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目的:在果糖诱导大鼠产生高尿酸血症、高胰岛素血症等胰岛素抵抗综合征的基础上进一步研究果糖能否引起瘦素功能失调及抗高尿酸血症剂天然产物槲皮素和芦丁的改善作用。方法:大鼠饮用10%果糖水溶液共8周。第4周后分别口服给予大鼠槲皮素和芦丁,并以别嘌呤醇为阳性对照药。分别测定给药前及最后一次给药后血清尿酸和胰岛素等水平。选择血清和下丘脑瘦素水平及脂肪组织瘦素分泌水平为指标评价果糖诱导大鼠体内瘦素功能的变化。选择血清甘油三酯、高密度脂蛋白和低密度脂蛋白水平为指标评价果糖诱导大鼠体内血脂失调。结果:果糖显著提高大鼠血清尿酸、胰岛素和瘦素等水平,并伴有血脂失调。再者,果糖显著上调大鼠脂肪组织ob基因的表达以增加脂肪分泌瘦素的功能。槲皮素、芦丁及别嘌呤醇可显著逆转果糖所致大鼠血清瘦素、血脂及脂肪分泌瘦素功能的异常。进一步研究发现果糖显著降低大鼠下丘脑瘦素水平,而槲皮素、芦丁和别嘌呤醇却无明显改善作用。结论:果糖能诱导大鼠产生高瘦素血症及下丘脑瘦素缺乏症,这与果糖所诱导大鼠高胰岛素血症、高甘油三酯血症和高尿酸血症等胰岛素抵抗综合征密切相关。天然降尿酸剂槲皮素和芦丁可通过逆转果糖所诱导大鼠高胰岛素血症及血脂失调症的作用改善果糖所致大鼠瘦素功能失调。本研究为果糖引起高瘦素血症与高尿酸血症之间的联系提供了直接的证据,并从药理学的角度进一步解释了降尿酸剂改善果糖所致胰岛素抵抗综合征大鼠的高尿酸血症和瘦素功能紊乱的作用机制。
OBJECTIVE: To further investigate whether fructose can cause leptin dysfunction and the natural products quercetin and rutin against hyperuricemia on the basis of fructose-induced insulin resistance syndromes such as hyperuricemia and hyperinsulinemia in rats. The improvement effect. Methods: Rats drank 10% aqueous fructose for 8 weeks. After the fourth week, rats were orally given quercetin and rutin, and allopurinol was used as a positive control. Serum uric acid and insulin levels were measured before and after the last administration. Serum and hypothalamic leptin levels and adipose tissue leptin secretion were selected as indexes to evaluate the changes of leptin function in fructose-induced rats. Serum triglyceride, high-density lipoprotein, and low-density lipoprotein levels were selected as indicators to evaluate fructose-induced dyslipidemia in rats. RESULTS: Fructose significantly increased serum uric acid, insulin, and leptin levels in rats and was associated with dyslipidemia. Furthermore, fructose significantly up-regulated the expression of ob gene in rat adipose tissue to increase the function of fat to secrete leptin. Quercetin, rutin and allopurinol significantly reversed the abnormality of serum leptin, lipids, and leptin secretion in rats induced by fructose. Further research found that fructose significantly reduced the rat’s hypothalamus leptin levels, while quercetin, rutin and allopurinol had no significant improvement. CONCLUSION: Fructose can induce hyperleptinemia and hypothalamus leptin deficiency in rats, which is closely related to insulin resistance syndrome such as hyperinsulinemia, hypertriglyceridemia and hyperuricemia induced by fructose in rats. The natural uric acid lowering agents quercetin and rutin can improve fructose-induced leptin dysfunction in rats by reversing fructose-induced hyperinsulinemia and dyslipidemia. This study provided direct evidence for the link between hyperleptinemia and hyperuricemia induced by fructose, and further explained the pharmacological perspective of uric acid lowering the hyperuricemia in rats with insulin resistance syndrome caused by fructose. The mechanism of action of leptin dysfunction.