Intra-uterine programming of the endocrine pancreas
Why this work is in the frame
A frame that forgets how it found something cannot be audited. These are the routes that admitted this work.
Bibliographic record
Abstract
In altricial species such as the rat and mouse, there is good evidence for the intra-uterine programming of the endocrine pancreas. Changes in the intra-uterine nutritional environment cause alterations in the structure and function of the islets which have life-long effects and predispose the animal to glucose intolerance and diabetes in later life. In rodents, the islets develop relatively late in gestation and undergo substantial remodelling in the period immediately after birth. Hence, the critical window for islet development in these animals is short and readily accessible for experimental manipulation. The short life-span of these species also means that elderly animals can be studied within a reasonable time frame. In precocious species, such as guinea pigs and farm animals, intra-uterine programming of the endocrine pancreas is less well established. In part, this may be due to difficulties in identifying the critical window for development as islet formation and remodelling begin at an earlier stage of gestation and continue for longer after birth. The long life-span of these animals and the relative insulin resistance of adult ruminants compared to other species also make it difficult to establish whether fetal changes in islet development have long-term consequences. In the human, the main phase of islet development occurs during the second trimester, although remodelling occurs throughout late gestation and early childhood. There is, therefore, a relatively long period in which early changes in islet development could be reversed or ameliorated in the human. Although the human epidemiological observations suggest that the fetal origin of adult glucose intolerance is due primarily to changes in insulin sensitivity rather than to defective insulin secretion, subtle changes in islet morphology and function sustained in utero may well contribute to the increased susceptibility to type 2 diabetes observed in adults who were growth-retarded in utero.
Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.
Full frame distilled prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. Learned from the 10,348 direct Codex labels and 10,348 direct Gemma labels. Candidate is the union of thresholded teacher heads; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels or direct frontier model labels.
Codex and Gemma teacher scores by category
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.000 | 0.004 |
| Meta-epidemiology (narrow) | 0.000 | 0.000 |
| Meta-epidemiology (broad) | 0.002 | 0.001 |
| Bibliometrics | 0.000 | 0.000 |
| Science and technology studies | 0.000 | 0.000 |
| Scholarly communication | 0.000 | 0.000 |
| Open science | 0.000 | 0.000 |
| Research integrity | 0.000 | 0.001 |
| Insufficient payload (model declined to judge) | 0.019 | 0.000 |
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 it