Pharmacological effect of ZYGK1, a novel glucokinase activator, in hyperglycemic and sulfonylurea-resistant type 2 diabetes in mice models.

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Tác giả: Mukul Jain, Amit Joharapurkar, Samadhan Kshirsagar, Ashutosh Kumar, Sunil Metiya, Kalpesh Patani, Rajesh Sundar

Ngôn ngữ: eng

Ký hiệu phân loại: 729.6 Decoration in veneer and incrustation

Thông tin xuất bản: United States : Journal of diabetes and its complications , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 643397

OBJECTIVES: Type 2 diabetes is caused due to inadequate glucose utilization in the liver and pancreas due to insulin resistance. Glucokinase enzyme plays a key role in metabolism of glucose and insulin release and hence glucokinase activation can be a useful therapeutic target for treatment of type 2 diabetes. METHODS: Present study was conducted to investigate the effect of a novel glucokinase activator ZYGK1 in the preclinical models of diabetes in mice. The activity of ZYGK1 was evaluated using recombinant glucokinase, and isolated islets and hepatocytes. Acute effect on glucose disposal was evaluated in C57 mice and repeated dose effect was assessed in db/db mice, along with the evaluation in sulfonylurea-resistance db/db mice. RESULTS: ZYGK1 has potent glucokinase stimulating activity with EC50 of 43 nM and increased glucokinase activity in islets and hepatocytes in a dose-related manner. Oral administration of ZYGK1 (0.1 to 10 mg/kg) showed dose dependently improved glucose disposal and glucose dependent insulin secretion in oral glucose tolerance test (OGTT) in C57 mice. Repeated dose administration of ZYGK1 improved glucose homeostasis and nondiabetic as well as diabetic mice and sulfonylurea-resistant db/db mice. CONCLUSION: ZYGK1 appears to be a potential therapeutic option for the treatment of type 2 diabetes owing to its action in the liver and pancreas, and in conditions resistant to sulfonylurea therapy.
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