糖尿病发展对初级和次级胆汁酸浓度药理学的调节性纳米/微米效应。
Modulatory Nano/Micro Effects of Diabetes Development on Pharmacology of Primary and Secondary Bile Acids Concentrations.
作者信息
Mooranian Armin, Zamani Nassim, Takechi Ryu, Luna Giuseppe, Mikov Momir, Goločorbin-Kon Svetlana, Kovacevic Bozica, Arfuso Frank, Al-Salami Hani
机构信息
Biotechnology and Drug Development Research Laboratory, School of Pharmacy and Biomedical Sciences, Curtin Health Innovation Research Institute, Curtin University, Perth, Western Australia, Australia.
School of Public Health, Curtin Health Innovation Research Institute, Curtin University, Perth, Western Australia, Australia.
出版信息
Curr Diabetes Rev. 2020;16(8):900-909. doi: 10.2174/1389450121666200204115121.
BACKGROUND
Recent studies have suggested that hyperglycaemia influences the bile acid profile and concentrations of secondary bile acids in the gut.
INTRODUCTION
This study aimed to measure changes in the bile acid profile in the gut, tissues, and faeces in type 1 Diabetes (T1D) and Type 2 Diabetes (T2D).
METHODS
T1D and T2D were established in a mouse model. Twenty-one seven-weeks old balb/c mice were randomly divided into three equal groups, healthy, T1D and T2D. Blood, tissue, urine and faeces samples were collected for bile acid measurements.
RESULTS
Compared with healthy mice, T1D and T2D mice showed lower levels of the primary bile acid, chenodeoxycholic acid, in the plasma, intestine, and brain, and higher levels of the secondary bile acid, lithocholic acid, in the plasma and pancreas. Levels of the bile acid ursodeoxycholic acid were undetected in healthy mice but were found to be elevated in T1D and T2D mice.
CONCLUSION
Bile acid profiles in other organs were variably influenced by T1D and T2D development, which suggests similarity in effects of T1D and T2D on the bile acid profile, but these effects were not always consistent among all organs, possibly since feedback mechanisms controlling enterohepatic recirculation and bile acid profiles and biotransformation are different in T1D and T2D.
背景
近期研究表明，高血糖会影响肠道中胆汁酸谱及次级胆汁酸的浓度。
引言
本研究旨在测量1型糖尿病（T1D）和2型糖尿病（T2D）小鼠肠道、组织和粪便中胆汁酸谱的变化。
方法
在小鼠模型中建立T1D和T2D。将21只7周龄的balb/c小鼠随机分为三组，即健康组、T1D组和T2D组。采集血液、组织、尿液和粪便样本进行胆汁酸测量。
结果
与健康小鼠相比，T1D和T2D小鼠血浆、肠道和大脑中的初级胆汁酸鹅去氧胆酸水平较低，而血浆和胰腺中的次级胆汁酸石胆酸水平较高。健康小鼠中未检测到熊去氧胆酸水平，但在T1D和T2D小鼠中发现其升高。
结论
T1D和T2D的发展对其他器官的胆汁酸谱有不同程度的影响，这表明T1D和T2D对胆汁酸谱的影响具有相似性，但这些影响在所有器官中并不总是一致的，可能是因为T1D和T2D中控制肠肝循环、胆汁酸谱和生物转化的反馈机制不同。
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