Curcumin Improved Glucose Intolerance, Renal Injury, and Nonalcoholic Fatty Liver Disease and Decreased Chromium Loss through Urine in Obese Mice
Curcumin Improved Glucose Intolerance, Renal Injury, and Nonalcoholic Fatty Liver Disease and Decreased Chromium Loss through Urine in Obese Mice
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DOI：
10.3390/pr9071132
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发表时间：
2021-07-01
期刊：
影响因子：
3.5
通讯作者：
Lin, Chuen-Fu
中科院分区：
文献类型：
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作者：
Chang, Geng-Ruei;Hsieh, Wen-Tsong;Lin, Chuen-Fu
肥胖相关的高血糖是胰岛素抵抗、糖耐量异常和相关代谢紊乱的基础，包括2型糖尿病、肾脏损害和非酒精性脂肪性肝病。姜黄根在亚洲普遍使用，姜黄素是其药理成分之一，可起到预防和治疗某些慢性生理疾病的作用。因此，这项研究考察了姜黄素如何通过改变小鼠脂肪肝评分、铬分布和肾脏损伤来降低高脂饮食(HFD)引起的高血糖和高脂血症。与对照组相比，同样饲喂高脂饲料的姜黄素组小鼠体重减轻，脂肪细胞体积变小，日摄食效率、血尿素氮和肌酐水平、血清丙氨酸氨基转移酶和天冬氨酸氨基转移酶水平、血清和肝脏甘油三酯水平以及肝脂调节标志物的表达也较低。姜黄素治疗肥胖组的空腹血糖显著降低，糖耐量减低，Akt磷酸化和葡萄糖转运蛋白4(GLUT4)表达增加，血清胰岛素水平升高。此外，这组患者表现出肾脏损伤，肿瘤坏死因子-α表达降低，同时肾脏抗氧化酶数量增加，包括超氧化物歧化酶、谷胱甘肽过氧化物酶和过氧化氢酶。姜黄素治疗的肥胖小鼠的肝脏组织学显示，与对照组相比，脂肪渗透明显增加，FASN和PNPLA3蛋白减少。姜黄素通过减少尿液中铬的损失量，有助于创造正的铬平衡，导致缓解高血糖所需的铬动员。因此，研究结果表明，姜黄素可预防高脂饮食引起的糖耐量减低、肾脏损伤和非酒精性脂肪性肝病。
Obesity-associated hyperglycemia underlies insulin resistance, glucose intolerance, and related metabolic disorders including type 2 diabetes, renal damage, and nonalcoholic fatty liver disease. Turmeric root is commonly used in Asia, and curcumin, one of its pharmacological components, can play a role in preventing and treating certain chronic physiological disorders. Accordingly, this study examined how high-fat diet (HFD)-induced hyperglycemia and hyperlipidemia are reduced by curcumin through changes in fatty liver scores, chromium distribution, and renal injury in mice. Relative to the control group, also fed an HFD, the curcumin group weighed less and had smaller adipocytes; it also had lower daily food efficiency, blood urea nitrogen and creatinine levels, serum alanine aminotransferase and aspartate aminotransferase levels, serum and hepatic triglyceride levels, and hepatic lipid regulation marker expression. The curcumin-treated obese group exhibited significantly lower fasting blood glucose, was less glucose intolerant, had higher Akt phosphorylation and glucose transporter 4 (GLUT4) expression, and had greater serum insulin levels. Moreover, the group showed renal damage with lower TNF-alpha expression along with more numerous renal antioxidative enzymes that included superoxide dismutase, glutathione peroxidase, and catalase. The liver histology of the curcumin-treated obese mice showed superior lipid infiltration and fewer FASN and PNPLA3 proteins in comparison with the control mice. Curcumin contributed to creating a positive chromium balance by decreasing the amount of chromium lost through urine, leading to the chromium mobilization needed to mitigate hyperglycemia. Thus, the results suggest that curcumin prevents HFD-induced glucose intolerance, kidney injury, and nonalcoholic fatty liver disease.