Skeletal muscle as a source of IGFBP-2 in a murine model of metabolic dysfunction associated with steatotic liver disease.
Bibliographic record
Abstract
Insulin-like Growth Factor Binding Protein (IGFBP)-2 is lower in serum during obesity and metabolic dysfunction. We have previously shown that the decrease in serum IGFBP-2 follows a diminished expression in liver and heart, both associated with the progression of steatotic liver disease. We aimed to identify, in a murine model, the synthesis of IGFBP-2 in extrahepatic tissues involved in metabolic dysfunction: skeletal muscle and adipose tissue. Samples of hamstring muscle, and epididymal adipose tissue were obtained from male C57BL/6 mice, fed a high-fat diet supplemented with sucrose and fructose (42g/L) in the beverage during 6 months. All procedures were approved by the Institutional Committee of Care and Use of Laboratory Animals at the School of Medicine, UNAM (FM/DI/005/2022). Four groups were included: Control; Metabolic dysfunction (MD), exhibiting increased bodyweight and adiposity; MD with steatosis (MD+SS); and MD+SS with fibrosis (MD+SS+F). Total protein was isolated in a protease inhibitor cocktail. Protein integrity was assessed by SDS-PAGE. IGFBP-2 was assayed by ELISA. Data was shown as Mean±SD, analyzed by one-way ANOVA; Student´s t test was applied to compare 2 groups. P<0.05 was considered significant. IGFBP-2 expression was 6-fold increased in control skeletal muscle compared to control adipose tissue. In epididymal adipose tissue, IGFBP-2 expression significantly decreased in MD+SS+F compared to Controls, and MD. In contrast, the hamstring showed increased IGFBP-2 expression in mice showing metabolic dysfunction associated with steatotic liver disease: MD+SS and MD+SS+F. The percentage of adiposity significantly increased in MD subjects whereas no changes were observed regarding muscle mass, suggesting hypertrophy might be key. Our results show that metabolic dysfunction (MD) associated with MASLD have a role in inhibiting IGFBP-2 expression in adipose tissue. In contrast, skeletal muscle increases its synthesis. These results suggest a role for skeletal muscle in the reversion of MASLD through IGFBP-2 expression. More studies are needed to identify the roles of skeletal muscle and its hypertrophic state in MASLD.
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.
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 | 0.000 | 0.000 |
| Meta-epidemiology (narrow) | 0.000 | 0.000 |
| Meta-epidemiology (broad) | 0.001 | 0.000 |
| 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 | 0.000 |
| 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".