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SS-LUP-332 Before and After: Comparison Table
The following table compares physiological and metabolic parameters before SS-LUP-332 administration (baseline/sedentary state) versus after 28 days of compound exposure at research doses, based on published preclinical data. All measurements from C57BL/6 mous
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- The following table compares physiological and metabolic parameters before SS-LUP-332 administration (baseline/sedentary state) versus after 28 days of compound exposure at research doses, based on published preclinical data. All measurements from C57BL/6 mouse models unless noted.
- Mitochondrial Density (% muscle volume)
- 2.3%
- 5.8%
- 6.1%
- Transmission electron microscopy
- ERRα agonism produces mitochondrial expansion comparable to structured endurance training without mechanical stimulus
- Treadmill Endurance (minutes to exhaustion)
- 42 min
- 61 min (45% increase)
- 64 min (52% increase)
- Graded treadmill protocol at 70% VO2 max
- Performance gains without training suggest metabolic, not muscular, adaptation as the primary mechanism
- Glucose Tolerance (AUC during OGTT)
- 28,400 mg/dL·min
- 23,300 mg/dL·min (18% improvement)
- 22,800 mg/dL·min (20% improvement)
- Oral glucose tolerance test with serial blood sampling
- Insulin-independent glucose disposal improves via increased GLUT4 translocation in skeletal muscle
- Respiratory Exchange Ratio (RER at rest)
- 0.92 (glucose-dominant)
- 0.78 (fat-dominant)
- 0.76 (fat-dominant)
- Indirect calorimetry
- Substrate preference shifts from carbohydrate to lipid oxidation at baseline metabolic rate
- Type I Oxidative Muscle Fibers (% of total)
- 22%
- 39%
- 43%
- Immunohistochemical staining for myosin heavy chain isoforms
- Fiber type remodeling occurs without mechanical load—ERRα drives genetic reprogramming independent of contraction
- Liver Triglyceride Content (mg/g tissue)
- 18.4 mg/g
- 12.7 mg/g (31% reduction)
- 11.9 mg/g (35% reduction)
- Biochemical lipid extraction and enzymatic assay
- Hepatic fat oxidation increases via ERRα-driven upregulation of CPT1A (carnitine shuttle enzyme)