Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2001 May;221(1-2):109-15.
doi: 10.1023/a:1010965527221.

Effect of oleoyl-estrone treatment on the expression of beta1- beta2- and beta3-adrenoreceptors in rat adipose tissues

Affiliations

Effect of oleoyl-estrone treatment on the expression of beta1- beta2- and beta3-adrenoreceptors in rat adipose tissues

C Cabot et al. Mol Cell Biochem. 2001 May.

Abstract

Adult female rats received a constant i.v. infusion of oleoyl-estrone (3.5 pmol/kg day) in a lipidic suspension for 14 days. On days 0 (no treatment), 3, 6, 10 and 14, as well as on day 14 for controls (receiving only the lipid); the rats were killed and the expression of the beta1-, beta2- and beta3-adrenoceptor genes, in brown adipose tissue and in subcutaneous and periovaric white adipose tissue, were measured by RNA protection assay, and compared with that of cyclophyllin. The beta3-adrenoceptor was the most expressed in all adipose tissues, whereas beta2 was the less expressed in brown adipose tissue. Oleoyl-estrone significantly, but moderately, increased the expression of beta-adrenoceptors in the three adipose tissues: beta1 increased in subcutaneous, beta2 and beta3 in periovaric and beta3 in brown adipose tissue. Oleoyl-estrone also decreased beta3 expression in subcutaneous white adipose tissue. On day 10, adipocytes isolated from periovaric white adipose tissue of oleoyl-estrone-treated rats showed higher cAMP response to an isoproterenol challenge than the controls. The mechanism by which oleoyl-estrone elicits the wasting of fat reserves could be mediated by adrenergic pathways, at least in part.

PubMed Disclaimer

Similar articles

Cited by

References

    1. Int J Obes Relat Metab Disord. 1997 Sep;21(9):789-95 - PubMed
    1. Mol Pharmacol. 1992 Oct;42(4):634-7 - PubMed
    1. Arch Physiol Biochem. 1997 Dec;105(7):663-72 - PubMed
    1. Am J Physiol. 1994 Mar;266(3 Pt 2):R905-13 - PubMed
    1. DNA. 1988 May;7(4):261-7 - PubMed

Publication types

MeSH terms

LinkOut - more resources