Inhibition of glucose metabolism by progesterone in adipocytes: role of protein synthesis

1991 ◽  
Vol 69 (12) ◽  
pp. 1861-1867 ◽  
Author(s):  
P. Cordoba ◽  
A. Kaaya ◽  
O. Richard ◽  
M.-Th. Sutter-Dub
Keyword(s):  
Protein Synthesis ◽  
Glucose Metabolism ◽  
Glucose Transport ◽  
Glucose Oxidation ◽  
Actinomycin D ◽  
Inhibitory Effect ◽  
Leucine Incorporation ◽  
Female Rat ◽  
Sds Page

Progesterone decreases [1-14C]glucose oxidation in isolated female rat adipocytes within 20 min of incubation. Because steroids regulate transcription mechanisms, the relationship between protein synthesis and glucose metabolism was studied in the presence of progesterone. Actinomycin D does not affect basal glucose oxidation or the progesterone effects on it; cycloheximide and puromycin decrease basal glucose oxidation, but only puromycin decreases the inhibitory progesterone effect. Although puromycin inhibits glucose transport, the common site of action of puromycin and progesterone does not seem to be glucose transport, which, as we showed previously, is not modified by the steroid. Incorporation of [3H]leucine into acid-precipitable proteins is decreased by puromycin and cycloheximide but not by actinomycin D or progesterone; moreover, the action of these inhibitors does not change in the presence of the steroid. As shown by electrophoresis (SDS–PAGE) and autoradiography, L-leucine is incorporated into adipocyte proteins as early as 20 min and progesterone increases this incorporation into five proteins. Leucine is a ketogenic amino acid that is also incorporated into lipids; progesterone depresses L-leucine incorporation into fatty acids by a glucose-dependent mechanism. These results suggest that the inhibitory effect of progesterone on glucose metabolism is related to an enhanced protein synthesis counterbalanced by decreased fatty acid synthesis.Key words: adipocytes, glucose metabolism, progesterone, protein synthesis, gel autoradiography.

Inhibition of hexose transport in adipocytes by dexamethasone: role of protein synthesis

1985 ◽  
Vol 248 (2) ◽  
pp. E215-E223
Author(s):  
C. Carter-Su ◽  
K. Okamoto
Keyword(s):  
Protein Synthesis ◽  
Effective Dose ◽  
Glucose Oxidation ◽  
Actinomycin D ◽  
Hexose Transport ◽  
Hormone Action ◽  
Transport Assay ◽  
Isolated Rat ◽  
Synthetic Glucocorticoid

The ability of the synthetic glucocorticoid, dexamethasone, to alter 3-O-methylglucose transport was investigated using isolated rat adipocytes. A maximally effective dose of dexamethasone (10(-7) M) inhibited transport up to 80% within 60–90 min. Inhibition of transport was evident as early as 15–30 min after addition of steroid, and was prevented by both actinomycin D and cycloheximide. When added within 45 or 60 min after dexamethasone, actinomycin D interfered with the cells' ability to respond to the steroid but had no effect when added between 60 and 90 min or longer after the steroid. Cycloheximide interfered with steroid-induced inhibition of transport when added at any time before the 15- to 30-min period immediately preceding the transport assay. This interference with hormone action appeared to be independent of the length of time cells were exposed to dexamethasone before addition of cycloheximide. Thus cells that were maximally inhibited by dexamethasone by 90 min became only partially inhibited when cycloheximide was added at 90 or 120 min, and cells were incubated for an additional 60 or 30 min, respectively. These findings are consistent with the following: dexamethasone inhibits glucose oxidation as a result of inhibiting hexose transport; inhibition of transport by dexamethasone requires the synthesis of RNA during the first 45–60 min after steroid addition and requires protein synthesis during the entire incubation period with dexamethasone; and transport is inhibited within minutes after protein synthesis is initiated.

EFFECT OF ACTINOMYCIN D ON TSH-INDUCED STIMULATION OF THYROIDAL PROTEIN SYNTHESIS IN THE RAT

1974 ◽  
Vol 77 (1) ◽  
pp. 64-70 ◽  
Author(s):  
Gustav Wägar
Keyword(s):  
Protein Synthesis ◽  
Actinomycin D ◽  
The Other ◽  
Leucine Incorporation ◽  
Short Term ◽  
Other Hand ◽  
Thyroid Glands ◽  
Translational Level ◽  
Stimulation Of

ABSTRACT Whether the short-term regulation of thyroidal protein synthesis by TSH occurs at the transcriptional or the translational level was tested by measuring the effect of actinomycin D (act D) on the TSH-induced stimulation of L-14C-leucine incorporation into the thyroidal proteins of rats. TSH was injected 6 h before the rats were killed. The thyroid glands were then removed and incubated in vitro in the presence of L-14C-leucine for 2 h. The pronounced stimulation of leucine incorporation in the TSH-treated animals was depressed as compared with controls but still significant even when the animals had been pre-treated with 100 μg act D 24 and 7 h before sacrifice. On the other hand, act D strongly decreased incorporation of 3H-uridine into RNA. Short-term regulation of thyroidal protein synthesis by TSH appears to be partly but not wholly dependent on neosynthesis of RNA. Hence regulation may partly occur at the translation level of protein synthesis.

POSSIBLE ROLE OF 5α-ANDROSTANE-3α,17β-DIOL IN THE CONTROL OF FOLLICLE-STIMULATING HORMONE SECRETION IN THE IMMATURE FEMALE RAT

1982 ◽  
Vol 92 (1) ◽  
pp. 37-42 ◽  
Author(s):  
H. M. A. MEIJS-ROELOFS ◽  
P. KRAMER ◽  
L. GRIBLING-HEGGE
Keyword(s):  
Inhibitory Action ◽  
Combined Treatment ◽  
Hormone Secretion ◽  
Inhibitory Effect ◽  
Ovariectomized Rats ◽  
Female Rat ◽  
Immature Rat ◽  
Rat Strain ◽  
Intact Rats

A possible role of 5α-androstane-3α,17β-diol (3α-androstanediol) in the control of FSH secretion was studied at various ages in ovariectomized rats. In the rat strain used, vaginal opening, coincident with first ovulation, generally occurs between 37 and 42 days of age. If 3α-androstanediol alone was given as an ovarian substitute, an inhibitory effect on FSH release was evident with all three doses tested (50, 100, 300 μg/100 g body wt) between 13 and 30 days of age; at 33–35 days of age only the 300 μg dose caused some inhibition of FSH release. Results were more complex if 3α-androstanediol was given in combined treatment with oestradiol and progesterone. Given with progesterone, 3α-androstanediol showed a synergistic inhibitory action on FSH release between 20 and 30 days of age. However, when 3α-androstanediol was combined with oestradiol a clear decrease in effect, as compared to the effect of oestradiol alone, was found between 20 and 30 days of age. Also the effect of combined oestradiol and progesterone treatment was greater than the effect of combined treatment with oestradiol, progesterone and 3α-androstanediol. At all ages after day 20 none of the steroid combinations tested was capable of maintaining FSH levels in ovariectomized rats similar to those in intact rats. It is concluded that 3α-androstanediol might play a role in the control of FSH secretion in the immature rat, but after day 20 the potentially inhibitory action of 3α-androstanediol on FSH secretion is limited in the presence of oestradiol.

Lipopolysaccharide-induced sensitization of adenylyl cyclase activity in murine macrophages

2006 ◽  
Vol 290 (1) ◽  
pp. C143-C151 ◽  
Author(s):  
Y. Osawa ◽  
H. T. Lee ◽  
C. A. Hirshman ◽  
D. Xu ◽  
C. W. Emala
Keyword(s):  
Protein Synthesis ◽  
Adenylyl Cyclase ◽  
Actinomycin D ◽  
Inhibitory Effect ◽  
Cytokine Release ◽  
Adenylyl Cyclase Activity ◽  
Phosphorylation State ◽  
Murine Macrophages ◽  
Dependent Pathway ◽  
New Protein

LPS is known to modulate macrophage responses during sepsis, including cytokine release, phagocytosis, and proliferation. Although agents that elevate cAMP reverse LPS-induced macrophage functions, whether LPS itself modulates cAMP and whether LPS-induced decreases in proliferation are modulated via a cAMP-dependent pathway are not known. Murine macrophages (RAW264.7 cells) were treated with LPS in the presence or absence of inhibitors of prostaglandin signaling, protein kinases, CaM, Giproteins, and NF-κB translocation or transcription/translation. LPS effects on CaMKII phosphorylation and the expression of relevant adenylyl cyclase (AC) isoforms were measured. LPS caused a significant dose (5–10,000 ng/ml)- and time (1–8 h)-dependent increase in forskolin-stimulated AC activity that was abrogated by pretreatment with SN50 (an NF-κB inhibitor), actinomycin D, or cycloheximide, indicating that the effect is mediated via NF-κB-dependent transcription and new protein synthesis. Furthermore, LPS decreased the phosphorylation state of CaMKII, and pretreatment with a CaM antagonist attenuated the LPS-induced sensitization of AC. LPS, cAMP, or PKA activation each independently decreased macrophage proliferation. However, inhibition of NF-κB had no effect on LPS-induced decreased proliferation, indicating that LPS-induced decreased macrophage proliferation can proceed via PKA-independent signaling pathways. Taken together, these findings indicate that LPS induces sensitization of AC activity by augmenting the stimulatory effect of CaM and attenuating the inhibitory effect of CaMKII on isoforms of AC that are CaMK sensitive.

Abstract 15161: Adiponectin Exerts a Protective Role Against Vascular Remodeling During Hypertension

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Crystal M Ghantous ◽  
Sarah Hanache ◽  
Firas Kobaissy ◽  
Asad Zeidan
Keyword(s):  
Protein Synthesis ◽  
Vascular Remodeling ◽  
Mechanical Stretch ◽  
Protective Role ◽  
Leucine Incorporation ◽  
Rat Portal Vein ◽  
Length Relationship ◽  
Longitudinal Orientation ◽  
Ros Formation

Introduction: Hypertension is associated with leptin production and ROS formation in vascular smooth muscle cells (VSMC) and contributes to vascular remodeling. Adiponectin (ADQ) has a cardioprotective role on the heart, but the protective role of ADQ on VSMC during hypertension has not been fully elucidated yet. Hypothesis: Mechanical stretch/hypertension is associated with a low ADQ/leptin ratio in VSMC, leading to VSMC remodeling. Methods: To mimic hypertension, the rat portal vein was cultured either mechanically stretched with 1.2 gram weights (due to the force-length relationship normalized to the human force of stretch during hypertension and the longitudinal orientation of its VSMC) or left unstretched. ADQ, leptin, eNOS, p-ERK1/2 and p-AKT expression in VSMC was evaluated by Western blot. The protective effect of adiponectin (5-10 μg/ml; 15 min-24 hr) was investigated on ROS formation by DHE staining and on hypertrophy by protein synthesis via [ 3 H]leucine incorporation. Results: Mechanical stretch for 24 hr reduced the expression of ADQ in VSMC (0.49 ± 0.08 fold, n=6, p<0.05) and increased leptin (2.51 ± 0.39 fold, n=6, p<0.05) compared to controls. Stretch (24 hr) decreased ADQ mRNA expression by 0.31 ± 0.11 fold (n=7, p<0.05) and ADQ receptor R2 by 0.51 ± 0.21 fold (n=7, p<0.05) but had no effect on ADQ receptor R1 (n=8). This effect of stretch was associated with increased protein synthesis by 1.39 ± 0.06 fold (n=6, p<0.05), while exogenous ADQ significantly inhibited stretch-induced hypertrophy (n=6, p<0.05). Stretch (15 min) increased p-ERK1/2 and p-AKT by 2.10 ± 0.25 and 4.03 ± 0.61 fold respectively (n=5, p<0.05), but ADQ reduced p-ERK1/2 and p-AKT by 0.82 ± 0.26 and 0.55 ± 0.25 fold respectively (n=3, p<0.05) in stretched vessels. eNOS expression decreased by 0.70 ± 0.06 fold (n=5, p<0.05) after stretch for 24 hr, while ADQ increased eNOS in stretched veins by 2.02 ± 0.41 fold (n=3, p<0.05). Stretch for 1 hr increased ROS by 5.69 ± 0.13 fold (n=3, p<0.05), whereas ADQ significantly inhibited ROS in stretched vessels (1.71 ± 0.22 fold, n=3). Conclusion: Mechanical stretch reduces the ADQ/leptin ratio in VSMC. ADQ plays a protective role against vascular remodeling during hypertension by affecting eNOS, ERK, AKT, ROS and hypertrophy.

Abstract 579: Increased Role of COX-derived Prostanoids in Regulating Ang II Induced Uterine Artery Contraction at Early Pregnancy in a Transgenic Model of Preeclampsia

Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Victor M Pulgar ◽  
Liliya M Yamaleyeva ◽  
Jasmina Varagic ◽  
Carolynne M McGee ◽  
Michael Bader ◽  
...  
Keyword(s):  
Uterine Artery ◽  
Inhibitory Effect ◽  
Isometric Tension ◽  
Late Gestation ◽  
Female Rat ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Vascular Control ◽  
Human Renin

The balance between vasodilatory and vasoconstrictor prostanoids contributes to vascular control during pregnancy. Alterations in this balance are involved in the development of hypertensive pregnancy. The transgenic female rat containing the human angiotensinogen (hAGN) gene mated with the male transgenic containing human renin (hREN) is a model of preeclampsia (TgA), and shows hypertension and proteinuria at late gestation. We investigated the role COX-derived mediators have on contractility of the uterine artery (UA) in TgA rats before the hypertensive phenotype develops. UA were isolated from transgenic TgA (n=9) and Sprague-Dawley (n=7) control rats at 7 days of gestation. UA were mounted in a wire myograph for determinations of isometric tension (DMT USA, 620M). Responses to acetylcholine (ACh), phenylephrine (Phe) and sodium nitroprusside (SNP) were measured in control conditions and after preincubation with indomethacin (Indo, 10-5M). Data were fitted to a dose response curve, vasodilatation was expressed as percent of pre-constriction and sensitivity as pD2 (pD2= -Log [EC50]). Responses to ACh reached similar maximal relaxations (64±8 vs 75±6%, p>0.05), and an increased contraction in TgA UA at ACh >10μM (p<0.05) was eliminated by Indo. Contraction to Phe was similar in both groups with an inhibitory effect of Indo on TgA UA (p<0.05). Relaxation to SNP was lower in TgA vs SD UA (92±2 vs 74±5%, p<0.05), this difference was abolished by Indo. Thus, inhibition of COX enzymes had a greater effect on TgA UA suggesting an imbalance towards an increased prostanoids-derived constrictor tone in TgA UA. This imbalance appears before the hypertensive phenotype is established.

scholarly journals Stimulation of vascular protein synthesis by activation of oestrogen receptor beta

2001 ◽  
Vol 171 (3) ◽  
pp. 417-423 ◽  
Author(s):  
M Liang ◽  
E Ekblad ◽  
JA Gustafsson ◽  
BO Nilsson
Keyword(s):  
Protein Synthesis ◽  
Protein Expression ◽  
Oestrogen Receptor ◽  
Beta Agonist ◽  
Tissue Homogenate ◽  
Leucine Incorporation ◽  
Ovariectomized Mice ◽  
Sds Page ◽  
Genistein Treatment ◽  
Stimulation Of

The objective of this study was to investigate the effects of oestrogen receptor (ER) beta activation on vascular protein synthesis and protein expression. Nuclear immunoreactivity towards ER beta was observed abundantly in vascular smooth muscle and endothelial cells of mouse aorta. No ER alpha-positive cell nuclei were observed. In aorta from ovariectomized mice, treatment with the selective ER beta agonist genistein (100 nM) for 24 h increased [(3)H]leucine incorporation by about 30%. This effect was prevented by the ER blocker ICI 182780 (10 microM). Although genistein treatment stimulated protein synthesis, it caused no change in total protein determined either by the Lowry method on tissue homogenate or by densitometric scanning of protein bands (10-220 kDa) separated by SDS-PAGE. Separation of [(35)S]methionine-labelled proteins by SDS-PAGE did not reveal the protein(s) stimulated by genistein. DNA synthesis was not affected by 100 nM genistein, suggesting that genistein-induced stimulation of protein synthesis is not part of a growth response. Protein expression, determined by SDS-PAGE, was similar in aorta from ER beta-knockout and wild-type mice, suggesting that expression of vascular proteins does not depend solely on a functional ER beta gene. We suggest that activation of vascular ER beta stimulates synthesis of proteins and that this response is not associated with vascular growth.

Activation of Protein Synthesis in Aging Potato Tuber Slices

1971 ◽  
Vol 26 (10) ◽  
pp. 1064-1067 ◽  
Author(s):  
Günter Kahl
Keyword(s):  
Protein Synthesis ◽  
Potato Tuber ◽  
Actinomycin D ◽  
Leucine Incorporation ◽  
Amino Acid Incorporation ◽  
Acid Incorporation ◽  
Fresh Potato ◽  
Polyuridylic Acid ◽  
Storage Organs

Whereas ribosome preparations of freshly sliced potato disks do not show appreciable activity in an in-vitro amino acid incorporation system, aging of the tissue leads to a greatly enhanced incorporation activity which reaches its maximum 24 hours after slicing. If ribosomes from freshly excised disks are provided with polyuridylic acid, their activity in the incorporation of phenylalanine is increased about 8 fold.Moreover, an RNA-fraction can be dissociated by EDTA from ribosomes of aged potato tuber slices, which sediments at 15 —18S, has a base composition different from that of 16S — rRNA, 5S-and 4S —RNA, and is not present on ribosomes of fresh slices. Its appearance is inhibited by actinomycin D and therefore most probably dependent on transcription. This compound, purified from sucrose gradients, enhances in vitro leucine incorporation into peptide material by ribosomes of fresh potato slices.The possibility is discussed that this fraction-among other factors-is responsible for the enhanced protein synthesis after slicing plant storage organs, and is indicative of a general derepression phenomenon in these tissues.

Glucose metabolism in rat hypothalamus

1981 ◽  
Vol 98 (4) ◽  
pp. 481-487 ◽  
Author(s):  
Pentti Lautala ◽  
Julio M. Martin
Keyword(s):  
Glucose Metabolism ◽  
Glucose Transport ◽  
Glucose Concentration ◽  
Glucose Oxidation ◽  
Glucose Utilization ◽  
Rat Hypothalamus ◽  
Extracellular Glucose Concentration ◽  
Extracellular Glucose ◽  
Phenazine Methosulphate

Abstract. In vitro glucose oxidation and glucose transport in the rat medial (MH) and lateral (LH) hypothalamic areas was measured. Glucose oxidation was calculated from the conversion of [U-14C]glucose to 14C02 and glucose transport from 14C02 produced from [114C]glucose in the presence of phenazine methosulphate and NaF. Increasing glucose in the medium from 1 him to 20 mm enhanced glucose oxidation two-fold in MH and 40% in LH. Addition of insulin, 100 (iU/ml, to the medium decreased glucose oxidation 30% both in MH and LH at both 4 mm and 20 mm glucose. Fasting did not affect glucose oxidation in either of these hypothalamic areas. Glucose transport was not affected by insulin, but was increased significantly when glucose was raised from 0.25 mm to 1.0 mm. Fasting also increased glucose transport in both hypothalamic areas. In conclusion, extracellular glucose concentration seems to be the major regulator of glucose utilization by the rat hypothalamus. Insulin, rather than increasing, seems to decrease glucose oxidation while having no effect on glucose transport.

Genomic and nongenomic dose-dependent biphasic effect of aldosterone on Na+/H+ exchanger in proximal S3 segment: role of cytosolic calcium

2008 ◽  
Vol 295 (5) ◽  
pp. F1342-F1352 ◽  
Author(s):  
D. C. A. Leite-Dellova ◽  
M. Oliveira-Souza ◽  
G. Malnic ◽  
M. Mello-Aires
Keyword(s):  
Actinomycin D ◽  
Cytosolic Calcium ◽  
Inhibitory Effect ◽  
Ru 486 ◽  
Nongenomic Action ◽  
Biphasic Effect ◽  
S3 Segment ◽  
Dose Dependent Increase ◽  
Dose Dependent

The effects of aldosterone on the intracellular pH recovery rate (pHirr) via Na+/H+ exchanger and on the [Ca2+]i were investigated in isolated rat S3 segment. Aldosterone [10−12, 10−10, or 10−8 M with 1-h, 15- or 2-min preincubation (pi)] caused a dose-dependent increase in the pHirr, but aldosterone (10−6 M with 1-h, 15- or 2-min pi) decreased it (these effects were prevented by HOE694 but not by S3226). After 1 min of aldosterone pi, there was a transient and dose-dependent increase of the [Ca2+]i and after 6-min pi there was a new increase of [Ca2+]i that persisted after 1 h. Spironolactone, actinomycin D, or cycloheximide did not affect the effects of aldosterone (15- or 2-min pi) but inhibited the effects of aldosterone (1-h pi) on pHirr and on [Ca2+]i. RU 486 prevented the stimulatory effect of aldosterone (10−12 M, 15- or 2-min pi) on both parameters and maintained the inhibitory effect of aldosterone (10−6 M, 15- or 2-min pi) on the pHirr but reversed its stimulatory effect on the [Ca2+]i to an inhibitory effect. The data indicate a genomic (1 h, via MR) and a nongenomic action (15 or 2 min, probably via GR) on [Ca2+]i and on the basolateral NHE1 and are compatible with stimulation of the NHE1 by increases in [Ca2+]i in the lower range (at 10−12 M aldosterone) and inhibition by increases at high levels (at 10−6 M aldosterone) or decreases in [Ca2+]i (at 10−6 M aldosterone plus RU 486).

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