Glucocorticoid receptor is indispensable for mineralocorticoid receptor‐dependent induction of colonic epithelial Na+ channels

Glucocorticoid hormones (GCs) are important regulators of lipid metabolism, promoting lipolysis with acute treatment but lipogenesis with chronic exposure. Conventional wisdom posits that these disparate outcomes are mediated by the classical glucocorticoid receptor GRα. There is insufficient knowledge of the GC receptors (GRα and GRβ) in metabolic conditions such as obesity and diabetes. We present acute models of GC exposure that induce lipolysis, such as exercise, as well as chronic-excess models that cause obesity and lipid accumulation in the liver, such as hepatic steatosis. Alternative mechanisms are then proposed for the lipogenic actions of GCs, including induction of GC resistance by the GRβ isoform, and promotion of lipogenesis by GC activation of the mineralocorticoid receptor (MR). Finally, the potential involvement of chaperone proteins in the regulation of adipogenesis is considered. This reevaluation may prove useful to future studies on the steroidal basis of adipogenesis and obesity.

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Glucocorticoid receptor is indispensable for physiological responses to aldosterone in epithelial Na+ channel induction via the mineralocorticoid receptor in a human colonic cell line

European Journal of Cell Biology ◽

10.1016/j.ejcb.2011.01.001 ◽

2011 ◽

Vol 90 (5) ◽

pp. 432-439 ◽

Cited By ~ 17

Author(s):

Theresa Bergann ◽

Anja Fromm ◽

Steffen A. Borden ◽

Michael Fromm ◽

Jörg D. Schulzke

Keyword(s):

Glucocorticoid Receptor ◽

Cell Line ◽

Mineralocorticoid Receptor ◽

Physiological Responses ◽

Na Channel ◽

Epithelial Na Channel

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Cloning of glucocorticoid receptor and mineralocorticoid receptor cDNA and gene expression in the central nervous system of the tree shrew (Tupaia belangeri)

Molecular Brain Research ◽

10.1016/s0169-328x(98)00004-7 ◽

1998 ◽

Vol 55 (2) ◽

pp. 243-253 ◽

Cited By ~ 39

Author(s):

Ute Meyer ◽

Mogens Kruhøffer ◽

Gabriele Flügge ◽

Eberhard Fuchs

Keyword(s):

Gene Expression ◽

Central Nervous System ◽

Nervous System ◽

Glucocorticoid Receptor ◽

Mineralocorticoid Receptor ◽

Tree Shrew ◽

Tupaia Belangeri ◽

The Central Nervous System ◽

Receptor Cdna

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Immunolocalisation of 11β-HSD-1 and -2, glucocorticoid receptor, mineralocorticoid receptor and Na+K+-ATPase during the postnatal development of the rat epididymis

Journal of Anatomy ◽

10.1111/j.1469-7580.2012.01481.x ◽

2012 ◽

Vol 220 (4) ◽

pp. 350-362 ◽

Cited By ~ 4

Author(s):

Gwyneth H. Gladstones ◽

Peter J. Burton ◽

Peter J. Mark ◽

Brendan J. Waddell ◽

Peter Roberts

Keyword(s):

Glucocorticoid Receptor ◽

Postnatal Development ◽

Mineralocorticoid Receptor ◽

Rat Epididymis

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Mechanisms and sequelae of increased alveolar fluid clearance in hyperoxic rats

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.1997.272.3.l407 ◽

1997 ◽

Vol 272 (3) ◽

pp. L407-L412 ◽

Cited By ~ 35

Author(s):

G. Yue ◽

S. Matalon

Keyword(s):

Alveolar Epithelial Cells ◽

Na Channels ◽

Alveolar Fluid Clearance ◽

Na Transport ◽

Alveolar Epithelial ◽

Lung Fluid ◽

Isotonic Fluid ◽

Epithelial Na Channels ◽

Alveolar Edema

We instilled 4 ml isotonic fluid containing trace amounts of fluorescently labeled dextran (molecular mass 150 kDa) in the lungs of rats exposed to either 85% O(2) for 7 days or to 85% O(2) for 7 days and 100% O(2) for 3 days. We withdrew the fluid every hour for a 3-h period and calculated alveolar fluid clearance (AFC) from changes in dextran concentration. Postinstillation (3 h), AFC values in the control and the two hyperoxic groups were 51 +/- 1, 63 +/- 2, and 62 +/- 3 (SE), respectively (%instilled volume; n > or = 5; P < 0.05). Addition of either 1 mM amiloride or N-ethyl-N-isopropyl amiloride (EIPA) in the instillate decreased the AFC values in all groups 3 h later to approximately 30% of instilled volume. Instillation of phenamil, an irreversible blocker of epithelial Na+ channels into the lungs of rats exposed to 85% O(2) for 7 days and 100% O(2) for 2 days, resulted in a significant increase of their extravascular lung fluid volumes 24 h later. These results demonstrate the existence of EIPA-inhibitable Na+ channels in alveolar epithelial cells in vivo and indicate that an increase in Na+ transport plays an important role in limiting the amount of alveolar edema in O(2)-damaged lungs.

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