Beta cell function: difference between revisions
Diff·revision 12 → 13·12:40, 26 Feb 2025
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| Revision 12 — 13:50, 31 Jan 2025 PriorAuthPaz (talk) split §Physiology from §Pharmacological exploitation 4,328 bytes ±0 | Revision 13 — 12:40, 26 Feb 2025 LeanMassLars (talk) rm a duplicated category 4,916 bytes +588 | ||
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| 6 | | Confounder = Prevailing insulin sensitivity | 6 | | Confounder = Prevailing insulin sensitivity |
| 7 | }} | 7 | }} |
| + | 8 | {{technical|talk=Readability of the indices section}} | |
| 8 | 9 | ||
| 9 | '''Beta cell function''' is the capacity of the pancreatic beta cell to secrete insulin in amounts appropriate to the prevailing glucose concentration and to the prevailing insulin sensitivity. It is not a single quantity and cannot be measured directly in a living person; every clinical measure is an inference from insulin or [[C-peptide]] concentrations under some defined stimulus.{{r|rorsman2013}} | 10 | '''Beta cell function''' is the capacity of the pancreatic beta cell to secrete insulin in amounts appropriate to the prevailing glucose concentration and to the prevailing insulin sensitivity. It is not a single quantity and cannot be measured directly in a living person; every clinical measure is an inference from insulin or [[C-peptide]] concentrations under some defined stimulus.{{r|rorsman2013}} |
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| 31 | The disposition index is conceptually the strongest of these because it embodies the hyperbolic relationship between secretion and sensitivity: for a given individual the product is approximately constant, and a fall in the product indicates genuine deterioration rather than compensation. Its practical weakness is that it inherits the error of both component measurements.{{r|bergman2002}} | 32 | The disposition index is conceptually the strongest of these because it embodies the hyperbolic relationship between secretion and sensitivity: for a given individual the product is approximately constant, and a fall in the product indicates genuine deterioration rather than compensation. Its practical weakness is that it inherits the error of both component measurements.{{r|bergman2002}} |
| 32 | 33 | ||
| + | 34 | Reference intervals for all of these are population- and assay-specific. A HOMA-B value quoted without the insulin assay it was derived from is not interpretable, because insulin immunoassays differ in cross-reactivity with proinsulin.{{r|rorsman2013,matthews1985}} | |
| + | 35 | ||
| 33 | == References == | 36 | == References == |
| 34 | {{reflist}} | 37 | {{reflist}} |
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| 36 | <ref name="bergman2002">Bergman RN, Ader M, Huecking K, Van Citters G. "Accurate assessment of beta-cell function: the hyperbolic correction." ''Diabetes'' 51 Suppl 1:S212–S220 (2002). PMID 11815482.</ref> | 39 | <ref name="bergman2002">Bergman RN, Ader M, Huecking K, Van Citters G. "Accurate assessment of beta-cell function: the hyperbolic correction." ''Diabetes'' 51 Suppl 1:S212–S220 (2002). PMID 11815482.</ref> |
| 37 | <ref name="drucker2018">Drucker DJ. "Mechanisms of action and therapeutic application of glucagon-like peptide-1." ''Cell Metabolism'' 27(4):740–756 (2018). PMID 29617641.</ref> | 40 | <ref name="drucker2018">Drucker DJ. "Mechanisms of action and therapeutic application of glucagon-like peptide-1." ''Cell Metabolism'' 27(4):740–756 (2018). PMID 29617641.</ref> |
| + | 41 | <ref name="matthews1985">Matthews DR, Hosker JP, Rudenski AS, et al. "Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man." ''Diabetologia'' 28(7):412–419 (1985). PMID 3899825.</ref> | |
| 38 | 42 | ||
| 39 | == See also == | 43 | == See also == |