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绿原酸对高脂饮食诱导肥胖大鼠糖耐量及其曲线特征的影响

[Effects of chlorogenic acid on glucose tolerance and its curve characteristics in high-fat diet-induced obesity rats].

作者信息

Guo C C, Zhang X Y, Wang Y X, Xie L, Chang C Q

机构信息

Institute of Sports Medicine, Peking University Third Hospital, Beijing 100191, China.

出版信息

Beijing Da Xue Xue Bao Yi Xue Ban. 2020 Apr 18;52(2):269-274. doi: 10.19723/j.issn.1671-167X.2020.02.012.

Abstract

OBJECTIVE

To observe the effect of chlorogenic acid (chlorogenic acid, CGA) on the glucose tolerance and its curve characteristics in high fat diet-induced obesity (diet-induced-obesity, DIO) rats, so as to provide scientific grounds for the development and utilization of CGA in early prevention and reversal of prediabetes.

METHODS

Eight of forty-six male Sprague-Dawley rats were randomly selected as the normal diet group (CON group), and the rest were fed with high-fat diet. After 4 weeks, 24 high-fat-induced obese rats were screened according to the criteria and then randomly divided into high fat diet group (HFD group), 50% CGA group and 98% CGA group. The CGA groups received intragastric administrations of 50% CGA and 98% CGA orally via a gavage needle once a day for 8 weeks, respectively, while the CON and HFD groups received a carrier solution (phosphate buffer saline, PBS). Their body weights were measured weekly and oral glucose tolerance test (OGTT) was performed every 4 weeks. Fasting insulin and insulin release were measured at the end of the study. Meanwhile, HOMA-IR and visceral fat percentage were calculated. Histopathological examination by hematoxylin and eosin staining method were evaluated in the pancreatic tissues.

RESULTS

Before the intervention of chlorogenic acid, blood glucose levels 120 min after glucose loading (P<0.05) and AUC-G (P<0.05) were increased in the HFD group when compared with the CON group, and the time to glucose peak was delayed after 4 weeks of chlorogenic acid intervention (P<0.05). After 8 weeks of intervention, the HOMA-IR index, the insulin levels at 0 min, 30 min, 60 min, and 120 min after glucose loading and AUC-I increased (P<0.05), and the histopathological examination showed obvious hyperplasia of pancreatic islets (P<0.05). Compared with the HFD group, there was no significant change in glucose tolerance and glucose peak time in 50%CGA and 98%CGA groups at the end of 4 weeks of intervention. However, after 8 weeks of intervention, OGTT-60min,OGTT-120min blood glucose (P<0.05) were lower, HOMA-IR index and OGTT-0min, OGTT-120min serum insulin level decreased (P<0.05), the time to glucose peak shifted to an earlier timepoint (P<0.05), abnormal islet hyperplasia attenuated (P<0.05) in 50% CGA and 98% CGA groups. Also, the OGTT-30min serum insulin level was decreased (P<0.05) in 50% CGA group.

CONCLUSION

Delay in time to glucose peak during the OGTT was one of the manifestations of impaired glucose tolerance in DIO rats, and 50% and 98% CGA could improve the glucose tolerance and delay in glucose peak time.

摘要

目的

观察绿原酸(chlorogenic acid,CGA)对高脂饮食诱导肥胖(diet-induced-obesity,DIO)大鼠糖耐量及其曲线特征的影响,为绿原酸在糖尿病前期的早期预防和逆转中的开发利用提供科学依据。

方法

46只雄性Sprague-Dawley大鼠中随机选取8只作为正常饮食组(CON组),其余大鼠给予高脂饮食。4周后,根据标准筛选出24只高脂诱导肥胖大鼠,再随机分为高脂饮食组(HFD组)、50%CGA组和98%CGA组。CGA组分别通过灌胃针每日1次口服给予50%CGA和98%CGA,持续8周,而CON组和HFD组给予载体溶液(磷酸盐缓冲盐水,PBS)。每周测量大鼠体重,每4周进行口服葡萄糖耐量试验(OGTT)。在研究结束时测量空腹胰岛素和胰岛素释放。同时,计算HOMA-IR和内脏脂肪百分比。采用苏木精-伊红染色法对胰腺组织进行组织病理学检查。

结果

在绿原酸干预前,与CON组相比,HFD组葡萄糖负荷后120分钟血糖水平(P<0.05)和AUC-G(P<0.05)升高,绿原酸干预4周后血糖峰值时间延迟(P<0.05)。干预8周后,HOMA-IR指数、葡萄糖负荷后0分钟、30分钟、60分钟和120分钟胰岛素水平及AUC-I升高(P<0.05),组织病理学检查显示胰岛明显增生(P<0.05)。与HFD组相比,干预4周结束时50%CGA和98%CGA组糖耐量和血糖峰值时间无显著变化。然而,干预8周后,50%CGA和98%CGA组OGTT-60min、OGTT-120min血糖水平降低(P<0.05),HOMA-IR指数及OGTT-0min、OGTT-120min血清胰岛素水平降低(P<0.05),血糖峰值时间提前(P<0.05),胰岛异常增生减轻(P<0.05)。此外,50%CGA组OGTT-30min血清胰岛素水平降低(P<0.05)。

结论

OGTT期间血糖峰值时间延迟是DIO大鼠糖耐量受损的表现之一,50%和98%的CGA可改善糖耐量并延迟血糖峰值时间。

相似文献

2
[Establishment of high-fat diet-induced obesity and insulin resistance model in rats].[高脂饮食诱导大鼠肥胖及胰岛素抵抗模型的建立]
Beijing Da Xue Xue Bao Yi Xue Ban. 2020 Jun 18;52(3):557-563. doi: 10.19723/j.issn.1671-167X.2020.03.024.

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