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Why the IFG Versus IGT Distinction Matters for an Amylin Agent
The two main prediabetes phenotypes are not interchangeable, and the distinction is directly relevant to how an amylin analogue might be expected to behave. Isolated impaired fasting glucose (IFG) is dominated by defects in basal hepatic glucose output and, to
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- The two main prediabetes phenotypes are not interchangeable, and the distinction is directly relevant to how an amylin analogue might be expected to behave. Isolated impaired fasting glucose (IFG) is dominated by defects in basal hepatic glucose output and, to a degree, early-phase insulin secretion, whereas isolated impaired glucose tolerance (IGT) reflects primarily impaired peripheral glucose disposal and exaggerated post-load excursions. An agent whose mechanism includes slowing gastric emptying and blunting the postprandial glucose spike—both amylin-class effects—would, on paper, be expected to influence the post-meal (IGT-type) abnormality more readily than the fasting (IFG-type) abnormality. This is a mechanistic prediction, not a demonstrated result for cagrilintide, but it illustrates why a serious prediabetes trial would need to stratify participants by phenotype: an intervention could show a real benefit in one subgroup that is diluted or masked when phenotypes are pooled. F