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Copper regulates cyclic-AMP-dependent lipolysis. 2016
Lakshmi Krishnamoorthy, and
Joseph A Cotruvo, and
Jefferson Chan, and
Harini Kaluarachchi, and
Abigael Muchenditsi, and
Venkata S Pendyala, and
Shang Jia, and
Allegra T Aron, and
Cheri M Ackerman, and
Mark N Vander Wal, and
Timothy Guan, and
Lukas P Smaga, and
Samouil L Farhi, and
Elizabeth J New, and
Svetlana Lutsenko, and
Christopher J Chang
Department of Chemistry, University of California, Berkeley, California, USA.
Cell signaling relies extensively on dynamic pools of redox-inactive metal ions such as sodium, potassium, calcium and zinc, but their redox-active transition metal counterparts such as copper and iron have been studied primarily as static enzyme cofactors. Here we report that copper is an endogenous regulator of lipolysis, the breakdown of fat, which is an essential process in maintaining body weight and energy stores. Using a mouse model of genetic copper misregulation, in combination with pharmacological alterations in copper status and imaging studies in a 3T3-L1 white adipocyte model, we found that copper regulates lipolysis at the level of the second messenger, cyclic AMP (cAMP), by altering the activity of the cAMP-degrading phosphodiesterase PDE3B. Biochemical studies of the copper-PDE3B interaction establish copper-dependent inhibition of enzyme activity and identify a key conserved cysteine residue in a PDE3-specific loop that is essential for the observed copper-dependent lipolytic phenotype.
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