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腺嘌呤诱导的慢性肾病和高胆固醇血症小鼠血浆脂质和动脉粥样硬化的反常降低

Paradoxical reduction of plasma lipids and atherosclerosis in mice with adenine-induced chronic kidney disease and hypercholesterolemia.

作者信息

Padalkar Mugdha V, Tsivitis Alexandra H, Gelfman Ylona, Kasiyanyk Mariya, Kaungumpillil Neil, Ma Danyang, Gao Michael, Borges Kelly A, Dhaliwal Puneet, Nasruddin Saud, Saji Sruthi, Gilani Hina, Schram Eric J, Singh Mohnish, Plummer Maria M, Savinova Olga V

机构信息

Department of Biomedical Sciences, New York Institute of Technology College of Osteopathic Medicine, Old Westbury, NY, United States.

Department of Clinical Specialties, New York Institute of Technology College of Osteopathic Medicine, Old Westbury, NY, United States.

出版信息

Front Cardiovasc Med. 2023 Feb 9;10:1088015. doi: 10.3389/fcvm.2023.1088015. eCollection 2023.

Abstract

BACKGROUND

Atherosclerotic cardiovascular disease is prevalent among patients with chronic kidney disease (CKD). In this study, we initially aimed to test whether vascular calcification associated with CKD can worsen atherosclerosis. However, a paradoxical finding emerged from attempting to test this hypothesis in a mouse model of adenine-induced CKD.

METHODS

We combined adenine-induced CKD and diet-induced atherosclerosis in mice with a mutation in the low-density lipoprotein receptor gene. In the first study, mice were co-treated with 0.2% adenine in a western diet for 8 weeks to induce CKD and atherosclerosis simultaneously. In the second study, mice were pre-treated with adenine in a regular diet for 8 weeks, followed by a western diet for another 8 weeks.

RESULTS

Co-treatment with adenine and a western diet resulted in a reduction of plasma triglycerides and cholesterol, liver lipid contents, and atherosclerosis in co-treated mice when compared with the western-only group, despite a fully penetrant CKD phenotype developed in response to adenine. In the two-step model, renal tubulointerstitial damage and polyuria persisted after the discontinuation of adenine in the adenine-pre-treated mice. The mice, however, had similar plasma triglycerides, cholesterol, liver lipid contents, and aortic root atherosclerosis after being fed a western diet, irrespective of adenine pre-treatment. Unexpectedly, adenine pre-treated mice consumed twice the calories from the diet as those not pre-treated without showing an increase in body weight.

CONCLUSION

The adenine-induced CKD model does not recapitulate accelerated atherosclerosis, limiting its use in pre-clinical studies. The results indicate that excessive adenine intake impacts lipid metabolism.

摘要

背景

动脉粥样硬化性心血管疾病在慢性肾脏病(CKD)患者中很常见。在本研究中,我们最初旨在测试与CKD相关的血管钙化是否会加重动脉粥样硬化。然而,在试图在腺嘌呤诱导的CKD小鼠模型中验证这一假设时出现了一个矛盾的发现。

方法

我们将腺嘌呤诱导的CKD与饮食诱导的动脉粥样硬化相结合,应用于低密度脂蛋白受体基因突变的小鼠。在第一项研究中,小鼠在西式饮食中同时接受0.2%腺嘌呤治疗8周,以同时诱导CKD和动脉粥样硬化。在第二项研究中,小鼠先在常规饮食中接受腺嘌呤预处理8周,然后再接受西式饮食8周。

结果

与仅接受西式饮食的组相比,腺嘌呤与西式饮食联合治疗导致联合治疗小鼠的血浆甘油三酯和胆固醇、肝脏脂质含量以及动脉粥样硬化减少,尽管对腺嘌呤产生了完全显性的CKD表型。在两步模型中,腺嘌呤预处理小鼠停止使用腺嘌呤后,肾小管间质损伤和多尿持续存在。然而,无论是否进行腺嘌呤预处理,这些小鼠在接受西式饮食后,其血浆甘油三酯、胆固醇、肝脏脂质含量和主动脉根部动脉粥样硬化情况相似。出乎意料的是,腺嘌呤预处理小鼠从饮食中摄入的热量是未预处理小鼠的两倍,但体重并未增加。

结论

腺嘌呤诱导的CKD模型不能重现加速的动脉粥样硬化,限制了其在临床前研究中的应用。结果表明,过量摄入腺嘌呤会影响脂质代谢。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c3aa/9947538/f749a082e790/fcvm-10-1088015-g001.jpg

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