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M511752200v1
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Papers In Press, published online ahead of print May 2, 2006
J. Biol. Chem, 10.1074/jbc.M511752200
Submitted on October 31, 2005
Revised on April 19, 2006
Accepted on May 2, 2006

The alternative stimulatory G protein alpha -subunit XLalpha s is a critical regulator of energy and glucose metabolism and sympathetic nerve activity in adult mice

Tao Xie, Antonius Plagge, Oksana Gavrilova, Stephanie Pack, William Jou, Edwin W. Lai, Marga Frontera, Gavin Kelsey, and Lee S. Weinstein

Metabolic Diseases Branch, NIDDK/NIH, Bethesda, MD 20892-1752

Corresponding Author: leew{at}amb.niddk.nih.gov

The complex imprinted Gnas locus encodes several gene products including Gsalpha , the ubiquitously expressed G protein alpha -subunit required for receptor-stimulated cAMP generation, and the neuroendocrine-specific Gsalpha isoform XLalpha s. XLalpha s is only expressed from the paternal allele, while Gsalpha is biallelically expressed in most tissues. XLalpha s knockout mice (Gnasxlm+/p-) have poor suckling and perinatal lethality, implicating XLalpha s as critical for postnatal feeding. We have now examined the metabolic phenotype of adult Gnasxlm+/p- mice. Gnasxlm+/p- mice had reduced fat mass and lipid accumulation in adipose tissue, with increased food intake and metabolic rates. Gene expression profiling was consistent with increased lipid metabolism in adipose tissue. These changes likely result from increased sympathetic nervous system activity rather than adipose cell-autonomous effects, as we found that XLalpha s is not normally expressed in adult adipose tissue and Gnasxlm+/p- mice had increased urinary norepinephrine levels but not increased metabolic responsiveness to a beta 3-adrenergic agonist. Gnasxlm+/p- mice were hypolipidemic and had increased glucose tolerance and insulin sensitivity. The similar metabolic profile observed in some prior paternal Gnas knockout models results from XLalpha s deficiency (or deficiency of the related alternative truncated protein XLN1). XLalpha s (or XLN1) is a negative regulator of sympathetic nervous system activity in mice.


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