Hormonal
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.
For those with established Type II diabetes, simply lowering insulin levels (if possible) or increasing receptor sensitivity is not enough because the cells' internal ability to process glucose is also damaged. Treatment must address both the signaling issue (receptors) and the internal processing issue (postreceptor defects), often requiring medication that bypasses or enhances these pathways.
In patients with fasting hyperglycemia, insulin resistance is due to both decreased insulin receptors and a postreceptor defect in the glucose disposal mechanisms.
Why this rating
Gold-standard euglycemic clamp technique confirms the reduction in maximal glucose disposal rate (Rd max) in diabetic subjects.
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
More from this paper
- In patients with impaired glucose tolerance, insulin resistance is caused solely by decreased insulin receptor numbers (receptor defect), resulting in a rightward shift of the dose-response curve without a reduction in maximal glucose disposal capacity.Strong
- 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.Strong
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