Insulin secretion: difference between revisions
Diff·revision 18 → 19·20:33, 12 Jul 2025
Difference between revision 18 and revision 19 of Insulin secretion. 2 lines changed; the page grew by 567 bytes.
| Revision 18 — 11:24, 22 Jun 2025 AnalyticalAnnie (talk) expand §Failure in type 2 diabetes 6,373 bytes ±0 | Revision 19 — 20:33, 12 Jul 2025 MicrodoseMagnus (talk) clarify that the receptor is expressed outside the pancreas 6,940 bytes +567 | ||
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| 39 | Beta-cell secretory failure, not insulin resistance alone, is what converts impaired glucose tolerance into diabetes. Cross-sectional data indicate a substantial loss of functional beta-cell capacity by the time of diagnosis, though estimates vary widely with the method used and post-mortem mass measurements do not track functional estimates closely.{{r|rorsman2013}} | 39 | Beta-cell secretory failure, not insulin resistance alone, is what converts impaired glucose tolerance into diabetes. Cross-sectional data indicate a substantial loss of functional beta-cell capacity by the time of diagnosis, though estimates vary widely with the method used and post-mortem mass measurements do not track functional estimates closely.{{r|rorsman2013}} |
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| + | 41 | Whether the loss is of cell number, of function, or of differentiated identity — beta cells dedifferentiating to a progenitor-like state — is actively debated, and the possibility of dedifferentiation is what makes partial functional recovery after substantial weight loss biologically plausible. Recovery of first-phase secretion has been reported in remission studies following large weight loss, which argues against irreversible loss of mass as the whole explanation.{{r|drucker2018}} See [[Beta cell function]] for the clinical assessment of this capacity. | |
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| 41 | == References == | 43 | == References == |
| 42 | {{reflist}} | 44 | {{reflist}} |