Abstract：
:G(s)α is a ubiquitously expressed G protein α-subunit that couples receptors to the generation of intracellular cyclic AMP. The G(s)α gene GNAS is a complex gene that undergoes genomic imprinting, an epigenetic phenomenon that leads to differential expression from the two parental alleles. G(s)α is imprinted in a tissue-specific manner, being expressed primarily from the maternal allele in a small number of tissues. Albright hereditary osteodystrophy is a monogenic obesity disorder caused by heterozygous G(s)α mutations but only when the mutations are maternally inherited. Studies in mice indicate a similar parent-of-origin effect on energy and glucose metabolism, with maternal but not paternal mutations leading to obesity, reduced sympathetic nerve activity and energy expenditure, glucose intolerance and insulin resistance, with no primary effect on food intake. These effects result from G(s)α imprinting leading to severe G(s)α deficiency in one or more regions of the central nervous system, and are associated with a specific defect in melanocortins to stimulate sympathetic nerve activity and energy expenditure.
journal_name
Eur J Pharmacoljournal_title
European journal of pharmacologyauthors
Chen M,Nemechek NM,Mema E,Wang J,Weinstein LSdoi
10.1016/j.ejphar.2010.10.105subject
Has Abstractpub_date
2011-06-11 00:00:00pages
119-24issue
1eissn
0014-2999issn
1879-0712pii
S0014-2999(10)01269-0journal_volume
660pub_type
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