[The glucose-pyruvate test in Friedreich's ataxia and Charcot-Marie-Tooth disease].
Explore the source record for details and available documents.
Adult↗
Biomedical subjects
R Avola
Publications and source records attributed to R Avola.
Phenformin increases insulin binding to human cultured breast cancer cells.
The effect of the hypoglycemic biguanide, phenformin, on the binding of insulin to MCF-7 cells, an in vitro line derived from a human breast cancer, has been investigated. Cells incubated for 24 h in the presence of 1.0 micrograms/ml of phenformin bound 62.2 +/- 8.1% (mean +/- SE) more 125I-insulin than did controls. The phenformin effect was dose-dependent over the concentration range of 0.1 micrograms/ml to 10.0 micrograms/ml. The increased binding was due to an increase in receptor number without a change in binding affinity. This demonstration of increased receptor number in response to phenformin exposure provides support for the hypothesis that one action of phenformin is to enhance tissue sensitivity to insulin.
Breast Neoplasms↗
Pyrimidine nucleotide synthesis in rat embryo cells infected with X14 or H-1 parvovirus.
The activity of some enzymes involved in pyrimidine nucleotide synthesis was studied in rat embryo cell (REC) cultures infected with X14 or H-1 parvovirus. dCMP aminohydrolase activity of the infected cells was 64--121% greater than that of the mock-infected cells. dTMP synthetase activity was 18% greater in X14 virus-infected cells and 34% lower in H-1 virus-infected cells. These results suggest some differences in the infected cells, as regards the biosynthesis of dTMP. Orotate phosphoribosyltransferase and orotidylate decarboxylase activities appeared nearly unmodified compared to the mock-infected cells. The addition of phosphoribosylpyrophosphate (PRPP) to the cell suspension incubated with [6-14C] orotate increased the specific radioactivity of acid-soluble uracil, 5-fold in the mock-infected cells and 15- --24-fold in the X14 or H-1 virus-infected cells (72 hr p.i.). This result suggests that the lowered pyrimidine nucleotide synthesis in infected cells depends to a large extent on the diminished PRPP pool.
Carboxy-Lyases↗
The dopaminergic system in hypertension.
Dopamine exerts cardiovascular and renal actions mediated through interaction with specific dopamine receptors. Dopamine receptors are cell surface receptors coupled to G-proteins and classified into two main super families based on biochemical, pharmacological and molecular characteristics. The dopamine D1-like receptor super family includes D1 and D5 receptors, known also in rodents as D1A and D1B sites. These receptors are linked to stimulation of adenylate cyclase. The dopamine D2-like receptor super family includes D2, D3 and D4 receptors. These receptors are linked to inhibition of adenylate cylase or not related with this enzyme activity. They also interfere with opening of Ca+2 channels and are linked to stimulation of K+ receptors. Dopamine receptor subtypes are expressed in brain as well as in extracerebral structures such as the heart, blood vessels, carotid body, kidney, adrenal gland, parathyroid gland and gastrointestinal tract. In the kidney, which represents the peripheral organ where dopamine receptors were more extensively investigated, dopamine receptors are involved in regulation of hemodynamic, electrolyte and water transport, as well as renin secretion. Hypertension-related dopamine receptor changes were also investigated primarily in the kidney. Defective renal dopamine production and/or dopamine receptor function have been reported in human primary hypertension as well as in genetic models of animal hypertension. There may be a primary defect in D1-like receptors and an altered signalling system in the proximal tubules that lead to reduced dopamine-mediated effects on renal sodium excretion in hypertension. Studies on the influence of hypertension on dopamine D2-like receptors are sparse Disruption of either D1A or D3 receptors at the gene level causes hypertension in mice. Using peripheral blood lymphocytes as possible markers of the status of dopamine receptors in essential hypertension, no changes of dopamine D1-like receptors were noticeable, whereas an increase of dopamine D2-like receptors likely representing an up-regulation mechanism was reported. Available information collectively indicates an involvement of peripheral dopaminergic system in hypertension consisting either in impaired receptor transduction mechanisms and/or in receptor loss. A better knowledge of molecular bases of these changes may contribute to the development of specific therapeutic approaches in the future.
Animals↗