Abstract 647: Hyperglycemia Increases Diet-Induced Coronary Artery Disease and Myocardial Infarction in SRBI Knockout ApoE-Hypomorphic Mice
Bibliographic record
Abstract
Background: Type I diabetes is characterized by high levels of glucose and free fatty acids in plasma. Several epidemiological studies have established diabetes as an independent risk factor for the development of cardiovascular disease. Diabetic animal models have shown increased development of aortic atherosclerosis, however the impact on coronary artery (CA) disease is less clear. Conventional mouse models of atherosclerosis do not reproducibly develop CA atherosclerosis. The HDL receptor, SRBI, has been associated with protection against atherosclerosis. SRBI knockout (KO) ApoE-hypomorphic mice exhibit increased aortic sinus atherosclerosis and diet-induced occlusive CA atherosclerosis when compared to SRBI+/+ ApoE-hypomorphic mice. We assessed the hypothesis that diabetes will increase the development of CA and aortic atherosclerosis and myocardial infarction in SRBI KO ApoE-hypomorphic mice. Methods: Hyperglycemia was induced by multiple low-dose i.p. injections of streptozotocin (40 mg/kg body weight). Controls received vehicle. Mice were fed a regular chow diet for 11 weeks (n=6-7) or a high-fat/high-cholesterol diet for 4 weeks (n=14-15). CA and aortic atherosclerosis and cardiac fibrosis were evaluated. Results: Diabetic SRBI KO ApoE-hypomorphic mice maintained on normal chow diet exhibited small plaques in the aortic sinus and the burden of atherosclerosis in CA was low. No fibrosis in hearts was detected. When mice were challenged with a high-fat/high-cholesterol diet, survival was significantly reduced in the diabetic group (p<0.01 vs control). High-fat/high-cholesterol diet fed diabetic mice exhibited significantly larger plaques in the aortic sinus as well (p<0.05 vs control). CA atherosclerosis burden was increased (p<0.001 vs control) along with higher levels of cardiac fibrosis (p<0.01 vs control). Conclusion: Hyperglycemia significantly increased the burden of aortic and CA atherosclerosis and cardiac fibrosis in SRBI KO ApoE-hypomorphic mice fed a high-fat/high-cholesterol diet.
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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 | 0.000 | 0.000 |
| Meta-epidemiology (narrow) | 0.001 | 0.001 |
| Meta-epidemiology (broad) | 0.001 | 0.001 |
| Bibliometrics | 0.001 | 0.000 |
| Science and technology studies | 0.000 | 0.000 |
| Scholarly communication | 0.001 | 0.000 |
| Open science | 0.000 | 0.000 |
| Research integrity | 0.001 | 0.002 |
| Insufficient payload (model declined to judge) | 0.005 | 0.001 |
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".