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₁- and ß₁-Adrenoceptor Signaling Fully Compensates for ß₃-Adrenoceptor Deficiency in Brown Adipocyte Norepinephrine-Stimulated Glucose Uptake

The Wenner-Gren Institute, The Arrhenius Laboratories F3, Stockholm University, SE-106 91 Stockholm, Sweden

Address all correspondence and requests for reprints to: Tore Bengtsson, The Wenner-Gren Institute, The Arrhenius Laboratories F3, Stockholm University, SE-106 91 Stockholm, Sweden. E-mail: tore.bengtsson{at}zoofys.su.se.

To assess the relative roles and potential contribution of adrenergic receptor subtypes other than the ß₃-adrenergic receptor in norepinephrine-mediated glucose uptake in brown adipocytes, we have here analyzed adrenergic activation of glucose uptake in primary cultures of brown adipocytes from wild-type and ß₃-adrenergic receptor knockout (KO) mice. In control cells in addition to high levels of ß₃-adrenergic receptor mRNA, there were relatively low _1A-, _1D-, and moderate ß₁-adrenergic receptor mRNA levels with no apparent expression of other adrenergic receptors. The levels of _1A-, _1D-, and ß₁-adrenergic receptor mRNA were not changed in the ß₃-KO brown adipocytes, indicating that the ß₃-adrenergic receptor ablation does not influence adrenergic gene expression in brown adipocytes in culture. As expected, the ß₃-adrenergic receptor agonists BRL-37344 and CL-316 243 did not induce 2-deoxy-D-glucose uptake in ß₃-KO brown adipocytes. Surprisingly, the endogenous adrenergic neurotransmitter norepinephrine induced the same concentration-dependent 2-deoxy-D-glucose uptake in wild-type and ß₃-KO brown adipocytes. This study demonstrates that ß₁-adrenergic receptors, and to a smaller degree ₁-adrenergic receptors, functionally compensate for the lack of ß₃-adrenergic receptors in glucose uptake. ß₁-Adrenergic receptors activate glucose uptake through a cAMP/protein kinase A/phosphatidylinositol 3-kinase pathway, stimulating conventional and novel protein kinase Cs. The ₁-adrenergic receptor component (that is not evident in wild-type cells) stimulates glucose uptake through a phosphatidylinositol 3-kinase and protein kinase C pathway in the ß₃-KO cells.

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