Abstract
Beta-adrenergic activation stimulates uncoupling protein 1 (UCP1), enhancing metabolic rate. In vitro, most work has studied brown adipocytes, however, few have investigated more established adipocyte lines such as the murine 3T3-L1 line. To assess the effect of beta-adrenergic activation, mature 3T3-L1s were treated for 6 or 48 hours with or without isoproterenol (10 and 100 μM) following standard differentiation supplemented with thyroid hormone (T3; 1 nM). The highest dose of isoproterenol increased lipid content following 48 hours of treatment. This concentration enhanced UCP1 mRNA and protein expression. The increase in UCP1 following 48 hours of isoproterenol increased oxygen consumption rate. Further, coupling efficiency of the electron transport chain was disturbed and an enhancement of glycolytic rate was measured alongside this, indicating an attempt to meet the energy demands of the cell. Lastly, markers of beige adipocytes (protein content of CD137 and gene transcript of CITED1) were also found to be upregulated at 48 hours of isoproterenol treatment. This data indicates that mature 3T3-L1 adipocytes are responsive to isoproterenol and induce UCP1 expression and activity. Further, this finding provides a model for further pharmaceutical and nutraceutical investigation of UCP1 in 3T3-L1s.
Highlights
Uncoupling proteins (UCPs) reside on the mitochondrial membranes and disrupt the proton gradient that drives the electron transport chain [1]
In the unadjusted AdipoRed assay 6 hours of isoproterenol treatment proved to be insignificant in the amount of lipid determined, a significant difference was measured between isoproterenol doses following 48 hours of treatment (p
Following adjustment for viable cells, isoproterenol treatment for 48 hours resulted in increased adjusted lipid content in a dose dependent fashion with the highest dose having the largest amount of lipid in viable cells (p
Summary
Uncoupling proteins (UCPs) reside on the mitochondrial membranes and disrupt the proton gradient that drives the electron transport chain [1]. This results in the loss of protons as heat and subsequently causes increased fatty acid oxidation to meet the energy demands of the cell. Because of this property, the upregulation of UCPs have been targeted as a potential panacea for anti-obesity research [2]. Several isoforms of UCPs exist and further are found to populate.
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