The role of nitric oxide in the metabolism of labeled glucose in isolated rat uterus. Influence of 17β-estradiol

González, Ezequiel; Jawerbaum, Alicia; Novaro, Virginia; Faletti, A.; Gimeno, M.F.

doi:10.1016/0090-6980(95)00122-0

Cited by 5 publications

(4 citation statements)

References 22 publications

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“…This effect was reverted by the addition of NAME and indomethacin. Furthermore SNP, a yielded exogenous NO, stimulated glucose metabolism, confirming the findings of other authors [8].…”

Section: Discussionsupporting

confidence: 90%

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Glucose metabolism in isolated uteri of immature rats. Influence of prostaglandins and nitric oxide

2006

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-We studied the contractile activity and glucose metabolism, in terms of production of 14 CO 2 from [ 14 C] glucose, in isolated uteri of immature rats. Immaturity was due to age or exposure to a restricted diet. The contractile activity in both prepubertal groups persisted for a period of 60 minutes and fell when indomethacin was added to the KRB medium. The production of 14 CO 2 was greater than for adult rats and fell as a result of the addition of indomethacin. The metabolism of [ 14 C] arachidonic acid showed that the percentage of eicosanoids released in age related immature uteri was greater than that in restricted diet related immature uteri. In animals that are immature as a result of exposure to a restricted diet, 14 CO 2 fell due to the effect of NAME. Sodium nitroprusside and L-arginine increased the production of 14 CO 2 . This effect was reverted by NAME and indomethacin. Conversely, the uteri of age related prepubertal rats were not affected. The level of activity of nitric oxide synthase was higher in restricted diet related immature animals and fell following the addition of NS-398. We may conclude that in rats exposed to a restricted diet, NO and COX-2 participate in glucose metabolism whereas they would not be involved in age related prepubertal animals.immature rats / glucose metabolism / nitric oxide / arachidonic acid

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“…This effect was reverted by the addition of NAME and indomethacin. Furthermore SNP, a yielded exogenous NO, stimulated glucose metabolism, confirming the findings of other authors [8].…”

Section: Discussionsupporting

confidence: 90%

“…Furthermore, nitric oxide (NO), synthesized from arginine by nitric oxide synthase (NOS) is involved in numerous physiological processes [7], amongst which lies glucose metabolism [8,9]. In a previous study on fasting rats we demonstrated that inhibitors of NOS prevent the increase of glucose metabolism induced by indomethacin [9].…”

Section: Introductionmentioning

confidence: 99%

Glucose metabolism in isolated uteri of immature rats. Influence of prostaglandins and nitric oxide

2006

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“…Thus, it is possible that some of the effects of estrogen are mediated by an increase in NO production by type I NOS. Glucose utilization by uterine strips obtained from estrogen-treated ovariectomized rats increases when the strips are exposed to the NO donor sodium nitroprusside, and it is decreased by high concentrations of NOS inhibitors [43].…”

Section: Discussionmentioning

confidence: 99%

Nonpregnant Sheep Uterine Type I and Type III Nitric Oxide Synthase Expression Is Differentially Regulated by Estrogen1

Zhang

Massmann

Mirabile

et al. 1999

Biology of Reproduction

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The aim of this study was to characterize the effect of estrogen on the expression of neuronal and endothelial isoforms of nitric oxide (NO) synthase (NOS) in myometrium, endometrium, and caruncle (nonglandular endometrium) in nonpregnant sheep. Twenty sheep were castrated during synchronized estrus (Days 14-16) and 4 days after surgery treated i.v. through the jugular with 100 microg/day of estradiol-17beta for 5 (n = 6) or 8 (n = 6) days or with vehicle (n = 8). Nitric oxide synthase mRNA was measured by ribonuclease protection assay, and NOS protein mass was measured by Western immunoblotting. Data were analyzed by ANOVA and Tukey's test. The three distinct uterine compartments studied contained the mRNA and protein for the neuronal (type I NOS) and the endothelial (type III NOS) isoforms of NOS. However, no inducible NOS was detected. Estrogen exhibited a differential effect on NOS expression in a tissue compartment- and NOS isoform-specific manner. In myometrium and caruncles, but not in endometrium, type I NOS mRNA and protein mass increased significantly (p < 0.05) after 5 or 8 days of estrogen. In contrast, type III NOS increased significantly in myometrium only after 8 days, whereas in endometrium and caruncles the increase was significant in the 5-day treatment group (p < 0.05). We conclude that the expression of type I NOS and type III NOS in the uterus are differentially regulated by estrogen. This differential regulation suggests that the NO produced within the uterus serves more than one physiological role. In myometrium it may be a uterorelaxant and regulate glucose utilization, and in endometrium and myometrium it may regulate blood flow.

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“…This is the first study to provide evidence for a role for activation of soluble PKG, by cGMP, in the stimulation of oxidative metabolism in skeletal muscle. Glucose oxidation is activated by NO in smooth muscle [25]. NO increases rates of oxidation of glucose, pyruvate, palmitate and leucine (see Section 3), suggesting activation of a common mechanism for oxidation of all these substrates.…”

Section: Discussionmentioning

confidence: 99%

Fuel oxidation in skeletal muscle is increased by nitric oxide/cGMP – evidence for involvement of cGMP‐dependent protein kinase

Young¹,

Leighton²

1998

FEBS Letters

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The cyclic guanosine-3P,5P-monophosphate (cGMP) analogue, 8-bromo-cGMP (1 mM), increased glucose oxidation in isolated soleus muscle. The nitric oxide (NO) donor, sodium nitroprusside (SNP) (15 mM), increased glucose, pyruvate, palmitate and leucine oxidation. Removal of extracellular Ca 2+ did not affect SNP-stimulated glucose oxidation (or other glucose utilization parameters), thus eliminating the influx of Ca 2+ as a mechanism for the increases. The guanylate cyclase inhibitor, LY-83583 (10 W WM), inhibited SNP-stimulated palmitate oxidation and activation of cGMP-dependent protein kinase (PKG). Activation of PKG might supersede any inhibitory effects of NO on respiration to stimulate metabolic fuel oxidation in skeletal muscle.z 1998 Federation of European Biochemical Societies.

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The role of nitric oxide in the metabolism of labeled glucose in isolated rat uterus. Influence of 17β-estradiol

Cited by 5 publications

References 22 publications

Glucose metabolism in isolated uteri of immature rats. Influence of prostaglandins and nitric oxide

Glucose metabolism in isolated uteri of immature rats. Influence of prostaglandins and nitric oxide

Nonpregnant Sheep Uterine Type I and Type III Nitric Oxide Synthase Expression Is Differentially Regulated by Estrogen1

Fuel oxidation in skeletal muscle is increased by nitric oxide/cGMP – evidence for involvement of cGMP‐dependent protein kinase

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