Objective: To study the animal model and lipid metabolism of quail hyperuricemia.
Method: After giving quail high fat for 30 days, take adenine (50 mg/head) orally for 7 days to establish a quail hyperuricemia model. After 22 days of observation, blood will be collected to detect uric acid and xanthine oxidase in the blood. , Creatinine (CRE), urea nitrogen (BUN), triglycerides (TG), low density lipoprotein (LDL), high density lipoprotein (HDL), total cholesterol (CHO), xanthine oxidase (XOD), Liver lipase (HL)), lipoprotein lipase (LPL), adenosine dehydrogenase (ADA) lipid metabolism indicators require histopathological examination of joints and kidneys.
Results: The blood uric acid of the model control group animals increased significantly (P\u003c0.01), CRE, BUN, TG, LDL and XOD increased significantly (P\u003c0.05 or P\u003c0) ..01), serum CHO , LPL, ADA, HDL content was significantly reduced (P\u003c0.05). After modeling, the animal’s toe joints were significantly swollen, and the surrounding soft tissues were swollen. X-rays showed that the bone density of the toes was reduced, and part of the joint surface was damaged due to osteolytic injury. Pathological examination revealed that the joint synovial membrane was hyperplasia, inflammatory cells infiltrated a lot, part of which was replaced by fibrotic connective tissue, uric acid crystals in renal tubules and renal tissue, and the renal tubules were slightly dilated, indicating the proliferation of renal interstitial fibrosis. Many inflammatory cells infiltrate.
Conclusion: This model suffers from kidney diseases, such as joint swelling and kidney uric acid deposition, and is related to impaired lipid metabolism. The pathological mechanism is related to the activity of XOD and ADA-related lipid metabolism enzymes.