Fructose [7660-25-5]

• Modeling Mechanism：

  ① Fructose consumes ATP during liver metabolism, stimulates purine degradation to produce uric acid, and reduces uric acid excretion; ② Potassium oxalate inhibits uricase activity, blocks uric acid decomposition, and synergistically increases serum uric acid (UA) with fructose; ③ Long-term high fructose intake further induces insulin resistance, dyslipidemia, and liver and kidney damage, mimicking the pathological features of hyperuricemia combined with metabolic syndrome.

• Related Products：

  Fructose (T2954)

• Modeling Method：

  Experimental Subject：

  Rats, Wistar, Male, 7–8 weeks old, Body weight 200–220 g

  Dosage and Administration Route：

  Control group: Equivalent volume saline solution, Intraperitoneal injection (i.p.).
  Hyperuricaemia model group: Potassium oxalate 250 mg/kg, dissolved in physiological saline, intraperitoneal injection (i.p.).
  Hyperuricaemia+Fructose group: ① Potassium oxalate 250 mg/kg dissolved in physiological saline, administered intraperitoneally (i.p.); ② One hour later: Fructose 8 mg/kg dissolved in distilled water, administered via gastric lavage.
  Hyperuricaemia+L-carnitine intervention group: ① Potassium oxalate 250 mg/kg, dissolved in physiological saline, administered via intraperitoneal injection (i.p.); ② Two hours later: L-carnitine 500 mg/kg, administered via intraperitoneal injection (i.p.).
  Hyperuricaemia+Fructose+L-carnitine intervention group: ① Potassium oxalate 250 mg/kg, dissolved in physiological saline, intraperitoneal injection (i.p.);② One hour later: Fructose 8 mg/kg, dissolved in distilled water, oral gavage; ③ A further hour later: L-carnitine 500 mg/kg, intraperitoneal injection (i.p.).

  Dosing Frequency and Duration Model：

  Once daily for 4 consecutive weeks

• Validation：

  1. Biochemical indicators: - Serum UA was significantly elevated (p<0.001), and higher than that of the potassium oxalate model group alone; - Fasting blood glucose (FBG) and HOMA-IR (insulin resistance index) were significantly elevated (p<0.001); - Serum total cholesterol and triglycerides were elevated (p<0.001), and albumin was decreased (p<0.001); - Plasma MDA (malondialdehyde) was elevated, and TAC (total antioxidant capacity) was decreased (p<0.001); 2. Pathological indicators: - Liver: vacuolar degeneration of hepatocytes, fatty infiltration, inflammatory cell infiltration in the portal vein area, and necrosis in some areas; - Kidneys: glomerular atrophy, enlargement of Bowman's capsule, vacuolar degeneration of renal tubular epithelial cells, and hyaline cast formation; 3. Metabolic phenotype: BMI and waist circumference were significantly increased (p<0.05), showing characteristics of abdominal obesity.

*Precautions： The animals were euthanized after the experiment.

*References：El-Kafoury BMA,et,al. Possible role of l-carnitine in improvement of metabolic and hepatic changes in hyperuricemic and hyperuricemic-Fructose-supplemented rats. Physiol Rep. 2019 Nov;7(22):e14282.