Fasting insulin (revision 17)
Old revision·04:13, 15 Jun 2025·CategoryBot
| Fasting insulinLaboratory medicine | |
|---|---|
| Specimen | Fasting plasma or serum |
| Interpretable | Only alongside a simultaneous glucose |
| Standardisation | Poor between assays |
| Topic infobox · conventions | |
Fasting insulin is the concentration of insulin measured after an overnight fast. It is widely available and widely over-interpreted: an insulin value alone answers no question, because the same concentration means different things at different glucose concentrations.[1]
Insulin immunoassays are poorly standardised between manufacturers, differing in cross-reactivity with proinsulin and its split products. Values from different laboratories are not interchangeable, and derived indices inherit the discrepancy.[1]
Its principal use is as an input to derived indices, chiefly HOMA-IR and HOMA-B, which combine it with fasting glucose to estimate insulin resistance and secretory capacity respectively.[2]
Why it needs glucose alongside it
[edit]Insulin secretion is a response to glucose. A high fasting insulin with a normal fasting glucose indicates that normal glucose is being maintained at the cost of high insulin — the signature of insulin resistance with preserved secretion. The same insulin with a high glucose indicates resistance with inadequate compensation.[1]
A low insulin with a high glucose indicates secretory failure. A low insulin with a normal glucose is unremarkable. The four combinations mean four different things, and only two values together distinguish them.
This is why laboratory reports that give an insulin reference interval without reference to glucose are of limited use, and why the derived indices exist at all.[2]
Standardisation
[edit]Insulin assays differ in their response to proinsulin and to split proinsulin products, which circulate at higher relative concentrations in insulin-resistant states. An assay with more proinsulin cross-reactivity reads higher in exactly the population most likely to be tested.[1]
| Consequence | Effect |
|---|---|
| Between-assay differences | Values not interchangeable |
| Proinsulin cross-reactivity | Overestimation in resistant states |
| Derived indices | Inherit both problems |
| Published cut-offs | Assay-specific in origin |
A HOMA-IR threshold quoted without the assay it was derived from is not a threshold. This is the practical reason the index is better used to track change within an individual on one assay than to classify against a published cut-off.[2]
Behaviour under treatment
[edit]Fasting insulin falls with weight loss and with improved insulin sensitivity by any means, and the fall is a consequence of reduced demand rather than of reduced secretory capacity.[3]
Under incretin therapy the picture is mixed: secretion is amplified while the drug is present, and sensitivity improves with weight loss, so fasting insulin reflects both influences. Attributing a change to either alone is unsound.[1]
See also
References
- ^ a b c d e Wallace TM, Levy JC, Matthews DR. "Use and abuse of HOMA modeling." Diabetes Care 27(6):1487–1495 (2004). DOI:10.2337/diacare.27.6.1487. PMID 15161807.
- ^ a b c Matthews DR, Hosker JP, Rudenski AS, et al. "Homeostasis model assessment." Diabetologia 28(7):412–419 (1985). PMID 3899825.
- ^ Drucker DJ. "Mechanisms of action and therapeutic application of glucagon-like peptide-1." Cell Metabolism 27(4):740–756 (2018). PMID 29617641.