PMID- 21153133
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20121002
LR  - 20211020
IS  - 1355-008X (Print)
IS  - 1355-008X (Linking)
VI  - 3
IP  - 8
DP  - 1995 Aug
TI  - Reduced hepatic sterol carrier protein-2 expression in the streptozotocin treated 
      diabetic rat.
PG  - 563-71
LID - 10.1007/BF02953020 [doi]
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 
      17beta-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.
FAU - McLean, M P
AU  - McLean MP
AD  - Department of Obstetrics and Gynecology, University of South Florida College of 
      Medicine, 33606, Tampa, Florida.
FAU - Nanjo, K
AU  - Nanjo K
FAU - Irby, R B
AU  - Irby RB
FAU - Warden, K J
AU  - Warden KJ
FAU - Billheimer, J T
AU  - Billheimer JT
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Endocrine
JT  - Endocrine
JID - 9434444
EDAT- 1995/08/01 00:00
MHDA- 1995/08/01 00:01
CRDT- 2010/12/15 06:00
PHST- 1995/02/09 00:00 [received]
PHST- 1995/04/05 00:00 [accepted]
PHST- 2010/12/15 06:00 [entrez]
PHST- 1995/08/01 00:00 [pubmed]
PHST- 1995/08/01 00:01 [medline]
AID - 10.1007/BF02953020 [doi]
PST - ppublish
SO  - Endocrine. 1995 Aug;3(8):563-71. doi: 10.1007/BF02953020.