Hormonal
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.
If you have impaired glucose tolerance (pre-diabetes), your body's ability to process glucose at high insulin levels is likely intact. The primary issue is that you have fewer insulin receptors, so you need higher insulin levels to achieve the same glucose disposal as a healthy person. This suggests that lifestyle interventions improving insulin sensitivity (like exercise) can help compensate for the lower receptor count by making the existing receptors more efficient or by lowering the baseline insulin demand.
In the patients with the mildest disorders of carbohydrate homeostasis (patients with impaired glucose tolerance) the insulin resistance can be accounted for solely on the basis of decreased insulin receptors.
Why this rating
The study uses the euglycemic glucose-clamp technique, considered the gold standard for measuring in vivo insulin sensitivity, across multiple insulin infusion rates.
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 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
- 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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