Literature DB >> 33219494

Antidiabetic compounds 8a, 8b, 8k, and 9h enhance insulin secretion: activity and mechanism.

Hui Li1, Jian Zhang1, Yongli Fu1, Yixin Zhang1, Chunhui Zhang1, Xiaozhu Sun1, Fang Wu2, Jing He3.   

Abstract

PURPOSE: This study primarily investigated the effects of hypoglycemic compounds (Imeglimin derivatives) on insulin secretion in type 2 diabetes mellitus (T2DM), and further explored the possible mechanism underlying these effects.
METHODS: Firstly, Metformin was used as the initiating compound to synthesize three sets of derivatives which contained Imeglimin structure core. At the cellular level, we screened compounds with better effect on the activity of insulin receptor tyrosine protein kinase (IFcTPK) after the islet β cells were treated with the compounds of different concentrations. The insulin secretion was assessed using radioimmunoassay and the cytotoxicity to islet β cells was evaluated by means of MTT assay following treatment with the compounds. The Ca2+-related mechanism by which these compounds promote insulin secretion was elucidated with whole cell recordings from current-clamp mode.
RESULTS: Totally, 48 synthesized compounds were generated, wherein 10 compounds could increase the activity of IFcTPK in HIT-T15 cells better among these compounds. The modified Imeglimin, especially in the structure of hydrophilic hydroxyl or piperidine rings, could improve the activity of the compound to promote insulin secretion. Furthermore, the compounds 8a, 8b, 8k, and 9h revealed high insulin secretion-promoting activity. These compounds enhanced insulin secretion in islet β cells by repressing the ATP-sensitive K(+) and voltage-gated K+ pathway.
CONCLUSIONS: Our findings indicate that the hypoglycemic compounds 8a, 8b, 8k, and 9h confer better promotive effect on insulin secretion, which provides a reference for the development of drugs with better hypoglycemic activity.

Entities:  

Keywords:  ATP-sensitive K(+) channel; Hypoglycemic compounds; Imeglimin derivatives; Insulin secretion; Type 2 diabetes mellitus; Voltage-gated K+ channel

Year:  2020        PMID: 33219494     DOI: 10.1007/s12020-020-02537-5

Source DB:  PubMed          Journal:  Endocrine        ISSN: 1355-008X            Impact factor:   3.633


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