Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-nine women in premature labor were randomly assigned to a ritodrine (N = 14) or placebo (N = 15) treatment group. Thirteen serial blood samples were drawn during the first 12 hours of therapy by intravenous drug infusion and they were analyzed for a variety of metabolic substances. There was a significant increase in the blood glucose level in the ritodrine group after one hour and this persisted for the 12 hours of intravenous drug treatment. Plasma insulin levels similarly did not increase in the placebo but significantly rose in the ritodrine group by 30 minutes, peaked at 2 1/2 hours, and remained elevated throughout the infusion. There were no significant differences between levels of plasma glucagon, cholesterol triglyceride, human placental lactogen, or human chorionic gonadotropin in the two treatment groups. Ritodrine caused significant maternal and fetal tachycardia. Its use in women with carbohydrate abnormalities should be monitored carefully. The increased glucose levels may lead to an increased fetal weight.
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PMID:The acute effects of ritodrine infusion on maternal metabolism: measurements of levels of glucose, insulin, glucagon, triglycerides, cholesterol, placental lactogen and chorionic gonadotropin. 35 1

Since insulin is known to stimulate intracellular hydrogen peroxide production in rat epididymal fat cells, the effects of exogenous hydrogen peroxide on rates of basal and hormone-stimulated lipolysis were investigated in a perifusion system. H2O2 (60 microM) caused a weak and transient stimulation of basal lipolysis that did not interfere with subsequent activation of lipolysis by hormones. More importantly, lipolysis stimulated submaximally with ritodrine (10(-7) M) or glucagon (10(-9) M) was inhibited by H2O2 in a manner similar to insulin, although slight differences in time course were noted. Ritodrine served as a beta-adrenergic agonist resistant to oxidative destruction by H2O2. The inhibition of lipolysis was reversible upon cessation of perifusion with H2O2. These findings ruled out oxidative destruction of the hormone or cell death as explanations for the antilipolytic effect of H2O2. Like insulin, H2O2 also inhibited 1-methyl-3-isobutylxanthine (4 X 10(-6) M)-stimulated lipolysis, but whereas insulin inhibited lipolysis stimulated by dibutyryl-cAMP (4 X 10(-4) M), H2O2 further enhanced it. These findings add another case to the growing list of insulin effects on adipocytes that can be mimicked by exogenous H2O2, and they hint at a site where the mechanisms of action of the two agents may differ.
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PMID:Effects of hydrogen peroxide on basal and hormone-stimulated lipolysis in perifused rat fat cells in relation to the mechanism of action of insulin. 615 57