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Preclinical data suggest GIP receptor engagement modulates lipid partitioning pathways and may act synergistically with GLP-1 receptor signalling in energy-balance models
Recently, SLC1A3, as a crucial effector of p53, has been shown to support cell survival and growth in the absence of glutamine 149
In effect, adding prandial RAIs to the treatment regimen mimics the physiological meal-simulated insulin release, which is lost first as beta-cell function declines
Cell death: critical control points
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