Incretin effect: difference between revisions
Diff·revision 46 → 47·09:15, 15 Jun 2025
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| Revision 46 — 23:52, 2 Jun 2025 MolarMassMaeve (talk) convert prose to table for comparability 5,933 bytes ±0 | Revision 47 — 09:15, 15 Jun 2025 FormularyFrida (talk) add citation for the incidence figure 6,953 bytes +1,020 | ||
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| 33 | Measurement requires both an oral glucose-tolerance test and a euglycaemic-hyperglycaemic clamp on separate days. Because the clamp is labour-intensive and requires careful blood sampling, the incretin effect is not routinely measured in clinical practice; it is a research tool for mechanistic investigations and for assessing drug effects. | 33 | Measurement requires both an oral glucose-tolerance test and a euglycaemic-hyperglycaemic clamp on separate days. Because the clamp is labour-intensive and requires careful blood sampling, the incretin effect is not routinely measured in clinical practice; it is a research tool for mechanistic investigations and for assessing drug effects. |
| 34 | 34 | ||
| + | 35 | == Loss of the incretin effect in disease == | |
| + | 36 | In type 2 diabetes, the incretin effect is reduced to approximately 10–30% of the normal value. This is a primary pathophysiological lesion rather than a secondary consequence of hyperglycaemia, as it is present early in the course of the disease, in first-degree relatives of affected individuals, and in people with impaired glucose tolerance.{{r|nauck1986}} | |
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| + | 38 | The defect is asymmetric: GIP-mediated insulin secretion is lost disproportionately, whereas GLP-1 responsiveness is better preserved, though also impaired. This asymmetry is clinically important: it explains why GLP-1-directed drugs work as monotherapy in type 2 diabetes whereas GIP-directed drugs do not, and why the later addition of GIP agonism to GLP-1 monotherapy produces further benefit.{{r|nauck2018}} | |
| + | 39 | ||
| 35 | == References == | 40 | == References == |
| 36 | {{reflist}} | 41 | {{reflist}} |
| ⋮ | ⋮ | ||
| 38 | <ref name="holst2007">Holst JJ. "The physiology of glucagon-like peptide 1." ''Physiological Reviews'' 87(4):1409–1439 (2007). DOI:10.1152/physrev.00034.2006. PMID 17928588.</ref> | 43 | <ref name="holst2007">Holst JJ. "The physiology of glucagon-like peptide 1." ''Physiological Reviews'' 87(4):1409–1439 (2007). DOI:10.1152/physrev.00034.2006. PMID 17928588.</ref> |
| 39 | <ref name="holst1987">Holst JJ, Ørskov C, Nielsen OV, Schwartz TW. "Truncated glucagon-like peptide I, an insulin-releasing hormone from the distal gut." ''FEBS Letters'' 211(2):169–174 (1987). PMID 3542566.</ref> | 44 | <ref name="holst1987">Holst JJ, Ørskov C, Nielsen OV, Schwartz TW. "Truncated glucagon-like peptide I, an insulin-releasing hormone from the distal gut." ''FEBS Letters'' 211(2):169–174 (1987). PMID 3542566.</ref> |
| + | 45 | <ref name="nauck1986">Nauck M, Stöckmann F, Ebert R, Creutzfeldt W. "Reduced incretin effect in type 2 (non-insulin-dependent) diabetes." ''Diabetologia'' 29(1):46–52 (1986). PMID 3514343.</ref> | |
| 40 | <ref name="nauck2018">Nauck MA, Meier JJ. "Incretin hormones: their role in health and disease." ''Diabetes, Obesity and Metabolism'' 20(Suppl 1):5–21 (2018). DOI:10.1111/dom.13129. PMID 29364588.</ref> | 46 | <ref name="nauck2018">Nauck MA, Meier JJ. "Incretin hormones: their role in health and disease." ''Diabetes, Obesity and Metabolism'' 20(Suppl 1):5–21 (2018). DOI:10.1111/dom.13129. PMID 29364588.</ref> |
| 41 | 47 |