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Taken together, GH excess associated with poorly controlled T1DM induces podocyte injury, characterized by podocyte hypertrophy, apoptosis, dedifferentiation of podocytes (epithelialmesenchymal transition) and/or cross-linking of the basement membrane resulting in increased podocyte permeability to albumin and detachment of podocytes from the glomerular basement membrane (Fig

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Combining them in experimental models allows researchers to study synergistic effects on GH release pathways and receptor cross-talk

David Beck, MD, Ochsner Medical Center, New Orleans, LA