Depot- and obesity-related differences in adipogenesisAdipocyte hypertrophy and hyperplasia are known to facilitate lipid storage in adipose tissues by increasing adipocyte cell size and number, respectively. Adipogenesis is the process resulting in adipose tissue hyperplasia. Although depot-specific differences and obesity-related modulation of adipocyte size are well documented, available data on adipogenesis and adipose tissue hyperplasia are less conclusive. Most studies support a reduction of adipogenesis in the obese state. Preadipocytes of the subcutaneous fat depot appear to be more responsive to adipogenic stimulation compared with those from visceral fat compartments in most studies. A number of studies support the notion that adipose tissue expansion through hyperplasia reduces ectopic lipid excess and obesity-related complications. Several genetic variants have been identified in the genes coding for adipogenesis-regulating proteins. While some of these variants have been clearly associated with the phenotypes of obesity and obesity-related alterations, available data highlight the importance of considering gene–gene and gene–diet interactions.
Bibliographic record
Abstract
Adipocyte hypertrophy and hyperplasia are known to facilitate lipid storage in adipose tissues by increasing adipocyte cell size and number, respectively. Adipogenesis is the process resulting in adipose tissue hyperplasia.Although depot-specific differences and obesity-related modulation of adipocyte size are well documented,available data on adipogenesis and adipose tissue hyperplasia are less conclusive. Most studies support a reduction of adipogenesis in the obese state. Preadipocytes of the subcutaneous fat depot appear to be more responsive to adipogenic stimulation compared with those from visceral fat compartments in most studies. A number of studies support the notion that adipose tissue expansion through hyperplasia reduces ectopic lipid excess and obesity-related complications. Several genetic variants have been identified in the genes coding for adipogenesis-regulating proteins. While some of these variants have been clearly associated with the phenotypes of obesity and obesity-related alterations, available data highlight the importance of considering gene–gene and gene–diet interactions.
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How this classification was reachedexpand
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 | 0.003 | 0.002 |
| Meta-epidemiology (narrow) | 0.001 | 0.001 |
| Meta-epidemiology (broad) | 0.002 | 0.000 |
| Bibliometrics | 0.000 | 0.001 |
| Science and technology studies | 0.001 | 0.002 |
| Scholarly communication | 0.000 | 0.001 |
| Open science | 0.001 | 0.001 |
| Research integrity | 0.000 | 0.000 |
| Insufficient payload (model declined to judge) | 0.000 | 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 itClassification
machine, unvalidatedMachine predicted; a candidate call from one teacher head, 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".