Endogenous epinephrine protects against obesity induced insulin resistance.
ABSTRACT Epinephrine (E) is a hormone released from the adrenal medulla in response to low blood sugar and other stresses. E and related β2-adrenergic agonists are used to treat asthma, but a side effect is high blood sugar. C57BL/6 mice prone to overfeeding induced type II diabetes had the PNMT gene knocked out to prevent E synthesis. These E deficient mice were very similar to control animals on a 14% fat diet. On a 40.6% fat diet they gained 20 to 33% more weight than control animals and increased their blood glucose response to a glucose tolerance test because they became resistant to insulin. Although the short term effect of β2-agonists such as E is to raise blood glucose, some long acting β2-agonists improve muscle glucose uptake. Endogenous E protects against overfeeding induced diabetes. Since adrenal E release can be impaired with aging and diabetes, endogenous E may help prevent adult onset diabetes.
Article: [The beta-hCG subunit, CA 125 and CA 19-9 antigen in the women with non-trophoblastic malignancy of genital tract. Endometrial cancer].[show abstract] [hide abstract]
ABSTRACT: There are few conflicting reports in regards of markers appearing in the patients with endometrial cancer. The aim of this study was to evaluate the serum levels: CA 125 antigen, CA 19-9 antigen and beta-hCG subunit in this group of patients and comparing obtained results with normal controls. In both groups--with endometrial cancer (n = 43)- and controls-(n = 214)--CA125 antigen, CA 19-9 antigen and beta-hCG subunit the serum level were determined two = site of immunometric method. The differences of the means, correlations, specificity, sensitivity, positive predictive value, negative predictive value and efficiency were calculated. The women with endometrial cancer exhibited the significantly higher level of all antigens. The positive correlation between CA 125 serum level and staging and grading and between beta-hCG subunit and endometrial cancer staging was found. The positive test had: specificity--62%, sensitivity--93%, positive predictive value--66%, negative predictive value--92% and efficiency--92.5%. In the women with endometrial cancer appears non-specific antigens characteristic for the müllerian duct derivatives tissue, exhibiting Lewis blood group antigen and involving in membrane cell structures in normal and cancer cells. The level of these antigens correlates with grading and staging of the neoplasms.Ginekologia polska 08/2000; 71(7):623-7. · 0.41 Impact Factor
Article: Nonadrenal epinephrine-forming enzymes in humans. Characteristics, distribution, regulation, and relationship to epinephrine levels.[show abstract] [hide abstract]
ABSTRACT: Animal studies indicate that nonadrenal tissues may synthesize epinephrine (E). Here we demonstrate phenylethanolamine N-methyltransferase (PNMT) and/or nonspecific N-methyltransferase (NMT) enzymatic activity in human lung, kidney, heart, liver, spleen, and pancreas. There was a significant overall correlation (r = 0.34) between tissue PNMT and E. PNMT and NMT in human tissues differed in substrate and inhibitor specificity, thermal stability, and antigenicity. By these criteria, PNMT in human lung and in human bronchial epithelial cells were indistinguishable from adrenal PNMT. PNMT and/or NMT activity were present in red blood cells (RBCs), and cancer cell lines. Human kidney, lung, and pancreas showed immunohistochemical staining with an antibody to adrenal PNMT. RBC PNMT activity was lower in males than females and was increased in hyperthyroidism and decreased in hypothyroidism. PNMT activity in a human bronchial epithelial cell line was dramatically increased by incubation with dexamethasone. E and 3H-E levels in plasma and urine during an intravenous infusion of 3H-E into humans indicated that kidney may synthesize half of urinary E. We conclude that PNMT and NMT are widely distributed in human tissues, that they may synthesize E in vivo and are influenced by glucocorticoid and thyroid hormones.Journal of Clinical Investigation 07/1995; 95(6):2896-902. · 15.39 Impact Factor