ArticleThe Journal of biological chemistry2006
The alternative stimulatory G protein alpha-subunit XLalphas is a critical regulator of energy and glucose metabolism and sympathetic nerve activity in adult mice.
Article in The Journal of biological chemistry, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 97 citations in OpenAlex.
- Effects of Developmental Lead and Phthalate Exposures on DNA Methylation in Adult Mouse Blood, Brain, and Liver: A Focus on Genomic Imprinting by Tissue and Sex.Environmental health perspectives · 2024Article
- Mother's warmth from maternal genes: genomic imprinting of brown adipose tissue.Evolution, medicine, and public health · 2023Article
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- Extra-Large Gα Protein (XLαs) Deficiency Causes Severe Adenine-Induced Renal Injury with Massive FGF23 Elevation.Endocrinology · 2020Article
- Genomic imprinting and its effects on postnatal growth and adult metabolism.Cellular and molecular life sciences : CMLS · 2019Review
- A G protein-coupled, IP3/protein kinase C pathway controlling the synthesis of phosphaturic hormone FGF23.JCI insight · 2019Article
- Neuronatin deletion causes postnatal growth restriction and adult obesity in 129S2/Sv mice.Molecular metabolism · 2018Article
- Current Nomenclature of Pseudohypoparathyroidism: Inactivating Parathyroid Hormone/Parathyroid Hormone-Related Protein Signaling Disorder.Journal of clinical research in pediatric endocrinology · 2017Review
- Large G protein α-subunit XLαs limits clathrin-mediated endocytosis and regulates tissue iron levels in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- New Perspectives on Genomic Imprinting, an Essential and Multifaceted Mode of Epigenetic Control in the Developing and Adult Brain.Annual review of neuroscience · 2016Review
- Epidemiology and Diagnosis of Hypoparathyroidism.The Journal of clinical endocrinology and metabolism · 2016Review
- Reductions in hypothalamic Gfap expression, glial cells and α-tanycytes in lean and hypermetabolic Gnasxl-deficient mice.Molecular brain · 2016Article
- Maternal uniparental disomy of chromosome 20: a novel imprinting disorder of growth failure.Genetics in medicine : official journal of the American College of Medical Genetics · 2016Article
- The G protein α subunit variant XLαs promotes inositol 1,4,5-trisphosphate signaling and mediates the renal actions of parathyroid hormone in vivo.Science signaling · 2015Article
- GNAS Spectrum of Disorders.Current osteoporosis reports · 2015Review
- GNAS mutations in Pseudohypoparathyroidism type 1a and related disorders.Human mutation · 2015Review
- The role of genomic imprinting in biology and disease: an expanding view.Nature reviews. Genetics · 2014Review
- Postnatal establishment of allelic Gαs silencing as a plausible explanation for delayed onset of parathyroid hormone resistance owing to heterozygous Gαs disruption.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2014Article
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
The complex imprinted Gnas locus encodes several gene products including G(s)alpha, the ubiquitously expressed G protein alpha-subunit required for receptor-stimulated cAMP generation, and the neuroendocrine-specific G(s)alpha isoform XLalphas. XLalphas is only expressed from the paternal allele, whereas G(s)alpha is biallelically expressed in most tissues. XLalphas knock-out mice (Gnasxl(m+/p-)) have poor suckling and perinatal lethality, implicating XLalphas as critical for postnatal feeding. We have now examined the metabolic phenotype of adult Gnasxl(m+/p-) mice. Gnasxl(m+/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 XLalphas is not normally expressed in adult adipose tissue, and Gnasxl(m+/p-) mice had increased urinary norepinephrine levels but not increased metabolic responsiveness to a beta3-adrenergic agonist. Gnasxl(m+/p-) mice were hypolipidemic and had increased glucose tolerance and insulin sensitivity. The similar metabolic profile observed in some prior paternal Gnas knock-out models results from XLalphas deficiency (or deficiency of the related alternative truncated protein XLN1). XLalphas (or XLN1) is a negative regulator of sympathetic nervous system activity in mice.
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