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Now, to understand why this might matter, we need to zoom in on an underappreciated problem in human metabolism
These findings were not attributed to variations in food intake, which implies that the observed results were mediated by alterations in metabolic processes [1]
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In an experimental model, transgenic mice expressing a kinase-deficient IGF-1R -subunit (thus displaying reduced signal transduction in both IGF-1R and hybrid receptors) developed diabetes early on life [162, 236]
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