Research

Hormonal

Insulin's ability to suppress hepatic glucose output is preserved in both impaired glucose tolerance and Type II diabetes, with no postreceptor defect detected in the liver.

Even in Type II diabetes, the liver retains the ability to stop producing glucose when insulin levels are high enough. This suggests that therapies aiming to suppress hepatic glucose production (like metformin or GLP-1 agonists) may still be effective because the liver's basic response mechanism is not broken, just less sensitive.

StrongRefutesHIGH confidence
no postreceptor defect was detected in any of the patient groups when insulin's ability to suppress hepatic glucose output was measured.
Orville Kolterman et al. · Journal of Clinical Investigation · 1981

Why this rating

Measured using primed continuous infusion of [3-3H]glucose to calculate hepatic glucose output.

Source

Receptor and postreceptor defects contribute to the insulin resistance in noninsulin-dependent diabetes mellitus.

Orville Kolterman et al. · Journal of Clinical Investigation · 1981

DOI 10.1172/jci110350

mechanism_only · n=45Cited 637×
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DOI resolved against Crossref · corpus check 2026-06-10

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