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皮下脂肪库中脂肪细胞增生的诱导减轻了肥胖小鼠的2型糖尿病症状。

Induction of adipocyte hyperplasia in subcutaneous fat depot alleviated type 2 diabetes symptoms in obese mice.

作者信息

Lu Qiqi, Li Mingming, Zou Yu, Cao Tong

机构信息

Faculty of Dentistry, National University of Singapore, Singapore, Singapore; Faculty of Dentistry NUS Graduate School for Integrative Science and Engineering, National University of Singapore, Singapore, Singapore.

出版信息

Obesity (Silver Spring). 2014 Jul;22(7):1623-31. doi: 10.1002/oby.20705. Epub 2014 Feb 11.

Abstract

OBJECTIVE

The role of subcutaneous adipose tissue (SAT) in the pathogenesis of type 2 diabetes is still under controversy. In this study, the metabolic effects of inducing adipocyte hyperplasia in SAT depots in obese mice were investigated.

METHODS

High fat diet was used to induce obesity and type 2 diabetes symptoms in C57BL6/J mice. To induce SAT expansion through hyperplasia, acellular adipogenic cocktails were injected around the SAT depots in high fat diet-induced obese mice.

RESULTS

Ten weeks after injections, significant neoadipogenesis was induced, which not only obviously expanded the volume of SATs but also significantly increased the adipocyte density within the whole SAT depots. Importantly, these mice exhibited improved glucose tolerance and insulin sensitivity (homeostatic model assessment) when compared to control group. Further studies suggested that these beneficial metabolic effects were associated with elevation of serum high-molecular-weight adiponectin level and reduction of ectopic lipid accumulation in liver.

CONCLUSIONS

These findings not only further supported the protective role of SAT in the pathogenesis of type 2 diabetes but also highlighted the importance of adipocyte hyperplasia in this protective effect.

摘要

目的

皮下脂肪组织(SAT)在2型糖尿病发病机制中的作用仍存在争议。本研究调查了在肥胖小鼠的SAT库中诱导脂肪细胞增生的代谢效应。

方法

采用高脂饮食诱导C57BL6/J小鼠肥胖和2型糖尿病症状。为通过增生诱导SAT扩张,向高脂饮食诱导的肥胖小鼠的SAT库周围注射无细胞脂肪生成混合物。

结果

注射后10周,诱导了显著的新生脂肪形成,这不仅明显扩大了SAT的体积,还显著增加了整个SAT库内的脂肪细胞密度。重要的是,与对照组相比,这些小鼠表现出改善的葡萄糖耐量和胰岛素敏感性(稳态模型评估)。进一步研究表明,这些有益的代谢效应与血清高分子量脂联素水平升高和肝脏异位脂质积累减少有关。

结论

这些发现不仅进一步支持了SAT在2型糖尿病发病机制中的保护作用,还突出了脂肪细胞增生在这种保护作用中的重要性。

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