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重塑脂肪组织炎性小体用于2型糖尿病治疗:当前观点与转化策略

Remodeling adipose tissue inflammasome for type 2 diabetes mellitus treatment: Current perspective and translational strategies.

作者信息

Banerjee Amrita, Singh Jagdish

机构信息

Department of Pharmaceutical Sciences North Dakota State University Fargo North Dakota.

出版信息

Bioeng Transl Med. 2019 Dec 13;5(2):e10150. doi: 10.1002/btm2.10150. eCollection 2020 May.

DOI:10.1002/btm2.10150
PMID:32440558
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7237149/
Abstract

Obesity-associated type 2 diabetes mellitus (T2DM) is characterized by low-grade chronic systemic inflammation that arises primarily from the white adipose tissue. The interplay between various adipose tissue-derived chemokines drives insulin resistance in T2DM and has therefore become a subject of rigorous investigation. The adipocytokines strongly associated with glucose homeostasis include tumor necrosis factor-α, various interleukins, monocyte chemoattractant protein-1, adiponectin, and leptin, among others. Remodeling the adipose tissue inflammasome in obesity-associated T2DM is likely to treat the underlying cause of the disease and bring significant therapeutic benefit. Various strategies have been adopted or are being investigated to modulate the serum/tissue levels of pro- and anti-inflammatory adipocytokines to improve glucose homeostasis in T2DM. These include use of small molecule agonists/inhibitors, mimetics, antibodies, gene therapy, and other novel formulations. Here, we discuss adipocytokines that are strongly associated with insulin activity and therapies that are under investigation for modulation of their levels in the treatment of T2DM.

摘要

肥胖相关的2型糖尿病(T2DM)的特征是主要源自白色脂肪组织的低度慢性全身炎症。各种脂肪组织衍生的趋化因子之间的相互作用导致T2DM中的胰岛素抵抗,因此已成为严格研究的对象。与葡萄糖稳态密切相关的脂肪细胞因子包括肿瘤坏死因子-α、各种白细胞介素、单核细胞趋化蛋白-1、脂联素和瘦素等。重塑肥胖相关T2DM中的脂肪组织炎性小体可能会治疗该疾病的根本原因并带来显著的治疗益处。已经采用或正在研究各种策略来调节促炎和抗炎脂肪细胞因子的血清/组织水平,以改善T2DM中的葡萄糖稳态。这些策略包括使用小分子激动剂/抑制剂、模拟物、抗体、基因治疗和其他新型制剂。在这里,我们讨论与胰岛素活性密切相关的脂肪细胞因子以及正在研究的用于调节其水平以治疗T2DM的疗法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e93/7237149/491343dd0297/BTM2-5-e10150-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e93/7237149/ab1bcfc977af/BTM2-5-e10150-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e93/7237149/d62ca8778a9a/BTM2-5-e10150-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e93/7237149/fd4d6a9d968e/BTM2-5-e10150-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e93/7237149/491343dd0297/BTM2-5-e10150-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e93/7237149/ab1bcfc977af/BTM2-5-e10150-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e93/7237149/d62ca8778a9a/BTM2-5-e10150-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e93/7237149/fd4d6a9d968e/BTM2-5-e10150-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e93/7237149/491343dd0297/BTM2-5-e10150-g004.jpg

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