diabetic rats treated with estradiol (1 cm silastic implant) or insulin (12 units/day). Data indicate that SCP2 protein levels were significantly reduced in the diabetic animals and that SCP2 protein expression in the liver was inversely related to the level of serum cholesterol in the diabetic animals. In contrast, SCP2 mRNA levels examined by slot blot, ribonuclease protection assay, and Northern blot analysis were significantly elevated. Both insulin and estradiol were able to enhance the expression of SCP2 protein in the liver following SZT treatment. The results of this investigation clearly indicate that hepatic SCP2 protein levels are significantly altered in the diabetic state suggesting that cholesterol transport capacity is reduced in the SZT-treated diabetic rat. The inverse relationship between serum cholesterol and hepatic SCP2 protein content suggests that the reduction in this protein may be a contributing factor in diabetic hypercholesterolemia.

AB - While a strong relationship between the hypercholesterolemia of diabetes and premature atherosclerosis is established, the etiology for the elevation in serum cholesterol in this disease is unknown. To determine whether diabetic hypercholesterolemia may be related to alterations in hepatic cholesterol transport capacity, sterol carrier protein-2 (SCP2) expression was examined in rats treated with streptozotocin (SZT). Furthermore, this study examined whether 17β-estradiol and insulin confer a protective effect on liver cholesterol homeostasis by maintaining hepatic SCP2 levels. SCP2 protein and mRNA expression were examined 13 days following SZT-induced diabetes onset and in diabetic rats treated with estradiol (1 cm silastic implant) or insulin (12 units/day). Data indicate that SCP2 protein levels were significantly reduced in the diabetic animals and that SCP2 protein expression in the liver was inversely related to the level of serum cholesterol in the diabetic animals. In contrast, SCP2 mRNA levels examined by slot blot, ribonuclease protection assay, and Northern blot analysis were significantly elevated. Both insulin and estradiol were able to enhance the expression of SCP2 protein in the liver following SZT treatment. The results of this investigation clearly indicate that hepatic SCP2 protein levels are significantly altered in the diabetic state suggesting that cholesterol transport capacity is reduced in the SZT-treated diabetic rat. The inverse relationship between serum cholesterol and hepatic SCP2 protein content suggests that the reduction in this protein may be a contributing factor in diabetic hypercholesterolemia.

UR - http://www.scopus.com/inward/record.url?scp=0029091611&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0029091611&partnerID=8YFLogxK

U2 - 10.1007/BF02953020

DO - 10.1007/BF02953020

M3 - Article

C2 - 21153133

AN - SCOPUS:0029091611

VL - 3

SP - 563

EP - 571

JO - Endocrine

JF - Endocrine

SN - 0969-711X

IS - 8

ER -