Electrophysiological effects of progesterone on hepatocytes

Waldegger, S; Beisse, F.; Apfel, H.; Breit, Sorin; Kolb, Hans-Peter; Häussinger, Dieter; Läng, Florian

doi:10.1016/0167-4889(94)00236-8

Cited by 27 publications

(13 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In search of specific steroid membrane binding sites and with regard to the reports on rapid progesterone effects on liver cell conductance (504) and progesterone membrane binding sites in hepatocytes (217,488), our group was able to characterize membrane progesterone binding sites (mPR) from porcine liver microsomes. After purification, the binding capacity corresponds to the enrichment of polypeptides of 28 and 56 kDa with the latter probably representing a dimer of the 28-kDa protein (139,301).…”

Section: Progesteronementioning

confidence: 99%

Nongenomic Steroid Action: Controversies, Questions, and Answers

Lösel

Falkenstein

Feuring

et al. 2003

Physiological Reviews

504

321

View full text Add to dashboard Cite

Lösel, Ralf M., Elisabeth Falkenstein, Martin Feuring, Armin Schultz, Hanns-Christian Tillmann, Karin Rossol-Haseroth, and Martin Wehling. Nongenomic Steroid Action: Controversies, Questions, and Answers. Physiol Rev 83: 965–1016, 2003; 10.1152/physrev.00003.2003.—Steroids may exert their action in living cells by several ways: 1) the well-known genomic pathway, involving hormone binding to cytosolic (classic) receptors and subsequent modulation of gene expression followed by protein synthesis. 2) Alternatively, pathways are operating that do not act on the genome, therefore indicating nongenomic action. Although it is comparatively easy to confirm the nongenomic nature of a particular phenomenon observed, e.g., by using inhibitors of transcription or translation, considerable controversy exists about the identity of receptors that mediate these responses. Many different approaches have been employed to answer this question, including pharmacology, knock-out animals, and numerous biochemical studies. Evidence is presented for and against both the participation of classic receptors, or proteins closely related to them, as well as for the involvement of yet poorly understood, novel membrane steroid receptors. In addition, clinical implications for a wide array of nongenomic steroid actions are outlined.

show abstract

Section: Progesteronementioning

confidence: 99%

Nongenomic Steroid Action: Controversies, Questions, and Answers

Lösel

Falkenstein

Feuring

et al. 2003

Physiological Reviews

504

321

View full text Add to dashboard Cite

show abstract

“…Progesterone receptor membrane component 1, a putative cell-surface receptor for progesterone (or a part of it) is believed to mediate non-genomic actions in various cells [23][24][25][26]. Based on evidence for a non-genomic mode of action we determined if this putative receptor is expressed in rat skeletal muscle.…”

Section: Expression Of Pgrmc1mentioning

confidence: 99%

Progesterone impairs cell respiration and suppresses a compensatory increase in glucose transport in isolated rat skeletal muscle: a non-genomic mechanism contributing to metabolic adaptation to late pregnancy?

et al. 2007

View full text Add to dashboard Cite

Aims/hypothesis The aim of the study was to gain better insight into the mechanisms responsible for impaired glucose metabolism during late pregnancy. We explored the direct effects of progesterone on glucose metabolism of skeletal muscle. Methods Specimens of skeletal muscle from untreated rats were incubated with progesterone and rates of substrate fluxes through the various pathways of glucose metabolism were analysed. Results Progesterone dose-dependently reduced the rates of glucose and pyruvate oxidation (insulin-stimulated rates after 5 h of exposure to 1 and 10 μmol/l progesterone: glucose oxidation, −6±4%, NS, and −39±4%, p<0.001; pyruvate oxidation, −28±2% and −55±4%, p<0.001 each) and increased lactate release (+28±4% and +58±9%, p<0.005 each), which indicated inhibition of mitochondrial respiratory function. Impairment of cell respiration, e.g. by the specific inhibitor rotenone, is known to trigger a compensatory increase in glucose transport, but this response was blunted in the case of progesterone (change of glucose transport in response to 10 μmol/l progesterone vs 60 nmol/l rotenone, both causing a reduction in glucose oxidation by −39%: progesterone, +14±8% vs rotenone, +84±23%, p< 0.03). Further experiments dealt with the underlying mechanisms and revealed a rapid mode of action (50 μmol/l progesterone, reduction in insulin-stimulated glucose oxidation after 30 min: −29±7%, p<0.01) not affected by blockers of gene expression or the nuclear progesterone receptor. Conclusions/interpretation Progesterone inhibits cell respiration and at the same time suppresses a compensatory increase in glucose transport, causing cellular carbohydrate deficiency in isolated rat skeletal muscle. This effect is mediated by a direct, rapid and non-genomic mechanism and could contribute to pregnancy-associated changes in glucose homeostasis.

show abstract

“…Using intracellular recording techniques, one report found that testosterone modified the resting membrane potential of neurons in the major pelvic ganglion by triggering a slow depolarization, but was without significant effect on the resting potential of coeliac ganglion neurons [23]. In rat hepatocytes, the addition of progesterone (1 -100 mmol/l) induces a rapid and completely reversible depolari- Original Basic zation of the cell membrane by decreasing its K + conductance [24].…”

Section: Discussionmentioning

confidence: 99%

“…The tip resistance used (15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25) is appropriate for the preferential impalement of cells with a size similar to that of Sertoli cells (L. Monti Bloch, personal communication). This tip diameter hardly permits the impalement of smaller (peritubular, myoid) cells.…”

Section: Methodsmentioning

confidence: 99%

Rapid Effect of Testosterone on Rat Sertoli Cell Membrane Potential. Relationship with K⁺ _ATPChannels

et al. 2002

View full text Add to dashboard Cite

For this study, we investigated the changes in the electrophysiological parameters of Sertoli cells in seminiferous tubules from 17 - 19 day-old rats induced by testosterone. Using conventional intracellular microelectrode techniques, we analysed the membrane potential and its input resistance. The entire tubules were fixed in a superfusion chamber continuously perfused with Krebs-Ringer bicarbonate buffer (pH 7.4, 32 degrees C). Visual control of cell impalement was achieved using an inverted microscope. The parameters analysed were passed through an amplifier and recorded using a proprietary software system. The topical application of testosterone (0.1 to 10 microM) led to an immediate (within 30 seconds) and significant dose-dependent depolarization of the membrane potential of the cell at all concentrations used. Concomitantly, the input resistance of the cell membrane underwent a significant increment at 30 seconds. These changes returned to resting values after washout. Topical administration of 17beta-estradiol or progesterone (10 microM) did not change the membrane potential. The addition of the K +ATP channel agonist diazoxide to the perfusion buffer nullified the depolarization effect of testosterone at 30 seconds. This result suggests that the immediate action of testosterone is associated with the closing of K +ATP channels, thereby depolarizing the membrane.

show abstract

Electrophysiological effects of progesterone on hepatocytes

Cited by 27 publications

References 9 publications

Nongenomic Steroid Action: Controversies, Questions, and Answers

Nongenomic Steroid Action: Controversies, Questions, and Answers

Progesterone impairs cell respiration and suppresses a compensatory increase in glucose transport in isolated rat skeletal muscle: a non-genomic mechanism contributing to metabolic adaptation to late pregnancy?

Rapid Effect of Testosterone on Rat Sertoli Cell Membrane Potential. Relationship with K⁺ _ATPChannels

Contact Info

Product

Resources

About

Electrophysiological effects of progesterone on hepatocytes

Cited by 27 publications

References 9 publications

Nongenomic Steroid Action: Controversies, Questions, and Answers

Nongenomic Steroid Action: Controversies, Questions, and Answers

Progesterone impairs cell respiration and suppresses a compensatory increase in glucose transport in isolated rat skeletal muscle: a non-genomic mechanism contributing to metabolic adaptation to late pregnancy?

Rapid Effect of Testosterone on Rat Sertoli Cell Membrane Potential. Relationship with K+ ATPChannels

Contact Info

Product

Resources

About

Rapid Effect of Testosterone on Rat Sertoli Cell Membrane Potential. Relationship with K⁺ _ATPChannels