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.
no postreceptor defect was detected in any of the patient groups when insulin's ability to suppress hepatic glucose output was measured.
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
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- In patients with Type II diabetes and fasting hyperglycemia, insulin resistance is caused by both decreased insulin receptors AND a postreceptor defect, leading to a reduced maximal rate of glucose disposal.Strong
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