Abstract:
:Apolipoprotein E (APOE) deficient mice exhibit unexplained hypercorticosteronemia. Given that APOE is also produced locally within the adrenals, we evaluated the effect of adrenal-specific APOE deficiency on the glucocorticoid function. Hereto, one adrenal containing or lacking APOE was transplanted into adrenalectomized wild-type mice. Adrenal APOE deficiency did not impact adrenal total cholesterol levels. Importantly, the ability of the two adrenal types to produce glucocorticoids was also not different as judged from the similar plasma corticosterone levels. Adrenal mRNA expression levels of HMG-CoA reductase and the LDL receptor were decreased by respectively 72% (p < 0.01) and 65% (p = 0.07), suggesting that cholesterol acquisition pathways were inhibited to possibly compensate the lack of APOE. In support, a parallel increase in the expression level of the cholesterol accumulation-associated ER stress marker CHOP was detected (+117%; p < 0.05). In conclusion, our studies show that elimination of adrenocortical APOE production does not impact glucocorticoid output in wild-type mice.
journal_name
Mol Cell Endocrinoljournal_title
Molecular and cellular endocrinologyauthors
van der Sluis RJ,Depuydt MAC,Verwilligen RAF,Hoekstra M,Van Eck Mdoi
10.1016/j.mce.2019.04.001subject
Has Abstractpub_date
2019-06-15 00:00:00pages
21-27eissn
0303-7207issn
1872-8057pii
S0303-7207(19)30101-7journal_volume
490pub_type
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