Peripheral Actions of Glucocorticoids

Leung, Kwok Nam; Munck, A

doi:10.1146/annurev.ph.37.030175.001333

Cited by 105 publications

(39 citation statements)

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“…In parallel with our data, Friedman et al (31) showed that adrenal removal in mice, leading to a markedly decreased corticosteroid level, did not affect hepatic PEPCK expression in the fasting state. Importantly, inhibition of glucose uptake is a consistently reproducible effect of glucocorticoids added at physiological concentrations to intact fat tissue as well as isolated adipocytes (32). Therefore, it is suggested that SR-BI-deficient mice suffer from fasting hypoglycemia as a consequence of increased peripheral glucose usage secondary to impaired glucocorticoid signaling.…”

Section: Discussionmentioning

confidence: 99%

Absence of HDL cholesteryl ester uptake in mice via SR-BI impairs an adequate adrenal glucocorticoid-mediated stress response to fasting

Hoekstra¹,

Meurs²,

Koenders³

et al. 2008

Journal of Lipid Research

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Receptor-mediated cholesterol uptake has been suggested to play a role in maintaining the adrenal intracellular free cholesterol pool and the ability to produce hormones. Therefore, in the current study, we evaluated the importance of scavenger receptor class B type I (SR-BI)-mediated cholesteryl ester uptake from HDL for adrenal glucocorticoid hormone synthesis in vivo. No difference was observed in the plasma level of corticosterone between SR-BI-deficient and wild-type mice under ad libitum feeding conditions. Overnight fasting (?16 h) stimulated the plasma level of corticosterone by 2-fold in wild-type mice. In contrast, no effect of fasting on plasma corticosterone levels was observed in SR-BI-deficient mice, leading to a 44% lower plasma corticosterone level compared with their wild-type littermate controls. In parallel, an almost complete depletion of lipid stores in the adrenal cortex of fasted SR-BIdeficient mice was observed. Plasma adrenocorticotropic hormone levels were increased by 5-fold in fasted SR-BIdeficient mice. SR-BI deficiency induced marked changes in the hepatic expression of the glucocorticoid-responsive genes cholesterol 7a-hydroxylase, HMG-CoA synthase, apolipoprotein A-IV, corticosteroid binding globulin, interleukin-6, and tumor necrosis factor-a, which coincided with a 42% decreased plasma glucose level under fasting conditions. In conclusion, we show that the absence of adrenal HDL cholesteryl ester uptake in SR-BI-deficient mice impairs the adrenal glucocorticoid-mediated stress response to fasting as a result of adrenal glucocorticoid insufficiency and attenuated liver glucocorticoid receptor signaling, leading to hypoglycemia under fasting conditions.-Hoekstra, M., I. Meurs, M. Koenders, R. Out, R. B. Hildebrand, J. K. Kruijt, M. Van Eck, and T. J. C. Van Berkel. Absence of HDL cholesteryl ester uptake in mice via SR-BI impairs an adequate adrenal glucocorticoid-mediated stress response to fasting. J. Lipid Res. 2008. 49: 738-745.

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Section: Discussionmentioning

confidence: 99%

Absence of HDL cholesteryl ester uptake in mice via SR-BI impairs an adequate adrenal glucocorticoid-mediated stress response to fasting

Hoekstra¹,

Meurs²,

Koenders³

et al. 2008

Journal of Lipid Research

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“…Both actions are seen in both OBand OC-cell types. The first action is a general inhibitory effect, which is also seen in many other tissues (23,24). The expectation is that this action would result in reduced bone formation as well as a reduced rate of bone resorption because of an inhibition of OB-and OC-cell proliferation and function.…”

Section: Discussionmentioning

confidence: 99%

Glucocorticoid Receptors and Actions in Subpopulations of Cultured Rat Bone Cells

Chen¹,

Feldman²

1979

J. Clin. Invest.

132

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“…Neben ihrer normalen Funktion in der Regulation der Entwicklung von Oligodendrocyten und anderen Zellen des ZNS [Bohn and Friedrich, 1982;Meyer, 1985;Kumar et al 1989;Poduslo et al, 1990;Vielkind et al, 1990], haben Glucocorticoide aufgrund ihrer anti-entzündlichen und das Immunsystem beeinflussenden Wirkung [Leung and Munck, 1975] [Cupps und Fauci, 1982;Culpepper und Lee, 1987;Taniguchi, 1988]. Nach bereits erfolgter Freisetzung von Cytokinen, konnte in verschiedenen Zellsystemen weiterhin eine anti-apoptotische Wirkung der Glucocorticoide beobachtet werden [Kull et al, 1988;Pagliacci et al, 1993;Cox et al, 1995;Cox and Austin, 1997;Wen et al, 1997].…”

Section: Vorläuferzellen?unclassified