Bibliographic record
Abstract
This is the third in a series of articles on presentations at the American Diabetes Association Annual Meeting, San Diego, California, 10–14 June 2005. Daniel Drucker (Toronto, Canada) reviewed evidence that the incretin effect, the phenomenon of enteral glucose loading increasing the insulin secretory response to an increase in blood glucose, is reduced in type 2 diabetes, and that the incretin glucagon-like peptide (GLP)-1 may ameliorate this defect. The major limitation to use of GLP-1 in clinical treatment is its rapid clearance by the enzyme dipeptidyl peptidase (DPP)-IV. GLP-1 stimulates insulin secretion, inhibits glucagon secretion, and delays gastric emptying. Loss-of-function studies with a mouse model not expressing the GLP-1 receptor (GLP-1R−/−), and with the GLP-1R antagonist exendin-(9-39), show effects of GLP-1 on the hypothalamic-pituitary-adrenal (HPA) axis, the reproductive system, the portal glucose receptor, gastric motility, and a number of other potential targets. GLP-1R−/− mice have normal insulin sensitivity, arguing against an effect of the system on insulin action, but have glucose intolerance, and administration of exendin-(9-39) similarly is associated with glucose intolerance in mice, in primates, and in humans. Drucker noted that there is controversy as to whether the product of DPP-IV degradation may act at a second GLP-1R, perhaps having additional effects on metabolism, but that GLP-1 does not lower glucose levels in GLP-1R−/− mice, arguing against such a receptor. In the model, pancreatic insulin mRNA levels are reduced and somatostatin mRNA levels are increased. The perfused pancreas isolated from GLP-1R−/− animals shows normal insulin response to glucose, although without response to GLP-1. GLP-1R−/− β-cells appear to have increased sensitivity to the incretin glucose-dependent insulinotropic polypeptide (GIP), perhaps representing an adaptive upregulation of GIP and/or of GIP response, and mice neither expressing the GLP-1 nor the GIP receptor show glucose intolerance with decreased insulin …
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How this classification was reachedexpand
Full frame machine prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.
Distilled classifier scores by category (both heads)
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.001 | 0.001 |
| Meta-epidemiology (narrow) | 0.001 | 0.000 |
| Meta-epidemiology (broad) | 0.001 | 0.001 |
| Bibliometrics | 0.001 | 0.001 |
| Science and technology studies | 0.001 | 0.001 |
| Scholarly communication | 0.003 | 0.002 |
| Open science | 0.001 | 0.002 |
| Research integrity | 0.002 | 0.002 |
| Insufficient payload (model declined to judge) | 0.070 | 0.036 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".