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- W2000383239 abstract "G-proteins are integral participants in many signalling cascades. Activation of G-protein is the principal mechanism through which activated heptahelical receptors generate changes in intracellular function. Abnormalities in regulation of G-proteins have been implicated in the pathogenesis of cardiovascular diseases, such as heart failure and hypertension. Also, common genetic polymorphisms of the components of G-proteins have been implicated in both cardiovascular and metabolic disease. In this issue of The Lancet, two research letters, by B Hocher and colleagues and A Gutersohn and colleagues, suggest the potential importance of a common G-protein polymorphism on aspects of fetal and maternal metabolism. These reports also highlight the challenges involved when attempts are made to translate genotypic differences into mechanisms that underlie complex phenotypes. G protein β3 subunit 825 TT genotype and post-pregnancy weight retentionPrimiparous homozygous carriers of the G protein β3 825T allele, a thrifty genotype, are at high risk of obesity and post-pregnancy weight retention if they do not exercise regularly. Full-Text PDF Association of maternal G protein β3 subunit 825T allele with low birthweightWeight at birth has been associated with an increased risk for cardiovascular disease and type 2 diabetes in adult life. We found an association between the maternal G protein β3 subunit 825T allele and low birthweight in babies born to women without other risks for reduced fetal growth. Full-Text PDF" @default.
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- W2000383239 date "2000-04-01" @default.
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- W2000383239 title "G-protein polymorphisms and maternal/neonatal metabolism: still a weight for the answer" @default.
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- W2000383239 doi "https://doi.org/10.1016/s0140-6736(00)02081-x" @default.
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