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This author has long recognized the need for a shift of clinical focus from glycemic status to insulin homeostasis for detecting and optimally managing adverse metabolic, proinflammatory, endothelial, developmental, and neurologic effects of hyperinsulinism (ref
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Absolute body weight reductions measured 10.2, 12.9, and 13.1 kg across the 2.4, 4.8, and 6 mg cohorts respectively vs
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