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Bone density and collagen synthesis pathway investigation

These abnormalities were previously regarded as secondary epiphenomena of metabolic dysfunction, but accumulating evidence now indicates that they arise from hyperglycaemia-driven OCTN2 impairment, insulin resistance, and oxidative stress, together forming a distinct carnitine-related metabolic signature

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A (served as the control), B (received 3 mg/kg CdCL2), C (received 100 mg/kg PREOG), D (received 200 mg/kg PREOG), E (received 100 mg/kg PREOG+3 mg/kg CdCL2) and F (received 200 mg/kg PREOG+3 mg/kg CdCL2) treatment continued to postnatal day 29 before weaning

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