Journalartikel

Jahr der Veröffentlichung: 2000

Seiten: 764-773

Zeitschrift: Molecular Endocrinology -Baltimore-

Bandnummer: 14

Heftnummer: 6

ISSN: 0888-8809

DOI Link: https://doi.org/10.1210/mend.14.6.0477

Verlag: Endocrine Society

Abstract: 
Cross-talk between insulin and the adrenergic system is important in the regulation of energy homeostasis. In cultured, differentiated mouse brown adipocytes, beta 3-adrenergic stimulation induced a 4.5-fold increase in uncoupling protein-1 (UCP-1) expression, which was diminished by 25% in the presence of insulin. beta 3-Adrenergic stimulation also activated mitogen-activated protein (MAP) kinase by 3.5-fold and caused a decrease in basal phosphoinositide (PI) 3-kinase activity detected in p1100 gamma- and G beta-subunit-immunoprecipitates in a time-dependent manner, whereas insulin stimulated p110 alpha- and phosphotyrosine-associated PI 3-kinase activity. Inhibition of MAP kinase or PI 3-kinase potentiated the beta 3-adrenergic effect on UCP-1 expression, both alone and in the presence of insulin. Thus, insulin inhibits beta 3-adrenergic stimulation of UCP-1, and both MAP kinase and PI 3-kinase are negative regulatory elements in the beta 3-adrenergic control of UCP-1 expression. Crosstalk between the adrenergic and insulin signaling systems end impaired regulation of UCP-1 might contribute to the development of a reduced energy balance, resulting in obesity and insulin resistance.

Harvard-Zitierstil: Klein, J., Fasshauer, M., Benito, M. and Kahn, C. (2000) Insulin and the β3-Adrenoceptor Differentially Regulate Uncoupling Protein-1 Expression, Molecular Endocrinology -Baltimore-, 14(6), pp. 764-773. https://doi.org/10.1210/mend.14.6.0477

APA-Zitierstil: Klein, J., Fasshauer, M., Benito, M., & Kahn, C. (2000). Insulin and the β3-Adrenoceptor Differentially Regulate Uncoupling Protein-1 Expression. Molecular Endocrinology -Baltimore-. 14(6), 764-773. https://doi.org/10.1210/mend.14.6.0477